The purpose of the Behavior Genetics Association is to promote scientific study of the interrelationship of genetic mechanisms and behavior, both human and animal; to encourage and aid the education and training of research workers in the field of behavior genetics; and to aid in the dissemination and interpretation to the general public of knowledge concerning the interrelationship of genetics and behavior, and its implications for health and human development and education.
For additional information about the Behavior Genetics Association, please contact Dr. Hermine Maes BGA Secretary, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Box 980003, Richmond VA 23298
| EXECUTIVE COMMITTEE | 1999-2000 | 2000-2001 |
| President President-Elect Past President Secretary Treasurer Member-at-Large Member-at-Large Member-at-Large | Richard Rose John Hewitt Norman Henderson Hermine Maes Pamela Madden Deborah Finkel Irwin Waldman Jennifer Harris | John Hewitt Matt McGue Richard Rose Hermine Maes Pam Madden Irwin Waldman Jennifer Harris Carol Prescott |
MEETING INFORMATION
The 30th Annual Meeting of the Behavior Genetics Association will be held at the Radisson Hotel, Burlington, Vermont, USA. Paper, poster and plenary sessions will be held throughout the day on June 29, 30, and July 1. The opening reception is scheduled to begin at 6:00 PM on June 28. The banquet will be held on June 30 starting at 6:00 PM.
Burlington, Vermont Called "The Queen City" of historic Lake Champlain, Burlington lies between the Green Mountains of Vermont and New York's Adirondack high peaks. Though relatively small, Burlington is a popular year-round tourist destination. The Radisson Hotel faces Waterfront Park and is adjacent to the historic Battery Street district and the Church Street Marketplace. A full range of shopping and eating establishments are a short walk from the hotel. A string of city parks are connected by a six mile recreation path along the lake. Bicycles and in-line skates are available for rental. Several excursion cruises and a seasonal passenger train originate near the hotel. Local attractions include resort areas, notably Stowe, Vermont, home of the "Sound of Music's" Trapp Family Lodge. Shelburne Museum, housing the world's largest collection of American folk art, is south of town. French-speaking Quebec is just to the north, with cosmopolitan Montreal less than a two hour drive away.
Local Host: Dr. Jim Hudziak, M.D.
Department of Psychiatry, UVM
Burlington, VT 05405
Tel: (802) 656-3272
E-mail: jhudziak@zoo.uvm.edu
| Year | Presidents | Dobzhansky Awardees | Thompson Awardees | Local Hosts |
| 1971 | R Osborne/B Ginsburg - Storrs CT | |||
| 1972 | Th. Dobzhansky | GE McClearn - Boulder CO | ||
| 1973 | John L. Fuller | WS Pollitzer - Chapel Hill NC | ||
| 1974 | Gerald E. McClearn | S Scarr - Minneapolis MN | ||
| 1975 | J. P. Scott | J Bruell - Austin TX | ||
| 1976 | Irving I. Gottesman | JC DeFries - Boulder CO | ||
| 1977 | W. R. Thompson | Steven Vandenberg | Nancy Galvin | R Wilson - Louisville KY |
| 1978 | Lee Ehrman | Elliott Slater | Gregory Carey | T Klein - Davis CA |
| 1979 | V. Elving Anderson | Ernst Caspari | Marla Sokolowski | C Lynch - Middletown CT |
| 1980 | John C. Loehlin | Benson Ginsburg | RD Bock - Chicago IL | |
| 1981 | Norman D. Henderson | Sheldon Reed | Michael Pogue-Geile | L Erhman - Purchase NY Rose/Guttman/Guttman - Jerusalem |
| 1982 | John C. DeFries | Gardner Lindzey | Paul Sharp | D Nash - Ft Collins CO |
| 1983 | David W. Fulker | Peter Broadhurst | Michael Neale | D Fulker - London |
| 1984 | Steven G. Vandenberg | Leonard Heston | Christine Michard & George Vogler | R Rose - Bloomington IN |
| 1985 | Sandra Scarr | Nikki Erlenmeyer-Kimling | Dorret Boomsma & Lucinda Miner | G McClearn - State College PA |
| 1986 | Ronald S. W ilson | Raymond Cattell | David Harder | G Ashton/R Johnson - Honolulu HI |
| 1987 | Peter A. Parsons | J L Fuller & J P Scott | J. S. de Belle | L Heston - Minneapolis |
| 1988 | Leonard L. Heston | Lee Erhman | Joanne Meyer | S Kerbusch - Nijmegen, Netherl. |
| 1989 | Robert Plomin | Gerald McClearn | Susan Parlour | S Scarr - Charlottesville VA |
| 1990 | Carol B. Lynch | Irving Gottesman | Lon Cardon & Philip Welbergen | P Roubertoux - Aussois, France |
| 1991 | Lindon J. Eaves | John Loehlin | Abel Bult & Lawrence Rodriguez | G Vogler - St Louis MO |
| 1992 | David A. Blizard | John DeFries | Deborah Finkel | J Wilson - Boulder CO |
| 1993 | Thomas J. Bouchard, Jr. | Peter Parsons | Hermine Maes | N Martin - Sydney, Australia |
| 1994 | Glayde Whitney | Aubrey Manning | Frans Sluyter | A Fernandez-Teruel/RM Escorihuela/A Tobena - Barcelona |
| 1995 | James Wilson | David Fulker | Soo HyunRhee & Stephen Petrill | J Meyer/L Eaves -Richmond |
| 1996 | Nicholas Martin | Stephanie Schmitz | G McClearn/G Vogler/D Blizard/B Jones - Pittsburgh PA | |
| 1997 | Nicholas Martin | Ron Johnston | Martine Thomis | Tony Vernon -Toronto, Canada |
| 1998 | Norm Henderson | Stephen Maxson | Javier Gayán & Alexander Weiss | N Pedersen - Stockholm, Sweden |
| 1999 | Richard Rose | Lindon Eaves | Danielle Posthuma & Danielle Dick | Kerry Jang, Vancouver, Canada |
BEHAVIOR GENETICS ASSOCIATION
30th ANNUAL MEETING
Burlington, VT, USA
June 28-July 1, 2000
WEDNESDAY JUNE 28
| 12:00 - 6:00
| REGISTRATION
| 4:00 - 5:00
| EXECUTIVE COMMITTEE MEETING
| 6:00 - 9:00
| WELCOME RECEPTION
| THURSDAY JUNE 29
| Thursday June 29th
| 8:30 - 10:45 PAPER SESSION I
| Nicotine and alcohol Chair: Nicholas G. Martin 8:30
| Defining the nicotine dependence phenotype
| Christina N. Lessov, Pamela A.F. Madden, Kathleen K. Bucholz, Alexandre A. Todorov, Nicholas G. Martin, Wendy S. Slutske, Laura J. Bierut, and Andrew C. Heath 8:45
| Heritability of heavy smoking in adult twins
| Pamela A.F. Madden, Andrew C. Heath, John P. Rice, Jaakko Kaprio, M. Koskenvuo, NancyL. Pedersen, AlexandreA. Todorov, Christina N. Lessov, and Nicholas G. Martin 9:00
| Understanding smoking patterns across adolescence: genetically informative analyses of trajectories of smoking and covariance with drinking
| Jaakko Kaprio, Danielle M. Dick, Richard J. Viken, Kalle Romanov, and Richard J. Rose 9:15
| Genetic analyses of smoking initiation, nicotine dependence, and smoking cessation
| Hermine H. Maes, Patrick F. Sullivan, Cindy Bulik, Michael C. Neale, Kenneth S. Kendler and Lindon J. Eaves 9:30
| Assortative mating for DSM-IV alcohol dependence: Evidence from the Australian Twin Study
| Julia D. Grant, Andrew C. Heath, Kathleen K. Bucholz, Pamela A. F. Madden, and Nicholas G. Martin 9:45
| Exploring Gene-Environment Interactions: Moderating Influences on Alcohol Use
| Danielle M. Dick, Richard J. Viken, Jaakko Kaprio, and Richard J. Rose 10:00
| Separating the influences of age, and age-related variables in the analysis of change in alcohol consumption among female twins
| Carol A. Prescott, and Kenneth S. Kendler 10:15
| Genetic and environmental correlations among antisociality, alcohol consumption, and alcohol problems.(T)
| Brian S. Mustanski, Richard J. Viken, Jaakko Kaprio, and Richard J. Rose 10:30 - 11:00
| Coffee
| 11:00 - 12:00
| PLENARY LECTURE
| Finding and identifying behavior genes in humans Professor Peter McGuffin 12:00 - 1:00
| Lunch
| Thursday June 29th
| 1:00 - 3:00 SYMPOSIUM I
| Cognitive decline and dementia Organizer and chair: Margaret Gatz Discussant: Jennifer Harris
| Contributions of perceptual and motor speed to heritablity of cognition in late adulthood
| Deborah Finkel
| Genetic and environmental influences on late-life cognitive decline
| Matt McGue, and Kaare Christensen
| Age, education, and bio-markers associated with cognitive decline in Swedish twins
| Chandra Reynolds
| Finding a satisfactory solution to influences on age at onset in dementia
| Nancy Pedersen, Margaret Gatz, Samuel Posner, and Samuli Ripatti Thursday June 29th
| 1:00 - 2:45 PAPER SESSION II
| QTL and other methodological issues Chair: John K. Hewitt 1:00
| Linkage disequilibrium analysis of pedigree data (T)
| Gonalo R. Abecasis, Lon R. Cardon, and W.O.C. Cookson 1:15
| Epistasis in QTL linkage analysis: interaction or main effect?(T)
| Shaun Purcell, and Pak C. Sham 1:30
| Effects of pedigree structure and genetic model on the power of QTL linkage analysis
| Fruhling V. Rijsdijk, and Pak C. Sham 1:45
| Genetic markers data in survival studies of siblings: the results of simulation study (T)
| Anatoli I. Yashin, Ivan A. Iachine, and Alexander Z. Begun 2:00
| Genetic analysis of multivariate ordinal data
| Michael C. Neale 2:15
| A review of family studies examining the etiology of comorbidity between two disorders
| Soo Hyun Rhee, John K. Hewitt, Robin P. Corley, and Michael C. Stallings 2:30
| Half-siblings and nonlinear genetic models
| Eric Turkheimer, and Mary Waldron 3:00 - 3:30
| Film
| Canine Kasper Hausers: A film by John L. Fuller on the effects of isolation on the behavior of dogs Presenter: Martin E. Hahn 3:30 - 4:00
| Coffee
| Thursday June 29th
| 4:00 - 6:00 POSTER SESSION
| 1
| Genetic structure of personality: Relationship between TCI and NEO
| Juko Ando, Naoko Onoda, and Yutaka Ono 2
| Candidate genes for frontal EEG asymmetry: preliminary results of a case-control study
| Andrey P. Anokhin, Nenad Svrakic, Andrei B. Vedeniapin, William Wu, Alison Goate, and John W. Rohrbaugh 3
| Effects of prenatal cocaine exposure upon a sequence of aggression situations in mice
| Robert H. Benno, Martin E. Hahn, and Norman Schanz 4
| Assessment of possible alterations of cholinergic basal forebrain in YAC polytransgenic mice: a mouse model of Down syndrome
| Igor Branchi, Zoë Bichler, Danièéle Migliore-Samour 5
| Alcohol dependence and depression in a national sample of Australian twins
| Kathleen K. Bucholz, Andrew C. Heath, Pamela A.F. Madden, Wendy S. Slutske, Laura J. Bierut, Dixie J. Statham, and Nicholas G. Martin 6
| An examination of the associations between DRD4 and personality traits (T)
| S. Alexandra Burt, Matthew K. McGue, and William G. Iacono 7
| Heritability of the Gender Identity Disorder
| Frederick L. Coolidge, Linda L. Thede, and Susan E. Young 8
| Longitudinal and developmental analysis of general cognitive ability and school performance: A sibling study
| Robin P. Corley, and Sally J. Wadsworth 9
| Sex differences in the genetic influences on motivations for drinking
| Rebecca J. Cross, Carol A. Prescott, John L. Horn, and Kenneth S. Kendler 10
| Differential genetic etiology of reading disability as a function of rapid automatized naming and phonological decoding (T)
| Chayna J. Davis, Valerie S. Knopik, Sally J. Wadsworth, Richard K. Olson, and John C. DeFries 11
| Genetic influences on aggression in preschoolers: Preliminary analyses
| Lisabeth F. DiLalla 12
| Partitioning the intergenerational transmission of parental smoking and child birth weight: The role of the children of twins methodology (T)
| Brian M. D'Onofrio, Eric Turkheimer, Linda A. Corey, Robert E. Emery, Mary Waldron, Kare Berg, and Lindon J. Eaves 13
| A study of the genetic and environmental etiology of stuttering in a selected twin sample
| Susan Felsenfeld, Katherine M. Kirk, Gu Zhu, Dixie J. Statham, Michael C. Neale, and Nicholas G. Martin 14
| Everyone Recalls the Same Items From a Word Recall Task
| Deborah Finkel 15
| Maternal sensitivity and measured common environmental factors: a twin study
| Nadine Forget-Dubois, Daniel Pérusse, George Tarabulsy, Bernard Boulerice, Marie-Claude Martel, Michel Boivin, and Richard E. Tremblay 16
| Genetic and Environmental Contributions Common And Specific to Suicidality: A Multivariate Analysis
| Qiang Fu, Andrew C. Heath, Kathleen K. Bucholz, Elliot Nelson, Jack Goldberg, Michael J. Lyons, Theodore Jacob, Seth A. Eisen, and William R. True 17
| Longitudinal analyses of teacher-rated temperament in early adolescence (T)
| Jeffrey R. Gagne, and Kimberly J. Saudino 18
| Effects of prenatal cocaine exposure upon maternal retrieval behavior in mice (T)
| Christopher W. Hess, Martin E. Hahn, Robert H. Benno, and Norman Schanz 19
| A population-based twin study of generalized anxiety disorder in men and women
| John .M. Hettema, Carol A. Prescott, and Kenneth S. Kendler 20
| The heritability of evolutionarily acquired mental mechanisms: A study on the Selection task with twin design
| Kai Hiraishi, Juko Ando, Yutaka Ono, and Toshikazu Hasegawa 21
| Sex Differences in the Genetic and Environmental Influences on the Development of Antisocial Behavior
| Kristen C. Jacobson, Carol A. Prescott, and Ken S. Kendler 22
| Change and stability of self-reported life satisfaction among adult twins - a 15 year follow-up 5
| Markku Koskenvuo, Kirsi Lillberg, Heli Koivumaa-Honkanen, and Jaakko Kaprio 23
| Gender Differences and Interactive Effects in the Etiology of Early Adolescent Substance Use (T)
| Lisa N. Legrand, Matt McGue, and William G. Iacono 24
| Population based survey of the EPQ in Southern England
| Neilson C. Martin, Lon R. Cardon, and Jonathan Flint 25
| Japanese twin study of co-morbidity of the depression and anxiety, and the effect of genetic and environmental factors
| T. Momose, Juko Ando, Naoko Onoda, and Yutaka Ono 26
| Neuro-ontogeny and development in the ataxic mouse mutant, hotfoot
| Donald J. Nash, and Laura J. Draski 27
| Genetic and environmental influences on "affectionless control" in Japanese population
| Naoko Onoda, Juko Ando, and Yutaka Ono 28
| Genetic influences on activity level in adolescence: Do the same genetic effects operate on parent ratings, self ratings and mechanical measures?
| Kimberly J. Saudino, Lee A. Thompson, and Jeffrey R. Gagne 29
| Personality structure in young adults and their parents
| Stephanie Schmitz, Robin P. Corley, and John K. Hewitt 30
| Twin Study of Suicidal Behavior: Replication and Extension
| Nancy L. Segal, and Alec Roy 31
| Power and robustness of candidate gene study designs
| Leo A. Sirota, and Dean H. Hamer 32
| Is divorce a var iant of bachelorhood?
| Susan L. Trumbetta, Irving I. Gottesman, and Eric N. Turkheimer 33
| Genetic covariance between antisociality and diffuse somatic symptoms in adolescent twins
| Richard J. Viken, Jaakko Kaprio, and Richard J. Rose 34
| Stability of genetic and environmental influences on reading performance from 7 to 16 years of age in the Colorado Adoption Project
| Sally J. Wadsworth, Robin P. Corley, John K. Hewitt, and J. C. DeFries 35
| Latent Class and Genetic Analysis on Nicotine Withdrawal in Men
| Hong Xian, Jeffrey Scherrer, Pamela AF Madden, Seth A Eisen, William R True, Jack Goldberg, Michael Lyons, and Ming Tsuang 36
| Another Answer to the Question, Why are Siblings in the Same Family So Different? (T)
| Mary Waldron, and Eric Turkheimer FRIDAY JUNE 30
| Friday June 30th
| 8:30 - 10:15 PAPER SESSION III
| Anxiety, depression, and personality Chair: Matt McGue 8:30
| Depression and anxiety disorders in a selected sample of Australian twins and their families: methodology
| Katherine M. Kirk, Gavin Andrews, and Nicholas G. Martin 8:45
| Depression and anxiety disorders in a selected sample of Australian twins and their families: models of family resemblance
| Nicholas G. Martin, and Katherine M. Kirk 9:00
| The structure of anxiety in 4-year-olds: a genetic analysis
| Thalia C. Eley, Derek Bolton, Thomas O'Connor, Sean Perrin, Patrick Smith, and Robert Plomin 9:15
| Demographic risk factors and moderators of genetic influence in separation anxiety disorder (T)
| Nikole J. Cronk, Wendy S. Slutske, Pamela A. F. Madden, Kathleen K. Bucholz, and Andrew C. Heath 9:30
| Change and continuity in temperament ages 4 to 7 years (T)
| Carol Van Hulle, Robin P. Corley, and John K. Hewitt 9:45
| Genetic and environmental relationships between normal and abnormal personality (T)
| Kristian E. Markon, Robert F. Krueger, and Thomas. J. Bouchard 10:00
| A biometric analysis of personality traits and externalizing disorders (T)
| Brian M. Hicks, Robert F. Krueger, William G. Iacono, and Matt McGue Friday June 30th
| 8:30 - 10:30 SYMPOSIUM II
| Genetics of brain function and information processing Organizer and chair: Dorret I. Boomsma Discussant: Nicholas G. Martin
| Genetic correlations between P300 and EEG pwer spectrum
| Andrey P. Anokhin, G. Caroline M. van Baal, Toos C.E.M. van Beijsterveldt, Julia D. Grant, Eco J.C. de Geus and Dorret I. Boomsma.
| Psychophysiological phenotypes of cognition: the P3 and SW components
| Margie Wright
| Memories are made of [TH]is
| G. Caroline M. van Baal, Danielle Posthuma, Eco J.C. de Geus, and Dorret I. Boomsma
| Genetic structure of visual/verbal working memory and its relationship with the ERP parameters
| Juko Ando, Kaname Mochizuki, Kai Hiraishi, Hiroshi Maruyama, Naoko Onoda, andYutaka Ono
| A twin study of psychometric intelligence and efficiency of information processing
| Glen Smith
| A genome scan for QTLs associated with general cognitive ability (`g')
| Robert Plomin 10:30 - 11:00
| Coffee
| Friday June 30th
| 11:00 - 12:00 PAPER SESSION IV
| Risk factors Chair: Michael Pogue-Geile 11:00
| Direction of causation modeling between personality, measures of perceived parenting and recently experienced psychiatric symptoms (T)
| Nathan Gillespie, David L. Duffy, and Nicholas G. Martin 11:15
| Gene-environment interaction and evocative gene-environment correlation: contributions of harsh discipline and parental psychopathology to problem adolescent behaviors
| Kristin Riggins-Caspers, Remi Cadoret, and John Knutson 11:30
| Differential deficit in working memory, not attention, associated with liability to schizophrenia: a sibling study of the expectancy AX-CPT (T)
| Angus W. MacDonald, III, Michael F. Pogue-Geile, Judy L. Thompson, Laura L. Ross, Tamika Allen, Melissa K. Johnson, Nicole D. Lollo, Allison R. Marquette, Eric J. Yablonski, and Cameron S. Carter 11:45
| Are opposite-sex twins sex-atypical? (T)
| Khytam Dawood, J. Michael Bailey, and Nicholas G. Martin Friday June 30th
| 11:00 - 12:15 PAPER SESSION V
| Cognitive abilities Chair: Caroline van Baal 11:00
| Longitudinal genetic analysis of intelligence at 5, 7, 10, and 12 years of age (T)
| Meike Bartels, Marjolein J.H. Rietveld, G.C.M. van Baal, and Dorret I. Boomsma 11:15
| A longitudinal twin study of specific cognitive abilities in preschool children (T)
| Thomas S. Price, Philip S. Dale, Jim Stevenson, Thalia C. Eley, and Robert Plomin 11:30
| Familial correlations between reading measures in a U.K. sib-pair cohort (T)
| Angela J. Marlow, Simon E. Fisher, Clyde Francks, Joel Talcott, Alex J. Richardson, Anthony P. Monaco, John F. Stein, and Lon R. Cardon 11:45
| The influence of genetic factors on choice response time and delayed response tasks (T)
| Michelle Luciano, Glen A. Smith, Gina M. Geffen, Margie J. Wright, Laurie B. Geffen, and Nicholas G. Martin 12:00
| Genetic influences on ERP slow wave measures of working memory in adolescence (T)
| Narelle K. Hansell, Margie J. Wright, Gina M. Geffen, Laurie B. Geffen, Glen A. Smith, and Nicholas G. Martin 12:00 - 1:00
| Lunch
| Friday June 30th
| 1:00 - 3:30 SYMPOSIUM III
| The Twin Mothers Project Organizer and chair: Jenae M. Neiderhiser Discussant: Robert Plomin
| The Twin Mothers Project
| David Reiss, Nancy Pedersen, Marianne Cederblad, Kjell Hansson, Paul Lichtenstein, Jenae M. Neiderhiser, Olof Elthammar
| An ecological exploration of factors influencing the parenting of adolescents using behavioral genetic techniques (T)
| Erica L. Spotts
| Genetic and environmental contributions to the associations between personality characteristics and adjustment in twin women: The role of mothering as a mediator
| Jenae M. Neiderhiser
| The etiology of genetic and environmental influences on marital relationships
| Paul Lichtenstein
| The nature of attachment
| Jody Ganiban, and Jenae Neiderhiser
| Mothering as an influence on the mother's own mental health
| Nancy L. Pedersen Friday June 30th
| 1:00 - 3:30 SYMPOSIUM IV
| Trisomy 21: from the clinic to the bench Organizer and chair: Pierre Roubertoux Discussant: Linda S. Crnic
| The mapping of Down syndrome phenotypic features
| J.M. Delabar
| Behavioral and neural phenotype of a mouse model of Down syndrome
| Linda S. Crnic, and Lynn A. Hyde
| Murine models with different expression levels of genes relevant to Down syndrome: a tool for understanding the role of single genes in neurophatological traits
| M. Dierssen, X. Altafaj, V. Fotaki, C. Casas, J. Visa, M.L. Arbonés, J. Guimerà, C. Fillat, C. Baamonde, C. Martinez-Cué, M. Lumbreras, J. Flórez, and X. Estivill
| Behavioral and cognitive performances of trangenic mice for Down Chromosomal Region (DCR)
| Caroline Chabert, and Pierre L. Roubertoux
| Spontaneous stereotypy in an animal model of Down syndrome (Ts65Dn mice)
| Mark H. Lewis, Cortney A. Turner, and Michael F. Presti 4:00 - 5:00
| BUSINESS MEETING
| 7:00
| BANQUET
| PRESIDENTIAL ADDRESS: BGA at 30 years: Reflections and projections Professor Richard J. Rose SATURDAY JULY 1
| Saturday July 1st
| 9:00 - 10:30 SYMPOSIUM V
| Behavior genetic perspectives on personality structure Organizers: Robert Krueger and Michael Stallings Chair: Robert F. Krueger Discussant: Andrew C. Heath
| Joint multivariate genetic analysis of personality dimensions from the TPQ, EPQ and KSP
| Michael C. Stallings, John K. Hewitt, Scott M. Hofer, Andrew C. Heath, and Lindon J. Eaves
| Phenotypic, genetic, and environmental parallels in the structure of personality: evidence from the Minnesota Twin Registry
| Robert F. Krueger
| Sources of structure: genetic, environmental, and artifactual influences on the covariance of personality traits
| Kerry Jang 10:30 - 11:00
| Coffee
| Saturday July 1st
| 11:00 - 12:00 PAPER SESSION VI
| Human association studies, transgenic mice Chair: Irwin D. Waldman 11:00
| Evidence of association between externalizing behavior and dopamine transporter genotype in young twins
| Susan E. Young, Andrew Smolen, Robin P. Corley, Michael C. Stallings, and John K. Hewitt 11:15
| Association and linkage between DRD3 and childhood disruptive behavior disorders
| Irwin D. Waldman, David C. Rowe, Craig Stever, L. Nicole Giedinghagen, Jaime M. C. Gard, H. Harrington Cleveland, Samantha T. Terris, Jennifer H. Mohr, and Stephanie Sherman 11:30
| [beta]-2 adrenergic receptor gene variations and blood pressure under stress in normal twins
| Andreas Busjahn, Guo-Hua Li, Hans-Dieter Faulhaber, Magda Rosenthal, Bernd Timmermann, Margret R. Hoehe, and Friedrich .C. Luft, 11:45
| Immunological disorders in transgenic mice for Down Syndrome Region
| Zoë Bichler, Marie-Claude Gonzalez, and Danièle Migliore-Samour Saturday July 1st
| 11:00 - 11:45 PAPER SESSION VII
| Social interactions, well-being, fertility Chair: David C. Rowe 11:00
| The friends of siblings: a test of social homogamy vs peer selection
| David C. Rowe, Michael Gilson, and Cathy B. Hunt 11:15
| Genetic and environmental sources for the correlation between dominance and subjective well-being in zoo chimpanzees (Pan troglodytes)
| Alexander Weiss, J.E. King, and R.M. Enns 11:30
| Behavior genetic modeling of human fertility: findings from a contemporary Danish twin study
| Joseph Lee Rodgers, Hans-Peter Kohler, Kirsten Kyvik, and Kaare Christensen | |||||
BEHAVIOR GENETICS ASSOCIATION
30th ANNUAL MEETING
Burlington, Vermont, USA June 28-July 1, 2000
Program Overview
WEDNESDAY JUNE 28 | ||
| 12:00 - 6:00 | REGISTRATION | |
| 4:00 - 5:00 | EXECUTIVE COMMITTEE MEETING | |
| 6:00 - 9:00 | WELCOME RECEPTION
Cocktails & Hors D'oeuvres | |
THURSDAY JUNE 29 | ||
| 8:00 - | REGISTRATION
Morning Continental | |
| 8:30 - 10:45 | PAPER SESSION I
Nicotine and Alcohol | |
| 11:15 - 12:00 | PLENARY LECTURE
Finding and identifying behavior genes in humans | |
| 1:00 - 3:00 | SYMPOSIUM I
Cognitive decline, dementia | PAPER SESSION II
QTL and other method issues |
| 3:00 - 3:30 | FILM
Canine Kasper Hausers | |
| 4:00 - 6:00 | POSTER SESSION | |
FRIDAY JUNE 30 | ||
| 8:30 - 10:30 | PAPER SESSION III
Anxiety, depression, personality | SYMPOSIUM II
Brain function |
| 11:00 - 12:00 | PAPER SESSION IV
Risk factors | PAPER SESSION V
Cognitive abilities |
| 1:00 - 3:30 | SYMPOSIUM III
Twin mothers project | SYMPOSIUM IV
Trisomy 21 |
| 4:00 - 5:00 | BUSINESS MEETING | |
| 6:00 | Bus Transportation | |
| 7:00 | BANQUET
Awards Ceremony & Presidential Address | |
SATURDAY JULY 1 | ||
| 9:00 - 10:30 | SYMPOSIUM V
Personality structure | |
| 11:00 -12:00 | PAPER SESSION VI
Human Association, Mouse Transgenics | PAPER SESSION VII
Social Interaction, Well-being, Fertility |
| 1:00 - 2:00 | EXECUTIVE COMMITTEE MEETING | |
Gonalo R. Abecasis, Lon R. Cardon, W.O.C. Cookson
In outbred populations, linkage disequilibrium is expected to extend for short distances and could provide a powerful gene-mapping tool. Family-based methods use measures of allelic transmission to construct tests that
are robust to population substructure (reviewed in G.R. Abecasis, W.O.C. Cookson, and L.R. Cardon, 2000, Eur. J. Hum. Genet. in press). In a variance components frame-work specific tests of linkage disequilibrium
can be constructed not only for case-parent triads, but for sib-pairs (D.W. Fulker, S.S. Cherny, P.C. Sham, and Hewitt J.K., 1999, Am. J. Hum. Genet. 64, 259-267) and larger families (G.R. Abecasis, L.R. Cardon,
W.O.C. Cookson, 2000, Am. J. Hum. Genet. 66, 279-292). We present QTDT, a computer program that provides a simple interface to these diverse methodologies. The program uses a general approach for
scoring allelic transmission that accommodates families of any size and uses all available genotypic information. The program allows for simple variance components and linkage analysis of discrete and quantitative traits. As
a practical application, we investigate the relationship between circulating angiotensin-1 converting enzyme (ACE) levels and polymorphisms in the ACE gene using previously published data. Juko Ando1, Kaname Mochizuki2, Kai Hiraishi3, Hiroshi Maruyama3, Naoko Onoda4, Yutaka Ono4
Working Memory (WM) is the active function of short-term memory which operates (operation) and stores (storage) relevant information, and is recently considered as the central component of the higher-order
information processing such as g (general ability)(Shah & Miyake, 1999). One of the current controversies is the structure and physiological correlates of WM; Whether WM is domain-specific or general? and What
kind of physiological evidence would support its domain-specificity (or generality)? In this study, 263 pairs of twins (MZf=122, MZm=49, DZf=41, DZm=19, DZo=32) took the visual(V) and spatial(S) WM
tasks which tapped both operation(o) and storage(s) functions (Vo, Vs, So, Ss). Some of them also took the visuo-spatial delayed response task that is thought to measure visual storage
function of WM and provides the ERP parameters (P3 and SW). The univariate analysis showed that all the WM functions (Vo, Vs, So, Ss) were explained by additive genetic and nonshared environmental factors (AE
model). The multivariate genetic analysis suggested that there might be one common and two domain -specific (visual and spatial) genetic factors. The relatinship between those factors and the ERP parameters
will be discussed. Juko Ando1, Naoko Onoda2, Yutaka Ono2
Two comrehensive personality inventories (NEO-PI-R and TCI) were taken by 301 pairs of Japanese twins (MZf=127, MZm=61, DZf=49, DZm=29, DZo=35 / age; 15-30 yrs). NEO-PI-R (Costa & McCrae, 1985,
Personality and Individual Differences, 6, 587-597) taps so called Big Five Factors(BFFs) that are known to provide the robust phenotypic structure of personality dimensions. The multivariate genetic analysis
revealed, however, that BFFs are not genetically independent. On the other hand, three temperament dimensions (novelty seeking(NS), harm avoidance(HA), reward dependence(RD)) assessed by TCI (Temperament
and Character Inventory, Cloninger, et al., 1993, Archives of Genetic Psychiatry, 50, 975-990) showed genetic independence, and the additive genetic component of persistencewas overlapped with those
of NS and HA< with no trait-specific genetic contribution. Among BFFs, the genetic compenents of neuroticisn(N), extraversion(E), and agreeableness(A) could be explained only by those of TCI's three
temeperament dimensions. Although Opneness to experience(I) and conscientiousness(C) were also genetically overlapped with NS, HA and RD, they showed their own tarit-specific genetic
contributions as well. [Poster] Andrey P. Anokhin1, G. Caroline M. van Baal2, Toos C.E.M. van Beijsterveldt2, Julia D. Grant1, Eco J.C. de Geus2and Dorret
I. Boomsma2
The P300 component of event-related brain potentials is elicited by task-relevant ("target") events and is believed to represent neuroelectricactivity associated with cognitive processing (e.g. contextual stimulus evaluation,
updating working memory conte nt, allocation of processing resources). Reduced P300 amplitude has been implicated in genetic risk for a variety of neuropsychiatric disorders, most notably, schizophrenia, alcoholism, and conduct
disorder. Previous studies have shown medium to high heri tability of P300. A number of studies suggest functional relationships between P300 amplitude and spontaneous EEG rhythms. Based on this evidence, we hypothesized
that P300 amplitude and low-frequency EEG activity may be influenced by common genetic facto rs. Three minutes of resting EEG and "visual oddball" P300 were recorded from sixteen year old MZ (n=91) and DZ (n=122)
twin pairs. P300 amplitude correlated significantly with spectral powers across different EEG frequency bands, most notably with delta and theta. To examine whether P300 and EEG characteristics are influenced by overlapping
genetic factors, we conducted bivariate genetic analysis (Cholesky decomposition) of P300 amplitude and the amount of delta activity (spectral power) measured at the same scalp locations. In males, delta power was highly
heritable (h2>90% for most scalp locations), whereas P300 amplitude showed lower heritability (h2~ 50%). The observed covariance between P300 and delta power was largely (>90%) accounted for
by shared genetic factors. Most genetic correlations between P300 and delta power (computed for AE model) were in the range of 0.6 to 0.9. In females, both delta power and P300 showed lower heritability than in males, yet
genetic correlatio n was also high (>0.6). The results suggest that individual variability of P300 amplitude is influenced largely by the same genetic factors that determine slow EEG rhythms. Genetic factors unique to P300 account
only for a modest portion (15-20 %) of the total P300 variance. Andrey P. Anokhin1, Nenad Svrakic1, Andrei B. Vedeniapin1, William Wu1, Alison Goate1, and John W. Rohrbaugh1
Individual differences in frontal brain asymmetry have been associated with temperament traits, affective style, and risk for mood disorders. Specifically, lower left than right anterior cortical activation is associated with
increased activity of behavio r inhibition system, withdrawal-avoidance behaviors, and higher risk for major depression and anxiety disorders. Conversely, greater left frontal activation is associated with the predominance of
behavior activation system, exploratory, approach, and rewa rd-seeking behaviors. Regional brain activation can be assessed using quantitative electroencephalography (EEG). Here we report preliminary results of a case control
association study of the frontal EEG asymmetry (FA) phenotype based on the data from the Washington University site of the Collaborative Study on the Genetics of Alcoholism (COGA). Alpha power of the resting EEG (an
inverse indicator of regional cortical activation) was measured at the left (F7) and right (F8) frontolateral sites (approximate ly corresponding to the dorsolateral prefrontal cortex) in 76 Caucasian individuals (42 females). The
effect of TaqA polymorphism of D2 dopamine receptor gene (DRD2) and polymorphism of the serotonin 1B receptor gene (5HT1B) on FA was studied using genera l linear models including age, gender, and alcoholism diagnosis
as covariates. The analysis has shown significant additive effects of both polymorphisms on the quantitative FA phenotype, indicating that allele A2 of the DRD2 (F[1, 72] =10.3, p=0.002) and t he "short" allele of the 5HT1B
(F[1, 72]=5.04, p=0.028) were associated with R>L pattern of frontal cortical activation (implicated in behavior inhibition and depression), whereas DRD2-A1 and 5HT1B-long alleles were associated with L>R asymmetry
(implicate d in reward-seeking "approach" behaviors). A combined genotype on both loci showed highly significant association with FA (F[2, 75] = 8.54, p<0.001). No significant interaction with age, sex, or alcoholism was
observed. These preliminary results suggest t hat individual pattern of frontal brain activation may be influenced by genetic polymorphisms related to dopaminergic and serotoninergic neurotransmission. [Poster] Meike Bartels1, M.J.H. Rietveld1, G.C.M. Van Baal1, and D.I. Boomsma1
Measures of intelligence were collected in 209 twin pairs at 5, 7, 10, and 12 years of age, as part of a longitudinal project on intelligence, brain function and behavioral problems. Intelligence was measured at 5, 7, and 10
years of age with the RAKIT, a well-known Dutch intelligence test, consisting of 6 subscales. At age 12 the complete WISC-RN was administered (12 subscales). Participation-rate is around 93% after 7 years. Inspection of
correlation coefficients over time suggest a simplex structure, that is, decreasing association with increasing time-interval, but all correlations are rather high across time: (r(5-7)= .64; r(5-10)= .65; r(5-12)=.59; r(7-10)=.71;
r(7-12)=.64 and r(10-12)=.73). Twin correlations for total IQ show a pattern that is consistent with a low heritability and substantial influence of shared family environment at age 5 and an increasing heritability with decreasing
shared environmental influences as children grow older. At age 12 there is no longer any influence of shared family environment on IQ scores. Cross-correlations for MZ and DZ twins suggest that stability in intelligence over
time is mainly due to genetic factors. Robert H. Benno, Martin E. Hahn and Norman Schanz
In the past we developed a model system using genetically standardized mice to investigate the effects of prenatal cocaine upon neural development and behavior, for example, aggressive behavior. We have found that prenatal
cocaine produced small effects upon the exposed offspring and that cocaine often interacted with genotype. Recently it has been suggested that the effects of prenatal cocaine are limited by the remarkable plasticity utilized by
the brain to offset the early perturbation of cocaine exposure. The cost of this early plasticity may be an inability to cope with a series of behavioral tasks presented to the animal in adulthood. In the current study we tested cocaine
exposed and control males in four social situations in sequence on four successive days. The animals were placed in: food competition, predatory aggression, and two intermale aggression situations, one the homogeneous set
design and the other the standard tester design. The cocaine and vehicle exposed males were the F1 offspring of C57BL/10J females paired with either a SJL/J, DBA/2J or BALB/cJ male. Mothers were injected daily
with either saline or 20 mg/kg of cocaine subcutaneously on gestational days 7-17, a dosage shown to produce minimal health consequences for pups and mothers. As expected, the results showed that there were significant genotype
effects on several measures of aggression and again cocaine had small but reliable effects. For example, cocaine increased the percentage of fighting in food competition and interacted with strain in the homogeneous set design
increasing fight latency in one F1 while decreasing it in another. Since we observed minimal differences due to drug treatment in the last test, intermale aggression in the homogeneous set design, the hypothesis that
repeated participation in social paradigms requiring aggressive responses would "overload" the animals is not supported. [Poster] Zoë Bichler, Marie-Claude Gonzalez, Danièle Migliore-Samour
Down syndrome is characterized, among various features, by immunological defects including a high prevalence of leukemia, susceptibility to infections and autoimmune disorders. Premature involution of thymus and
alterations of some lymphocytes immunological markers have been reported (L. Nespoli, G. R. Burgio, A. G. Ugazio, and R. Maccario, 1993, Journal of Intellectual Disability Research 37, 543-551). Transgenic
mice with four different inserts from human Down Chromosomal Region (DCR) have been developed (D. J. Smith, Y. Zhu, J-L. Zhang, J-F. Cheng, and E. M. Rubin, 1995, Genomics 27, 425-434). As thymus
was known to play an important part in differenciation, selection and maturation of T lymphocytes, we have investigated the expression of different specific immunological markers on thymocytes. Fluorescent antibodies were
employed and analyzed via flow cytofluorometry at six different ages from birth to adulthood in transgenic mice overexpressing a human chromosome 21 fragment. Variations in TCR, CD4, CD8 and CD25 marked cells were
observed pending the transgene over-expression. Igor Branchi, Zoë Bichler, Danièle Migliore-Samour
Down syndrome (DS) the most frequent genetic cause of mental retardation (1:700 live births), is due to an extra copy of chromosome 21. Structural and functional abnormalities in the central nervous system of DS individuals
have been widely reported. The first aim of DS research in recent years has been to identify the genetic bases of the different phenotypic aspects. For this purpose, YAC transgenic mouse models of DS have been developed by
inserting in the murine genome a Yeast Artificial Chromosome (YAC) bearing a fragment of the human Down syndrome Chromosomal Region (DCR). This region was reported to play an important role in the development of
typical DS features, including mental retardation. In YAC mice, trisomy is due to two copies of mouse chromosome 16 and one copy of homologous fragment of human chromosome 21 included in the YAC. Several works reported
a neurodegeneration of cholinergic neurons in DS brain, and, more recently, a treatment based on acetylcholinesterase inhibitors has been shown to improve cognitive abilities in DS patients. An assessment at developmental
and adult phase of neurobiological and behavioral deficits in YAC mice has been carried out. Abnormalities of basal forebrain cholinergic neurons have been investigated using specific neuronal markers, and behavioral impairments
have been monitored in a passive avoidance and a two-object recognition task. These analyses, performed on YAC mice bearing different fragments of the DCR, provided information to identify which part, or even gene, of such
region is responsible for the different features of cognitive impairment displayed by DS subjects. [Poster] Kathleen K. Bucholz1, Andrew C. Heath1, Pamela A.F. Madden1, Wendy S. Slutske2, Laura J. Bierut1, Dixie J.
Statham3, and Nicholas G. Martin3
The strong association between alcohol dependence and depression frequently observed in clinical samples has been confirmed in community samples, with alcoholics twice as likely as nonalcoholics to meet criteria for
major depression (Merikangas 1990Psych. Clinics N. America 13, 613-632). Both disorders are familial, but evidence from family studies has been equivocal in terms of a consistent explanation for the
co-segregation. Using data from young adult Australian twins, we studied the relative influences of genes and environment in the association between the two disorders. In 1996-97, Australian twins who 8 years earlier had
participated in a survey by mail were interviewed by telephone with a structured psychiatric diagnostic interview, from which lifetime DSM-IV alcohol dependence (AD) and major depression (MD) were derived. The mean
age of the twins was 29.4, 55.7% were female, and 50.3% were currently married. Complete pairs for study numbered 529 MZF, 415 DZF, 358 MZM, 296 DZM, and 498 DZOS, along with 798 single twins. Overall lifetime
prevalence of AD was 21.5% (F:14.8%, males 29.9%) and of MD 28.4% (F: 32.8% vs 22.7% M). Prevalence of MD was substantially elevated among those with AD: 49.5% vs. 30% in F, and 31.5% vs. 19.0% in M, and the
reverse was true as well. Tetrachoric correlations, ranging from .35-.56 for MZ, and .11-.38 for DZ, indicated substantial familial influences. Results of structural equation modeling indicated that genetic influences were
substantial for AD but less so for MD (44% and 34% of the variances in AD and MD respectively). The genetic and nonshared environmental correlations between AD and MD were similar (.31 and .28 respectively). These
analyses indicate some shared genetic influences in AD-MD comorbidity, but also a substantial role for nonshared environmental factors. The degree to which these findings will hold with different MD phenotypes will be
investigated. [Poster] S. Alexandra Burt1, Matthew K. McGue2, and William G. Iacono3
To date, evidence supporting positive associations between the 7-repeat allele of the D4 dopamine receptor (DRD4) exon III 48 bp polymorphism and Novelty-Seeking (originally reported by Ebstein, et al., 1996, Nature
Genetics12, 78-80) has been mixed. Some studies have replicated the association (Ekelund, J., 1999, American Journal of Psychiatry156(9), 1453-1455), while others have not (E.G. J”nsson, et
al., 1997, The American Journal of Psychiatry154:5, 697-699). In the present study, we examined the relationship between DRD4 polymorphisms and various personality traits, as measured by the
Multidimensional Personality Questionnaire (MPQ; A. Tellegen, 1982, Brief manual for the Differential Personality Questionnaire. Unpublished manuscript, University of Minnesota, Minneapolis). The sample consisted
of 71 DZ families (n=284) and 177 MZ families (n=531) assessed as part of the ongoing Minnesota Twin Family Study. Those with extreme scores on the MPQ validity scales (TRIN and VRIN) were dropped from the analyses.
In order to maximize the comparability of our results to those of other studies, genotypes were clustered in three distinct ways: genotypes containing alleles with two to five repeats (short) versus those with six or more repeats
(long), genotypes containing the 7-repeat allele versus those without, and genotypes 4, 4 versus 4, 7. We will report association results using both discordant sib pair analyses and the within-family transmission/disequilibrium.
[Poster] Andreas Busjahn1, Guo-Hua Li2, Hans-Dieter Faulhaber1, Magda Rosenthal1, Bernd Timmermann2, Margret R. Hoehe2,
Friedrich .C. Luft1
We tested the hypothesis that blood pressure responses to physical and mental stress are associated with polymorphisms in the [beta]-2 adrenergic receptor (AR) gene. We studied normotensive, young, monozygotic (MZ)
and dizygotic (DZ) twins. The subjects underwent automated blood pressure measurements at the brachial and digital arteries and were subjected to mental arithmetic and cold pressor stress. We used allele-specific PCR to
genotype the subjects in terms of four single nucleotide polymorphisms in the [beta]-2 AR gene. The most functionally-relevant polymorphism in the [beta]-2 AR gene, namely Arg16/Gly, was associated with systolic and diastolic
blood pressure under resting conditions, during mental arithmetic, and during the cold pressor test, as well as with the increase in diastolic blood pressure during both forms of stress. These findings underscore the importance
of the [beta]-2 AR gene to blood pressure regulation. They also indicate that the [beta]-2 AR gene influences regulation of not only resting but also stress-related blood pressure. Caroline Chabert1,3and Pierre L. Roubertoux1,2
DCR is the minimal region of human chromosome 21 that is implicated in Down syndrome. Four chromosomal segments covering this region were incorporated in Yeast Artificial Chromosomes (YACs) and were then
transfected into FVB mice genome by Rubin's group, 1997, Nature Genetics, 16, 28-36. As mouse chromosome 16 is synthenic with the human 21 chromosome, partialy trisomic mice for the DCR were obtained. Two
strain per one YAC were then used to produce transgenic mice. FVB transgenic males were crossed with C57BL/6 female mice to produce transgenic F1 mice. Behavioral examinations were performed (Morris water maze, elevated
plus maze, fear conditionning test). No difference was seen between the strains carrying the same YAC, suggesting that the transgene effect was not due to its insertion. Preliminary results indicate differences in cognitive abilities
between the four YACS and between the YACs and the control mice. Learning impairment was observed in mice carrying YACs, suggesting that DCR encompasses several genes linked to cognitive abilities. This YAC strategy
should pave the way to identify the functions of genes carried by DCR. Frederick L. Coolidge1, Linda L. Thede1, and Susan E. Young2
The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV, 1994; American Psychiatric Association, Author, Washington DC) bases the diagnosis of Gender Identity Disorder (GID) upon two necessary
components: (a) a strong and persistent cross-gender identification and (b) persistent discomfort with one's sex or gender role of that sex. Most twin studies to date, however, have investigated the genetic influence upon
homosexuality (sexual desire or behavior directed toward a person of one's own sex) but not GID, and no twin studies have investigated GID in a non-retrospective design. The present study was designed to address this lacuna.
The parents of 258 child twins (4-17 years old; 80 MZ and 49 DZ pairs) completed a standardized personality measure (Coolidge Personality and Neuropsychological Inventory [CPNI]; Coolidge, 1998, CPNI Manual,
Author, Colorado Springs) that contains a GID scale (six items answered on 4-point Likert scale; internal scale reliability = .71; test-retest reliability = .78). Preliminary analyses revealed a correlation between age and the GID
score, so the data were age-corrected and rank-normalized to reduce skewness. Univariate model fitting revealed that the MZ correlation was .61 and the DZ correlation was .16. Both the ADE model and the AE model fit the
data well, so the more parsimonious model (AE) was chosen to interpret the data. The heritability component was .61, and the nonshared environmental component was .39 (model fit: Chi square = 2.35, df = 5, p = .80, AIC =
-7.65). The results appear to indicate that GID has a strong genetic component. This finding is consistent with some prior studies (e.g., Buhrich, Bailey, & Martin, 1991, Behav. Genet.21, 75-96) who have found
that sexual orientation has a substantial genetic influence (at least in adult male twins with multivariate model-fitting analyses). Future studies will include multivariate model fitting, analyses by gender, and an increased sample
size. [Poster] Robin P. Corley1, and Sally Wadsworth1
We explore familial and developmental influences on three constructs: reading performance, mathematical performance, and general cognitive ability, using results from the Colorado Adoption Project, an ongoing longitudinal
study of 245 adoptive families, and a matching sample of 245 non-adoptive families. Comparing the similarity of biological full siblings and adoptive siblings at ages 7 and 12 indicates a high degree of overlap in the genetic
and environmental influences acting on the three constructs. Analysis of cross-construct influences between age 7 and age 12 indicates that age 7 cognitive ability predicts subsequent change in relative reading and mathematics
performance, but that the reciprocal effects of age 7 reading and mathematics on age 12 cognitive ability are less important. Developmental analyses between ages 7 and 12 indicate complete continuity in the genetic factors
for all three constructs and in the shared environmental influences acting on reading and general cognitive ability. Mathematical performance at age 12 may be influenced by newly emerging shared environmental influences.
Modeling developmental and reciprocal influences of performance and general cognitive ability leads to better understanding of ability- achievement discrepancies, which have been used as predictors of externalizing behaviors
and substance experimentation. [Poster] Linda S. Crnic1, 2, and Lynn A. Hyde2
The Ts65Dn mouse model of Down syndrome (DS) is segmentally trisomic, carrying an extra copy of the region of mouse Chromosome 16 syntenic to human Chromosome 21. These mice are hyperactive, and have difficulty
inhibiting behavior appropriately in mildly fearful situations, and difficulty with behavioral flexibility. Because hippocampus and cerebellum are selectively affected in DS, we have focused on these two regions. Individuals
with DS and TS65Dn mice show loss of basal forebrain cholinergic neurons (BFCN) early in life. Examining mice from 4-12 months of age, we demonstrated that the loss occurs between 4 and 6 months. Correlations between
loss of BFCN and impaired behavioral flexibility in spatial but not visual reversal learning will be presented. Other hippocampal tasks examined between 3 and 12 months of age and were also impaired in these mice only after
the age of loss of BFCN. While the cerebellum has been shown to be small in these mice (L. L.Baxter, T.H. Moran, J. T. Richtsmeier, J. Troncoso, and R. H. Reeves, 2000, Human Molec. Genet. 9, 195-202),
three different tests of motor learning show no impairment in mice younger or older than 6 months of age when training is gradual, whereas acquisition of motor tasks has been shown to be impaired if the mice are not trained
gradually (A. Costa, K. Walsh, and M. T. Davisson, 1999, Physiol. Behav. 68, 211-220). We have begun to remove individual genes from this segmental trisomy to determine their role in the phenotype, and
have found that the presence of the interferon alpha/beta receptor does not appear to account for the behavioral effects of the segmental trisomy observed to date. The behavioral and neural phenotype of the Ts65Dn model resembles
that of human DS and will be a useful model for determining the role of genes and gene regions in this disorder. Nikole J. Cronk1, Wendy S. Slutske1, Pamela A. F. Madden2, Kathleen K. Bucholz2, and Andrew C. Heath2
We examined the association between three demographic variables and lifetime history of separation anxiety disorder (SAD) symptoms in a population-based sample of 1, 991 female adolescent twin pairs. Twins were identified
from state of Missouri birth records, and histories of SAD symptoms were obtained by structured telephone interviews with the twins' biological mothers. The three demographic variables included race (African-American vs.
white), mother's current marital status (married vs. not married), and annual household income (less than $24, 000/year vs. $24, 000/year or more). African-American girls, girls from single-parent homes, and girls from low income
homes had signficantly higher mean levels of SAD symptoms than white girls, girls from dual-parent homes, and girls from higher income households, respectively. For example, 17.4% of African-American girls vs. 11.8% of
white girls, 17.7% of girls from single-parent homes vs. 11.2% of girls from dual-parent homes, and 19.4% of girls from low income homes vs. 10.9% of girls from higher income homes had 3 or more symptoms of SAD. Genetic
model-fitting revealed significant genetic effects on mother-reported lifetime separation anxiety disorder symptoms for the entire twin sample (a2=.56; c2=.16; e2=.28). There were also
significant genetic effects for all levels of race, marital status of mother, and household income, although estimates of genetic effects were significantly lower for African-American girls, girls from single-parent homes, and girls
from low income homes than for white girls, girls from dual-parent homes, and girls from higher income homes, respectively. These findings indicate that race, family composition, and socioeconomic status are important risk
factors for SAD and may also moderate genetic effects on SAD. Rebecca J. Cross1, Carol A. Prescott2, John L. Horn3, and Kenneth S. Kendler2
A large amount of evidence supports moderate to strong genetic influences on the etiology of alcoholism. Some research suggests alcoholism is associated with motivations for drinking. It is possible that some of the genetic
liability for alcoholism is mediated through genetic influences on the underlying motivations for drinking. We investigated this hypothesis using four scales from the Alcohol Use Inventory (AUI; K.W. Wanberg and J.L. Horn,
1983, American Psychologist 38, 1055-1069), which assess motivations for drinking including: drinking in social situations (SOCINT), to improve mental functioning (MENT), to relieve social anxiety (SOCANX),
and to manage mood states (MOOD). Complete AUI data from adult twins who were sampled from the population-based Virginia Twin Registry were available on 6, 795 individuals who had used alcohol, including members
of 300 MZ female, 185 DZ female, 550 MZ male, 384 DZ male, and 809 opposite sex DZ pairs. Structural models were used to test for sex differences in absolute magnitude of genetic influence, proportional genetic influence,
and sex-specific genetic sources. For SOCINT, MENT, and MOOD males and females had significantly different patterns of genetic and environmental contributions. In addition for MOOD, there was evidence of sex-specific
genetic sources. For SOCANX, males and females had equal genetic estimates but differed in the magnitude of common and specific environmental contributions. These results add to a growing literature on the importance of
genetic influences on the development of alcohol-related behaviors in women as well as men, and suggest the existence of sex-specific genetic influences on the development of drinking motivations. [Poster] Chayna J. Davis1, Valerie S. Knopik1, Sally J. Wadsworth1, Richard K. Olson1, and John C. DeFries1
Children with deficits in both rapid automatized naming (RAN) and phonological decoding (PD) have more severe reading difficulties than children with deficits in either RAN or PD alone (Wolf, 1999, Annals of
Dyslexia 49, 3-28). Because reading difficulties are highly heritable (DeFries & Alarcon, 1996, Mental Retardation and Developmental Disabilities Research Reviews 2, 39-47), the validity of
this typology may be tested by assessing the differential etiology of reading difficulties in the four different possible subtypes (children with deficits in RAN but not PD; PD but not RAN; the combined type; and neither RAN
nor PD). Composite reading performance, RAN, and PD data from 229 monozygotic and 178 same-sex dizygotic twin pairs in which at least one member of each pair was reading-disabled were subjected to DF multiple regression
analysis (DeFries & Fulker, 1985, Behavior Genetics 15, 467-473). RAN was measured using a variation of the subtests of Denckla and Rudel (1974, Cortex 10, 186-202), and PD was measured
using non-word reading tasks. Heritability of the group deficit in reading performance (h2g) across the full range of RAN and PD scores was .57. When the basic regression model was fitted
separately to data from twin pairs with standardized RAN scores below or above the mean, resulting estimates of h2g were .48 and .65, respectively, a nonsignificant difference (p < .28). In
contrast, when the basic regression model was fitted separately to data from twin pairs with standardized PD scores below or above the mean, resulting estimates of h2g were .30 and .67, respectively,
a significant difference (p < .02). Heritability estimates were also obtained by fitting the basic regression model to data from the children with deficits in RAN but not PD (h2g = .34), PD but
not RAN(h2g = .58), the combined type (h2g = .29), and neither RAN nor PD (h2g = .68). As expected, results of fitting
extended regression models to reading performance, RAN, and PD data simultaneously provided no evidence that the genetic etiology of reading disability differs as a function of RAN and PD jointly (p < .73). Thus, the results
of this study suggest that phonological decoding may be more important than RAN as a dimension to consider for possible differential diagnosis of reading difficulties. [Poster] Khytam Dawood, J. Michael Bailey, and Nick Martin
Animal work has suggested that opposite-sex fetuses can affect each other in utero. Results of these studies suggest that differential hormone exposure during development may modulate brain structure and function, and
thereby contribute to subsequent behavioral variation within and between sexes. The best established, and most theoretically explicable, effects are of male fetuses on female fetuses. The study of opposite-sex twins provides
a means of investigating prenatal hormonal influences on sexually dimorphic traits in humans. A few studies consistent with such effects have been reported. The objective of the present study is to identify whether females in
opposite-sex pairs are more masculine or less feminine than other females (and males more feminine or less masculine) on sexually dimorphic traits. Our study will be the best human study to date for the following reasons: a)
it has the largest sample size, b) it has more traits that are demonstrably sexually dimorphic, and c) the traits that it examines are those that have been best demonstrated to be sensitive to prenatal hormonal effects. Questionnaire
data from the Australian Twin Registry will be used. The sample includes 1908 complete twin pairs (980 MZ, 928 DZ), and 1085 singles. The questionnaire includes measures of sexual orientation, atypical gender role behavior
(childhood and adulthood), personality, interest in casual sex, attitudes toward homosexuality, juvenile delinquency, birth order, and sexual experience. We will identify sexually dimorphic variables in the questionnaire, and
focus on traits that may be especially sensitive to the effects of exposure to prenatal hormones. J.M.Delabar
Despite a vast amount of investigation of the pathology, biochemistry, and physiology of Down syndrome it is still not known how the individual genes on HSA21, either singly or in concert, produce the anatomical and
functional alterations associated with the trisomic state. However, what is known is that the phenotypic features that define the syndrome are attributable to the genes on HSA21 and are not the result of a non specific effect
of aneuploidy. The ultimate goal of constructing a phenotypic map is to define molecularly the chromosomal region and ultimately the genes that are responsible for particular phenotypic features. Due to the variability of the
phenotypic expression of a given trait among patients with full trisomy 21, the molecular data from many individuals must be combined to define small regions, optimally less than 2-3 Mb, that are suitable for molecular analysis.
Such a study has been performed on ten patients with partial trisomy 21 . After gene dosage characterization of the extent of the duplications a genotype-phenotype correlation study allowed to define regions duplications of
which might be associated with given features : a region of 2.3 Mb mapping in 21q22.2 should contain genes involved in 13 features including facial and hand features, joint hyperlaxity and mental retardation. This association
is also observed for a set of 50 patients collected in the ANEU21 database. Some of the genes from this region present a strong expression restricted to specific areas of the central nervous system and might be considered as
good candidate genes for some features. A second approach to relate specific components of the trisomic phenotype to the increased expression of genes is to construct mouse models with segmental trisomies or overexpressing
specific genes. First studies on these models seem to indicate that it will be possible to identify genes responsible for many components of the phenotype. Danielle M. Dick1, Richard J. Viken1, Jaakko Kaprio2, 3, and Richard J. Rose1
Gene-environment interactions have been demonstrated repeatedly in the animal literature in strain x rearing research designs, but they are difficult to document in human data. This is due, in part, to the large number of
twin pairs necessary to detect gene-environment interactions and other constraints inherent in modeling human gene-environment interactions. With data from FinnTwin16, a population-based sample of five consecutive
birth cohorts of twins, we have been exploring environmental moderation of genetic effects. Using Mx's raw data analysis feature, we fit moderation models to adolescent twins' drinking frequencies at age 16. Genetic and
environmental influences on adolescents' drinking patterns were moderated by family structure and sex. However, the interpretation of this interaction is complicated by the possible presence of both genetic and environmental
correlations with family structure. This presentation will explore the meaning of gene-environment interactions in the context of a complex set of intercorrelated factors--complexities likely to be the rule, rather than the exception,
in the real world. M. Dierssen, X. Altafaj, V. Fotaki, C. Casas, J. Visa, M.L. Arbonés, J. Guimerà, C. Fillat, C. Baamonde, C. Martinez-Cué, M. Lumbreras, J. Flórez and X. Estivill
Down syndrome (DS) phenotype results from overdosage of a cluster of proteins encoded by several human chromosome 21 (HSA21) genes. Our group has isolated several HSA21 encoded genes, and we have generated
murine models with different levels of expression of selected candidate genes for DS neuropathology. One of the selected genes is the human homologue (Dyrk1A) of Drosophila minibrain (mnb) that maps within theDS critical
region. mnb gene encodes a serine-threonine protein kinase, whose mutations result in defects in neurogenesis and perturbed visual, olfactory and motor behavior, as well as learning defects. To elucidate the contribution of Dyrk1A
to DS we have used three different experimental strategies. 1) We have generated mice carrying a targeted disrupted Dyrk1A gene and analyzed their neurobehavioral profile. Mice homozygous for the mutation are not viable,
but heterozygous mice are viable to adulthood and fertile. They are smaller in size and weight than wild-types and present delay in emergence of physical characteristics (eyelid and ear opening) and in some psychomotor aspects.
Adult heterozygous mice show alterations in regulation of locomotor activity. 2) We have also generated four lines of transgenic mice overexpressing the Dyrk1A gene (TgDyrk1A.) under the control of the sheep methallothionein
promoter. Neurobehavioral characterization of transgenic mice show retardation in neuromotor development. Adult TgDyrk1A show hyperactivity and some alterations in motor coordination. 3) Finally, the breeding of partial
trisomy 16 mice (Ts65Dn) with mice carrying the disrupted Dyrk1A gene gives rise to trisomic progeny with Dyrk1A in disomy. This progeny should allow to evaluate the reversal of parts of the phenotype seen in the Ts65Dn
mice.Supported by CEC/BIOMED2 BMH4-CT98-3039; SAF99-0092-CO2-01 and FIS 00/0795. V.F. has a Marie Curie Research Training Grant ERBFMBICT972278. Lisabeth F. DiLalla1
Genetic influences have been identified for adult violent behaviors, but less is known about genetic influences on aggressive behaviors in non-clinical samples of young children. Recent research has demonstrated a genetic
influence on parent- rated aggressive behaviors of adolescents. The current project assessed aggressive behaviors in preschoolers during unstructured free play with peers. This allows an extension of the research on genetic
influences of aggression to preschoolers and to behaviors children exhibit when interacting with peers rather than relying solely on parent ratings. Five-year-old twins were allowed to play one at a time with a same-sex, same-age
singleton child for 20 minutes in a lab playroom. Play was videotaped and later rated by trained coders. Children's aggressive behaviors were coded, including grabbing a toy from the other child, physical aggression, and verbal
threats. Parents also completed questionnaires, including the Child Behavior Checklist (CBCL) and the Behavioral Style Questionnaire (BSQ). An Aggression variable was computed by norming and then summing the Grab
score during play, the Mood and Activity scales of the BSQ, and the Delinquency and Aggression scales of the CBCL (Cronbach's alpha = .72). Intra-pair correlations showed that identical twins were more highly inter-correlated
than were fraternal twins, rMZ = .92 and rDZ = .52. Similar results were found when a partial correlation was conducted to control for the total amount of time the twins spent actually interacting
with the other child in the room. Analyses were repeated separately for boys with virtually identical results, rMZ = .91 and rDZ = .45. There were too few fraternal girls to calculate correlations at
this time. The results from this lab demonstrate for the first time that genetic influences are important for aggressive play behaviors in preschoolers during free play with unfamiliar peers. They augment other research relying
on parent reports for older children. [Poster] Brian M. D'Onofrio1, Eric Turkheimer1, Linda A. Corey2, Robert E. Emery1, Mary Waldron1, Kare Berg3, Lindon
J. Eaves2
The deleterious effects of maternal smoking on birth outcomes have been well documented, and in many cases, a causal relationship is implied. However, most of these studies do not assess the possibility that genetic factors
could account for the intergenerational relationships. The situation in which a common genetic component influences a parental behavior (measured as the environment) and an outcome in the child is referred to as a passive
gene-environment correlation because the parents provide both the environment and the genes to their children. Under these conditions, the correlation between the parental environment and the child outcome would not be
causal. The children of twins design, especially when spousal information is included, provides a powerful method to test parental and family environmental influences on children while controlling for genetic effects which
confound typical sociological or epidemiological studies of families. The current study utilizes the methodology to determine the degree to which common genetic factors and environmental pathways explain the relationship
between parental smoking and their children's birth weight. The study includes same-sex adult twins from Virginia and Norway, their spouses, and reports of their children's birth weight. Differing maternal and paternal effects
as well as the role of assortative mating are discussed. [Poster] Thalia C. Eley1, Derek Bolton2, Thomas O'Connor1, Sean Perrin2, Patrick Smith2, Robert Plomin1.
The structure of anxiety in pre-school children is not well understood. Measurement of such symptoms has tended to rely on the use of mother-reported global measures of emotional temperament or general internalizing
symptoms, and as such the behavioural genetic studies have tended to use these general measures. These have produced highly varied levels of heritability, which may be due to the mixture of symptoms within such general
measures. Previous analyses at 2- and 3- years from the Twins' Early Development Study (TEDS) found limited evidence for differentiation between two aspects of anxiety in young children: emotional temperament and anxiety
symptoms. Six factors of anxiety have been identified in the mother-reported data on around 2, 500 twin pairs aged four years. The measure included the anxiety and peer relationship scales from the Strengths and Difficulties
Questionnaire (Goodman, 1997, J. Child Psychol. Psychiat.38, 581-586), and various additional items assessing reflecting different types of anxiety symptom. These factors created were general anxiety, social
anxiety or shyness, peer-related anxiety, obsessive-compulsive symptoms, tics, and separation anxiety. Due to the extreme skew for some of the more rare symptoms (e.g. obsessive-compulsive symptoms and tics) threshold models
were fitted to the raw data. Preliminary univariate genetic analyses indicated quite different patterns of heritability for each of these dimensions of anxiety, both in the normal range and at the extremes. For example
obsessive-compulsive symptoms were highly heritable, as was shyness - the latter was predominantly influenced by non-additive genetic factors. In contrast, separation anxiety was significantly influenced by the shared environment.
Multivariate genetic analyses indicate some over-lapping genetic variance between the scales, and some scale specificity. These analyses validate the differing sub-scales of anxiety found in this dataset and suggest that we may
be able to distinguish between different types of anxiety in children as young as 4 years. Susan Felsenfeld1, Katherine M. Kirk2, Gu Zhu2, Dixie J. Statham2, M.C. Neale3, and N.G. Martin2
In this study, a population-based twin sample from the Australian Twin Registry (1567 pairs and 634 singles aged 17-29 years) was screened to identify twin pairs in which one or both members reported themselves to be
affected by stuttering at some point during their lifetime. From this sample, 331 cases (8.8%) identified themselves as stuttering-affected. Telephone interview-based diagnoses were subsequently obtained for 457 individuals
from the screening cohort (all contactable self-reported affected cases, all contactable cotwins of these cases, and a subgroup of controls) to determine whether the self-report was correct. Ultimately, 91 complete twin pairs (38
MZ and 53 DZ pairs) containing at least one stuttering member were identified in the interview phase of the study. To correct for ascertainment bias, a bivariate analysis of the final diagnosis in the selected sample with the screening
item in the full sample was performed, using the categorical raw data option of Mx 1.47c. After using bivariate analysis to correct the correlation and threshold values of the interview measure for ascertainment bias, the resulting
twin correlations suggested a strong genetic influence on the liability to stuttering (rMZ= 0.75; rDZ= 0.15). Multivariate structural equation modeling of these data revealed that approximately 70%
(95% confidence interval: 39-86%) of the variance in liability to stuttering in men and women was attributable to additive genetic effects, with the remainder due to non-shared environmental effects. The moderate correlation
between the screening item responses and an interview-based diagnosis obtained 5 to 7 year later (r= 0.60) highlights the importance of using sensitive diagnostic procedures for this disorder. [Poster] Deborah Finkel
Previous research has indicated that both perceptual speed (e.g., Salthouse, 1996) and sensorimotor functioning (Lindenberger & Baltes, 1997) mediate much of the age-related variance in cognitive functioning. The aim
of the present analysis was to examine genetic influences on cognitive ability in adulthood in the context of the relationship between perceptual speed, sensorimotor functioning, and cognitive aging. The heritability of cognitive
ability may result, at least in part, from genes that influence perceptual speed and sensorimotor measures instead of cognitive functioning, per se. Measures of motor performance, perceptual speed, and cognitive functioning in
four domains (crystallized, fluid, spatial, and memory) were available from the Swedish Adoption/Twin Study of Aging. The sample included 206 twin pairs ranging in age from 44 to 82 years. A Motor Speed factor was constructed
from 17 timed measures of motor performance. Heritability of Motor Speed was .26 in middle-aged twins and .00 in older twins. Results indicated that genetic variance in cognitive functioning in the middle-aged cohort may
be defined by motor speed, whereas genetic variance in the older cohort was defined by perceptual speed. Indications of a nonshared environmental component to the association among motor speed, perceptual speed, and spatial
abilities suggest possible frontal lobe involvement. Deborah Finkel1
Previous studies have demonstrated that MZ twins are more similar than DZ twins in the total number of items recalled on a word recall task. Heritability is about .55 (D. Finkel and M. McGue, 1993, Psych. Aging,
8, 527-537). As yet, no study has attempted to determine whether MZ twins are more likely than DZ twins to recall the same items from the original list. Seventy MZ twins and 40 DZ twins (aged 27-86) were presented
a list of 36 words as part of the Minnesota Twin Study of Adult Development and Aging (M. McGue, B. Hirsch, and D.T. Lykken, 1993, Psych. Aging, 8, 72-80). The mean percent of items recalled that were
recalled by both members of a twin pair was 76.5% for MZ twins and 75.0% for DZ twins. To determine whether twin similarity resulted from shared rearing effects or simply correlated environmental effects, word recall data
were collected from a sample of 40 singletons (aged 19-51). Twenty random pairs were created, matched on gender and age. The mean percent of items recalled that were recalled by both members of a random pair was 75.1%.
Results indicate that the higher than chance recall of identical items by MZ, DZ, and random pairs resulted from correlated environmental effects. Further analyses indicated that the high percentage of common items recalled
could not be explained by recency and primacy effects. [Poster] Nadine Forget-Dubois1, Daniel Pérusse1, George Tarabulsy2, Bernard Boulerice1, Marie-Claude Martel2, Michel
Boivin3, and Richard E. Tremblay1
A growing body of work aims to assess genetic and environmental influences on family relationships (Bussell et al., 1999, Developmental psychology 35, 1248-1259). The present study aimed to
identify the sources of variance on maternal sensitivity by including actual measures of the environment to a genetically sensitive analysis, rather than simply reporting proportions of variance attributable to genes, common, and
unique environment. Analysis were performed on a sample of 100 same-sex, five month-old twin pairs (50 MZ and 50 DZ pairs). Maternal sensitivity was assessed from spontaneous interactions videotaped in a laboratory setting,
using the Maternal Behavior Q-set (Pederson et al., 1990, Child Development 61, 1974-1983). Additional information concerning parents were obtained by questionnaires. We used multilevel hierarchical
analysis to fit genetic/environmental models to the data, separately for boys and girls. The best-fitting model for boys was a CE model and for girls, a model considering common and unique environment as well as an effect of
zygosity. Thus, no genetic effects on maternal sensitivity were found. We then added to these models variables related to SES and parents psychological. Preliminary results indicated that maternal psychological well being as
measure by the SCL-90-r (Derogatis, Lipman, and Covi, 1973, Psychopharmacology Bulletin9, 13-28) accounted for 25% of the variance between families (common environment) for girls. For boys, fathers
employment status explained 18% of the variance of the common environment. This study shows the importance of common environmental influence on parent-child relationships in infancy. It is suggested that the variables
included in the common environmentý category may vary according to gender. Finally, our results indicated mothers treated MZ girls more similarly than DZ girls. [Poster] Qiang Fu1, Andrew C. Heath1, Kathleen K. Bucholz1, Elliot Nelson1, Jack Goldberg2, Michael J. Lyons3, Theodore
Jacob4, Seth A. Eisen1, and William R. True5
Several studies have reported specific genes only predisposing to suicidal risk or increasing risks of suicidal behavior and psychiatric disorders (e.g. major depression, alcohol dependence and impulsiveness). The purpose
of this study was to investigate how much genetic risk could be explained by genes that are shared and specific to suicidality. Data were analyzed from 3, 361 middle aged male-male monozygotic and (MZ) and dizygotic (DZ)
twin pairs from the Vietnam Era Twin (VET) Registry who completed a telephone administration of the Diagnostic Interview Schedule Version 3 (Revised) in 1992. Lifetime persistent suicidal thoughts or attempts (suicidality)
were reported by 18% of the sample. Lifetime major depressive episode (MDE), antisocial personality disorder (ASPD), alcohol dependence (AD) and drug dependence (DD) were diagnosed according to DSM-III-R criteria.
Structural equation modeling was performed to estimate the additive genetic, shared environmental and unique environmental contributions common and specific to each condition simultaneously using Mx. A chi-squared test
of goodness-of- fit was used to assess overall fit of modelss. Under the best-fitting model (x2= 56.1, df=65, p=0.78), the results showed that additive genetic and unique environmental
influences accounted for 47% and 51% of the variance in risk for suicidality, respectively. The genetic and unique environmental risks for MDE explained 75% of the additive genetic and 39% of the unique environmental
variances in risk of suicidality, respectively. After adjustment for the overlapping genetic risk for MDE, 25% of the variance in genetic risk was specific to suicidality. Controlling for MDE, we did not find significant common
genetic and environmental factors between suicidality and other conditions. Our data suggest that genetic influences on suicidality in adult men are largely associated with MDE, but that there are also genetic effects specific
to suicidality. Unique environmental effects account for approximately one-half of the liability for suicidality. [Poster] Jeffrey R. Gagne1, and Kimberly J. Saudino1
Genetic and environmental influences on teacher reports of temperament in early adolescence were examined in the Colorado Adoption Project (CAP) using the adoptive/nonadoptive sibling design. The analyses included
adoptive sibling pairs participating in CAP with sample sizes that ranged from 60 at age 9 to 30 at age 12, and nonadoptive sibling pairs with sample sizes ranging from 73 at age 9 to 28 at age 12. Temperament was assessed
using the teacher version of the Colorado Childhood Temperament Inventory (CCTI) at ages 9, 10, 11, and 12 years. Sibling intraclass correlations suggested that teacher ratings of temperament are genetically influenced.
Nonadoptive siblings demonstrated moderate similarity for all dimensions at all ages, whereas adoptive siblings showed very little or no resemblance. Consistent with the pattern of intraclass correlations, pedigree model-fitting
analyses reveal that with the exception of activity, the CCTI temperament dimensions show moderate heritability. Heritabilities ranged from .19 to .49 for emotionality, from .08 to .62 for activity, from .31 to .61 for sociability,
and from .25 to .51 for attention, although as a result of small sample sizes, these findings were not significant. For most age-to-age comparisons the genetic correlations approach 1 suggesting that there is substantial genetic
overlap across age. In addition, the cross-age phenotypic correlations are largely due to genetic factors. Previous research indicates that neither parent ratings, nor self-reports of temperament on the CCTI displayed evidence of
genetic variance in adoptive/nonadoptive sibling analyses in CAP (K. J. Saudino & J. R. Gagne, 1998, paper presented at the 10th Annual Convention of the American Psychological Society, Washington, D.C.). The current
findings suggest that although we have different teachers rating temperament at different ages, there is genetic continuity in teacher perceptions of temperament in early adolescence. [Poster] Jody Ganiban1, Jenae Neiderhiser2
Attachment styles are typically viewed as products of relationship experiences. Yet, recent studies suggest that genetic factors also play a role (D. Finkel, D. Wille, A. Matheny, 1998, Behav. Genet.28, 1-8;
K. Lang, W.J. Livesley, P. Vernon, 1998, Eur. Jo. Person.12, 331-344). This study examined sources of genetic contributions to adult attachment, including personality and relationship experiences. This issue
was examined within adult female Swedish twin pairs participating in the Twin Mothers project. Two dimensions of attachment style (secure vs. avoidant attachment; degree of attachment anxiety), and personality characteristics
relevant to negative emotionality (irritability, psychic anxiety, somatic anxiety) were assessed. In regard to relationships, recollections of maternal warmth during childhood, and the quality of current marital relationships were
assessed. Data were analyzed using a Common Factor model, which also included unique factors for each of the four variables. Preliminary analyses suggest that: (a) collectively, genetic and shared environment contributions
to attachment style were explained by negative emotionality, maternal warmth, and marital quality; (b) only non-shared environment made unique contributions to attachment style. Nathan Gillespie1, David L. Duffy1, Nicholas G. Martin1
Under certain conditions, cross sectional analysis of cross-twin inter-trait correlations can provide important information about the direction of causation (DOC) between two variables. A community-based sample of 3269
Australian twin pairs aged between 18 to 28 years was mailed an extensive Health and Lifestyle Questionnaire (HLQ) which covered a wide range of health issues affecting younger people. Included were self-report measures
of recently experienced psychiatric symptoms (SCL & DSSI/sAD), measures of personality (EPQ & TPQ) as well as ratings of parents' rearing style (PBI). An advantage of using a younger cohort is that while the sample is
old enough to report symptoms of psychopathology, twins should still be young enough to recollect parental rearing style. Univariate analysis revealed that the best fitting model for the psychiatric symptoms, personality
dimensions and recollections of parental rearing style was an additive genetic and non-shared environmental effects (AE) model for male and female twins alike. Despite the inclusion of measurement error to relax the equality
constraint relating to rE, it was is not possible to model DOC between our phenotypes, since each has only two sources of variance, and results will give the same fit as the general bivariate model. We therefore modeled DOC
using a multiple indicator model (MIM) with its increased power to detect different modes of inheritance. Although the application of MIM's to to provide tests of the goodness of fit to reciprocal causation models (AUB) is
only possible with at least three sources of variance, the same procedure can provide tests of the goodness of fit to unidirectional causation models (A?B, or A?B) when only two sources of variation are present. Results of model
fitting and limitations of DOC modeling will be discussed. Julia D. Grant1, Andrew C. Heath1, Kathleen K. Bucholz1, Pamela A. F. Madden1, and Nicholas G. Martin2
We assessed spousal correlations for alcohol dependence in a sample of middle-aged Australian twins. Data from 5976 individuals who completed a telephone diagnostic interview for the Australian Twin Study ("1981 cohort";
2702 complete pairs: MZF=935, MZM=398, DZF=534, DZM=234, DZO=601; 572 individual respondents) were analyzed. Respondents had a mean age of 44.0 years at the time of interview. Based on self report data, 548
twins met DSM-IV lifetime criteria for alcohol dependence (AD). Twin reports of spouse history of alcohol problems were available for 5365 individuals (with 501 reporting a history of alcohol problems); spouse interview data
were available for 3814 individuals (with 668 meeting DSM-IV criteria for alcohol dependence). Genetic and nonshared environmental influences each accounted for 50% of the variance in twin alcohol dependence. When
examining twin reports of their own alcohol dependence and their spouse's history of alcohol problems, the spousal correlation was .37; when using self-reports of alcohol dependence from both the twin and the spouse, the spousal
correlation was .26. Both of these correlations were significant, consistent with positive assortative mating for alcohol dependence. The somewhat different magnitude of the spousal correlations could indicate that the twins
overestimate their similarity to their spouses, or could reflect a sampling bias in the spouses that completed the interview. Further analyses combining twin self-reports, twin reports of spouses, and spouse self-reports of alcohol
problems will be presented. Martin E. Hahn
Between 1946 and 1959 John Paul Scott and John L. Fuller led a project on the genetics and social behavior of dogs. Because of its scope and quality, the project is likely the finest example of work on genes and social behavior
ever completed. A part of the project which attracted considerable attention at its publication, was a set of isolation experiments with puppies. In those experiments, puppies were isolated from animal and human contact for 12
weeks, from three weeks of age through 15 weeks of age. During those weeks of isolation, some puppies were brought out for contact with humans, other puppies, and toys for very brief periods (a total of eight minutes per week).
Some puppies were allowed brief emergence from isolation but punished for approaching humans. Other puppies were maintained in isolation for the complete 12 weeks. The emergence of those puppies from isolation was of
special interest. Some of those puppies were given the tranquilizer, chlorpromazine, on emergence. A film documenting the experiments was in the library of John Fuller and is currently in the archives of The Jackson Laboratory.
The film, entitled Canine Kaspar Hausers, was photographed by John Fuller who also wrote an accompanying narration. The film with narration added, will be shown and discussed. As John concludes in the narration, "On the
basis of current findings, we suggest that early deprivation produces its effects indirectly by setting up conditions favorable to induction of fear by exposure to complex stimulation. The organism does not outgrow the capacity
to learn and normal psychological development can proceed if the fear block is removed. We have shown that at least one drug can aid in the lifting of the block." Narelle K. Hansell1, 2, Margie J. Wright1, Gina M. Geffen2, Laurie B. Geffen2, Glen A. Smith1, 3, and Nicholas G. Martin1
Genetic influences are examined for event-related potential (ERP) measures elicited in a delayed-response working memory task. These measures are being collected as part of a large ongoing twin study of cognition (the
Memory, Attention and Problem Solving study), as working memory is an important component of general cognitive functioning (E. Necka, 1992, Pers. Individ. Diff.13, 1031-1046). In ERP studies, delaying
response in a working memory task has been found to elicit a slow wave (SW) (P. Rama, S. Carlson, J. Kekoni, and H. Hamalainen, 1995, Electroencephalogr. Clin. Neurophysiol.94, 371-380). In our own
laboratory, increased SW negativity was found to reflect maintenance of target position during the delay period (G. M. Geffen, M. J. Wright, H. J. Green, N. A. Gillespie, D.C. Smyth, D. M. Evans, and L. B. Geffen, 1997, J.
Cogn. Neurosci.9, 743-757). No genetic studies have examined long latency ERP components such as SW, but there is evidence that other components such as P3 amplitude are genetically influenced (J. Katsanis,
W. G. Iacono, M. K. McGue, and S. R. Carlson, 1997, Psychophysiol.34, 47-58). In the present analyses, data collected from 327 twin pairs aged 16 years are used. All participants are required to touch the
remembered position of a target on a computer screen after a short (1 or 4 s) delay period while ERPs are recorded from 15 scalp locations. Memory trials are compared to sensory control trials that require no memory. Preliminary
analyses suggest that the SW is genetically influenced at more scalp locations in memory than sensory trials. Other patterns of genetic influence are expected to emerge and will be discussed. The present study is the first to examine
genetic influences on physiological measures of working memory. Christopher W. Hess, Martin E. Hahn, Robert H. Benno, and Norman Schanz
Previous studies have demonstrated impairment of maternal retrieval behavior as a result of acute cocaine exposure. In an effort to establish the influence of prenatal cocaine exposure on these same behaviors, we studied
maternal retrieval in mice of three genotypes. We prenatally exposed pups of three F1 genotypes by injecting their mothers (all C57BL/10J strain) with 20 mg/kg cocaine hydrochloride or saline subcutaneously on gestation days
7-17. After these animals matured, we mated females with males of the same genotype who were randomly selected for prenatal exposure to cocaine or saline. Following the births of litters from these pairs, we tested the retrieval
behavior of female subjects from control and treatment groups in both a two-choice apparatus on postpartum day 4 and an open field on day 5. Prenatal cocaine exposure exerted a significant effect upon retrieval latency. However,
this effect was confined to one genotype (BALB F1) and one measure of retrieval (two-choice apparatus on day 4). These results are in accordance with previous studies finding situation-specific deficits in the ability of prenatally
exposed subjects in at least one genotype to respond to environmental stressors and demands. [Poster] John .M. Hettema1, Carol A. Prescott1, and Kenneth S. Kendler1, 2
Background. As Generalized Anxiety Disorder (GAD) has undergone significant revisions over the last two decades, we continue to be uncertain of the role genetic factors has in its etiology. The data show higher rates of
GAD in women than men, yet we know even less about how gender may impact the genetics of GAD. Methods. We obtained a lifetime history of DSM-IIII-R and DSM-IV GAD, via face-to-face and telephone interviews, from
3, 100 complete male-male, female-female and male-female twin pairs, ascertained through a population-based registry. Varying definitions of illness were created to increase statistical power by broadening diagnostic criteria.
Biometrical twin modeling was utilized to estimate the relative contributions of genetic and environmental factors to liability for GAD, allowing for gender-specific effects. Results. The familial aggregation of GAD in this sample
was only modest. Due to the relatively small number of affected individuals, we were unable to definitively resolve competing genetic and non-genetic models of familial transmission. Although there was some inconsistency
across diagnostic definitions, overall the results suggested that the source of twin resemblance was largely genetic. In the best-fitting twin models, the heritability of liability to GAD was the same in men and women, estimated
at about 15-20%. Conclusions. GAD is a modestly familial disorder in which the predominant source of twin resemblance appears to be genetic in origin. Our data is consistent with the hypothesis that genetic risk factors impact
liability to GAD similarly in the two sexes. [Poster] Brian M. Hicks, Robert F. Krueger, William G. Iacono, and Matt McGue
Utilizing the 17-year old twin cohort of the Minnesota Twin Family Study, a community based longitudinal sample, we performed biometric analyses to delineate the genetic and environmental sources of covariation among
the externalizing disorders (substance use and antisocial behavior disorders) and personality traits reflecting disinhibition. Our sample consisted of 594 twin pairs (199 female MZ twin pairs, 188 male MZ twin pairs, 106 female
DZ twin pairs, and 101 male DZ twin pairs). Personality traits were assessed using the Multidimensional Personality Questionnaire (MPQ). Mental disorders were assessed using the Structured Clinical Interview for DSM-III-R,
the Substance Abuse Module from the Composite International Diagnostic Interview, and a specially-designed interview for the assessment of conduct disorder and adult antisocial behavior. We fit a series of biometric models
to these data: a Cholesky decomposition model, an independent pathway model, and a common pathway model. In addition, we attempted to replicate our findings at age 17 intake using data from an age 20 follow-up
assessment. Kai Hiraishi12, Juko Ando3, Yutaka Ono4, Toshikazu HASEGAWA1
This study attempts to bridge two research fields which thus far have developed in relative isolation from each other; behavioral genetics and evolutionary psychology. The Selection task is a reasoning task where the modal
answers change depending on the content of the problem. Evolutionary psychologists argue that evolutionarily acquired mental mechanisms lead to the modal answers on the Selection tasks. This argument implies small genetic
influence on the performances on the Selection task; since natural selection works to exclude disadvantageous traits, thus producing a genetically homogeneous population. On the other hand, taking the findings of behavioral
genetics regarding heritability of cognitive abilities, substantial genetic influence is expected. Thus we conducted a Selection task study with the twin design. Respondents were 219 pairs of twins participating in the Keio
Twin Project (MZ: 133, DZ: 86, 15- to 27-year-old, mean age: 20-year-old). They answered three types of Selection tasks: two with a deontic rule (social-contract or precaution) and one with an arbitrary rule. The probandwise
concordance rates for making modal answers were not significantly different from MZ twins to DZ twins on all the problems (Social-contract, MZ: 68% vs. DZ: 62%, NS, Precaution, MZ: 69% vs. DZ: 63%, NS, Abstract, MZ:
50% vs. DZ: 42%, NS). Likewise, the concordance rates for not-making modal answers did not significantly differ from MZ twins to DZ twins (Social-contract, MZ: 71% vs. DZ: 64%, NS, Precaution, MZ: 54% vs. DZ: 48%,
NS, Abstract, MZ: 55% vs. DZ: 67%, NS). The comparison of "similarity score" between MZ twins and DZ twins was also not significant. These results indicate small genetic influence on the performances, supporting the
evolutionary psychology hypothesis. $B!! (JHowever, given few literatures regarding heritability of performances on reasoning tasks, further research is required. [Poster] Kristen C. Jacobson, Carol A. Prescott, and Ken S. Kendler
This study investigates sex differences in the underlying genetic and environmental architecture of the development of antisocial behavior (AB). Retrospective reports of AB prior to age 15 (childhood), age 15-17 (adolescent),
and age 18 and older (adult) were obtained from a population-based sample of 6806 male-male, female-female, and opposite-sex adult twins. Structural equation modeling was used to examine sex differences in the underlying
genetic and environmental architecture of the development of AB. Results revealed both similarities and differences across sex in the pattern of genetic and environmental influences on the development of AB. There was no
evidence for sex-specific genes or shared family environments on the development of AB. In addition, for both sexes, a model that allowed for genetic influences on adolescent and adult AB that were not shared with childhood
AB fit better than a model with a single genetic factor, whereas shared environmental influences on adolescent and adult AB overlapped entirely with shared environmental influences on childhood AB. The heritability of AB
also increased substantially from childhood to adolescence and adulthood for both sexes. Two primary sex differences were found: the heritability of childhood AB was greater among females than among males;
conversely, shared environmental factors played a larger role in variation for childhood AB among males than among females. The magnitude of genetic and environmental influences on adolescent and adult AB were approximately
equal across sex. [Poster] Kerry L. Jang1, Robert R. McCrae2, W. John Livesley1, Rainer Riemann3, and Alois Angleitner3
The phenotypic structure of personality traits has been well described, but it has not yet been explained causally. Behavior genetic covariance analyses can identify the underlying causes of phenotypic structure; previous
behavior genetic research has suggested that the effects from genetic and non-shared environmental influences both mirror the phenotype. However, non-shared environmental effects are usually estimated as a residual term that
may also include systematic bias, such as that introduced by implicit personality theory. To reduce that bias, we supplemented data from Canadian and German twin studies with cross-observer correlations on the Revised NEO
Personality Inventory. The hypothesized five-factor structure was found in both the phenotypic and genetic covariances. When the residual covariance was decomposed into true non-shared environmental influences and method
bias, only the latter showed the five-factor structure. True non-shared environmental influences are not structured as genetic influences are, although there was some suggestion that they do affect two personality dimensions,
Conscientiousness and Love. Jaakko Kaprio1, 2, Danielle M. Dick3, Richard J. Viken3, Kalle Romanov1, and Richard J. Rose3
Understanding the factors influencing smoking habits is an important health priority, due to the numerous health risks related to smoking. Using a population-based sample of five birth cohorts of Finnish twins, we present
genetically informative analyses of influences on smoking across time and causes of covariance between smoking and drinking. With data from 724 concordantly smoking same-sex twin pairs, we ran trivariate Cholesky
decompositions of smoking frequency at ages 16, 17, and 18.5. Results indicated that genetic and environmental influences on smoking remained relatively stable across this age range, with genetic factors accounting for
approximately 50% of the variance, common environmental factors accounting for ~30% of the variance, and unique environmental factors accounting for ~20% of the variance, at all ages. The best-fitting model for the data
indicated that the same common environmental factors were acting across this age range, while genetic factors were both shared and age-specific. A bivariate analysis of smoking and drinking at age 16 suggested that largely
the same genetic factors were influencing smoking and drinking initiation. However, a parallel analysis of smoking and drinking frequency, among twin pairs concordantly smoking and drinking, indicated
that genetic influences on frequency of use were more substance-specific (r = .25). Common environmental factors for both initiation and frequency were correlated at approximately .50. No significant sex differences
were detected. Katherine M. Kirk1, Gavin Andrews2, and Nicholas G. Martin1
Multivariate modelling of anxiety and depression data in twins has suggested that the two phenotypes are largely underpinned by one genetic factor (K. S. Kendler, A. C. Heath, N. G. Martin, and L.J. Eaves, 1987, Arch.
Gen. Psychiatry 44451-457), while other studies have indicated a relationship between these disorders and neuroticism (e.g. R. Jardine, N.G. Martin, and A. S. Henderson, 1984, Genet. Epidemiol1,
89-107). As part of a study to identify quantitative trait loci for anxiety and depression, questionnaire responses and interviews of Australian twins and their family members conducted during the past 20 years were reviewed
to identify individuals with neuroticism, anxiety and depression scores in the top or bottom deciles of the population. This information was then used to identify extreme concordant and discordant sib pairs (N. Risch, and H.
Zhang, 1995, Science 268, 1584-1589). Extremely high participation rates were achieved in this study, with over 90% of contactable prospective participants completing the interview phase. Participation
bias arising from the nature of the selection variables was minimal, with only a small difference between rates of interview participation among prospective participants with high and low selection scores (p = 0.028). The
interview permitted the diagnosis of depression and several anxiety disorders (OCD, agoraphobia, panic disorder, generalised anxiety disorder) in this sample according to DSM-IV criteria. The methodology for selection of
prospective subjects was demonstrated to be extremely successful, with highly significant differences in depression and anxiety disorder prevalence rates between individuals in the two selection groups (p < 0.001 for most
phenotypes). Markku Koskenvuo1, 2, Kirsi Lillberg2, Heli Koivumaa-Honkanen3, and Jaakko Kaprio1, 4
Life satisfaction is an indicator of subjective well-being, and can be viewed as a global assessment of life based on the fit between personal goals and achievements. It has also been found to be predictive of various health
outcomes, including long term mortality (Koivumaa-Honkanen et al, Am. J. Epidemiol. , in press) and suicide. Using the older Finnish Twin Cohort, we carried out genetically informative analyses of a four-item
life satisfaction scale. Among the 11540 twin individuals born 1930-1957, who replied to questionnaires in 1975, 1981 and 1990, mean life satisfaction scores were very stable, and were not correlated with sex or age ('r's less
than 0.03). We identified 1431 MZ and 2636 like-sexed DZ pairs in which both co-twins had replied to all 3 questionnaires. Trivariate Cholesky decompositions of life satisfaction frequency in 1975, 1981 and 1990 was carried
out using Mx. Results indicated that genetic and environmental influences remained stable across measurement occasions, with additive genetic factors accounting for 25-30% of the variance at each occasion. Both genetic and
environmental factors were both shared and occasion-specific. Over 50% of the covariance between measurement occasions could be attributed to genetic factors. [Poster] Robert F. Kreuger1
How closely do observed, phenotypic personality structures correspond with underlying, genetic and environmental personality structures? This question was addressed using data from 2, 490 pairs of twins from the Minnesota
Twin Registry who completed the Multidimensional Personality Questionnaire (MPQ). Phenotypic, additive genetic, and non-shared environmental correlations were computed among the MPQ's eleven primary scales. Principal
component analyses of all three matrices revealed three broad, higher-order components that were readily interpreted as negative emotionality, positive emotionality, and constraint. The components from all three matrices were
highly congruent, suggesting that the observed, phenotypic structure of personality corresponds closely with the underlying, etiologic structure of personality. Lisa N. Legrand, Matt McGue, and William G. Iacono
A prior investigation of 591 male twins from the Minnesota Twin Family Study demonstrated gene-by-environment interactions in the development of early adolescent substance use. Genetic risk was estimated from parents'
substance-related diagnoses, and environmental risk from the boys' affiliations at age 11 with social groups likely to either encourage or discourage substance use. Regression analyses revealed both main effects and a significant
interactive effect between the genetic- and environmental-risk variables in the prediction of the number of different substances tried by age 14. Using the same-aged female cohort (N=605) we will investigate whether
a gene-environment interaction emerges with young adolescent females, as well. Preliminary analyses suggest that while main effects are significant, the interaction term is not. Furthermore, although teacher-rated externalizing
tendencies contributed to the prediction of the males' substance use independently from the environmental-risk variable, this does not appear to be the case for females. A comparison of the male and female data will be presented,
along with analyses exploring possible reasons for the different results for each gender. [Poster] Christina N. Lessov1, Pamela A.F. Madden1, Kathleen K. Bucholz1, Alexandre A. Todorov1, Nicholas G. Martin2, Wendy S.
Slutske3, Laura J. Bierut1, and Andrew C. Heath1
The DSM-IV and the Fagerstrom Test of Nicotine Dependence (FTND) are commonly used to assess nicotine dependence. The two measures are highly correlated, but the estimates of prevalence are highest under DSM-IV
criteria and will vary across gender under FTND criteria (DSM-IV: 35% for women, 36% for men; FTND: 12 % for women, 18% for men; data obtained from over 2000 pairs of Australian young adult twins). However, the
DSM-IV and FTND criteria yield similar heritability estimates (~60%), and there is no evidence for shared environmental effects. In addition, no gender differences in heritability are deteced under either criterion. We are
currently performing analyses to assess the degree to which the DSM-IV and FTND criteria may represent indices of the same underlying genetic liability to nicotine dependence. Mark H. Lewis1, Cortney A. Turner1, Michael F. Presti1, Howard A. Newman1, Charles J. Epstein2, and Linda Crnic3
Stereotyped behaviors (e.g., body rocking) occur at high rates in individuals with mental retardation (e.g., Down syndrome). To determine if spontaneous stereotypy occurs in an animal model of Down syndrome (Ts65Dn),
undisturbed Ts65Dn and control mice were videotaped in their home cages for 5 hours/day on two consecutive days during their dark cycle. Motor activity was assessed in novel automated test chambers. In order to provide an
additional assessment of the association of stereotyped behavior with environmental challenge, mice were tested in acoustic startle and rotor rod paradigms. In home cage observations, 3 of 9 (33%) Ts65Dn mice displayed
stereotyped jumping (up to 41% of time) with an additional 3 animals (33%) displaying cagetop twirling (20% of time), for a total of 67% exhibiting stereotypy. None of the control mice exhibited jumping and 9% (1/11) engaged
in cagetop twirling (35% of time). Ts65Dn mice exhibited significantly less locomotor activity and rearing than did controls, this difference being due primarily to the low level of activity of the stereotypic trisomic mice. On
the rotor rod, the Ts65Dn mice attained significantly lower rotor rod speeds than did controls and did not differ from controls in the amplitude of the acoustic startle response. These environmental challenges did not appreciably
increase stereotypy over that observed in the home cage. Additional observations were conducted on Ts1Cje mice that are trisomic for the distal portion of chromosome 16. These mice were not observed to exhibit stereotyped
behavior and were generally hypoactive relative to controls. These observations suggest that a restricted proximal segment of chromosome 16 must be triplicated in order for the spontaneous stereotypy observed to be expressed.
Paul Lichtenstein1
Behavior genetic research has shown that genetic effects are important for divorce rates. However, very little research has been done on marital quality or other types of marital processes. In the Twin Mom study one of the
main goals is to evaluate the etiology of genetic and environmental influences for marital relationships. Because there is ample evidence that stable personality traits are linked to marital quality, it is possible that genetic and
environmental influences for stable characteristic in the women mediate influences on marriage. Using the Twin Mom sample we investigated genetic and environmental influences on self-report and observer ratings of marital
quality (satisfaction, closeness, warmth and marital conflict. Further, we evaluated how genetic influences were mediated by the stable characteristics. Martial quality is influenced by nonshared environmental and genetic influences.
A major part of the genetic influences seem to be mediated by stable personality characteristics. These results should be taken into account when investigating the relationships among stable characteristics, marital processes,
and mid-life adjustment. Michelle Luciano1, 2, Glen A. Smith1, 3, Gina M. Geffen2, Margie J. Wright1, Laurie B. Geffen2, and Nicholas G. Martin1
Previous findings have shown a substantial contribution of genetic variance to basic measures of information processing (P.A. Vernon, 1989, Pers. Individ. Diff.10, 573-576; M. McGue, and T.J. Bouchard,
1989, in R.J. Sternberg, ed., Advances in Psychology of Human Intelligence, Lawrence Erlbaum Associates, New Jersey). These studies have either used a speed of processing component derived from an array of diverse
information processing tasks (varying in complexity) or a particular dependent variable from one task alone. Working memory, a higher information processing measure, has also shown genetic influence, although the degree
of heritability is largely dependent on the task used to measure memory (A. Thapar, S.A. Petrill, and L.A. Thompson, 1994, Behav. Genet.24, 155-160). In this study, 6 variables were assessed from a basic
information processing task (choice response time), and dependent measures (sensory and memory conditions) were recorded on a visuo-spatial delayed response task. 328 twin pairs who participated in the Memory, Attention
and Problem Solving Study were sampled. Univariate genetic analyses - adjusted for the stability of the test measure - revealed strong, but differing, degrees of genetic influence on choice response variables and sensory variables
from the delayed response task. Multivariate analyses were performed with results supporting the presence of more than one common genetic factor contributing to the covariance among information processes. Angus W. MacDonald, III, Michael F. Pogue-Geile, Judy L. Thompson, Laura L. Ross, Tamika Allen, Melissa K. Johnson, Nicole D. Lollo, Allison R. Marquette, Eric J. Yablonski, & Cameron
S. Carter.
Rationale: A number of sibling studies have shown that neuropsychological deficits in the healthy first-degree relatives of patients with schizophrenia may be linked to unexpressed genetic liability to this disorder.
Attention and working memory measures are particularly sensitive to unexpressed liability. However, these studies have not been able to establish whether 1) attention and maintenance processes are dissociable components
of genetic vulnerability, 2) they derive from a common deficit, or 3) they result from a generalized deficit. Methods: The current study evaluated the healthy adult siblings of patients with schizophrenia using expectancy
and delay manipulations of the AX-CPT paradigm. In this version, 80% of trials were AX pairs, with the rest AY, BX and BY pairs (B is any non-A cue, Y is any non-X probe). This expectancy manipulation increased AY
false alarms if the A was strongly represented and increased BX false alarms if the B was weakly represented. A delay (0 or 5 seconds) between the cue and the probe allowed us to examine how cue representations degraded over
time. Selective attention, response inhibition, and response-set maintenance were thereby dissociated. The study involved both letter and dot-pattern versions of the task, which allowed us to examine whether modality-specific
pathways were differentially influenced by the genes of liability. Results: Increased BX false alarms observed in the delay condition suggest that response dysinhibition in siblings of patients is a failure to maintain the
response set, rather than an attentional deficit. Because demographically-matched control subjects had absolutely more AY false alarms than siblings, this deficit is not the expression of a generalized deficit. The pattern of errors
was similar for both modalities. These findings suggest that specific measures of response set maintenance may be sensitive to genes associated with liability to schizophrenia. Correlations between CPT measures and
neuropsychological test scores will be discussed. Pamela A.F. Madden1, A.C. Heath1, J.P. Rice1, J. Kaprio2, M. Koskenvuo2, N.L. Pedersen3, A.A. Todorov1,
C. N. Lessov1, and N.G. Martin4
Questionnaire survey data obtained from large samples of male and female like-sexed twins, 18-45 years of age, from three different countries (Australia, N=2, 284 pairs; Sweden, N=10, 948 pairs; and Finland, N=8, 651
pairs) were used to examine the usefulness of heavy smoking as a phenotype for the ascertainment of families in a study designed to identify genes that contribute to risk of addiction to nicotine. Despite substantial differences
in prevalence (e.g., between 33-46% in the Australian women, and between 8-16% in the Scandinavian women), the magnitude of genetic influence for lifetime heavy smoking, defined as smoking on average 20 or more cigarettes
per day, was consistent across country, and across age groups for women (67% heritability, 95% CI: 47-73%) and for men (37%, 95% CI: 19-55%). Similar estimates of genetic effect were observed in men when the threshold
for heavy smoking was increased to 25 cigarettes per day (43%, 95% CI: 11-60%). Results suggest that ther! ! e are strong genetic influences on heavy smoking, and that the magnitude of genetic risk for the amount of cigarettes
smoked may differ in men and women. Because the amount of nicotine consumed may be partially determined by factors that vary by sex, it may be important to use sex-specific definitions of heavy smoking in the selection
of families for genotyping. Hermine H. Maes, Patrick F. Sullivan, Cindy Bulik, Michael C. Neale, Kenneth S. Kendler, and Lindon J. Eaves1
The development of nicotine dependence and smoking cessation require prior smoking initiation. We examined the relationship between genetic and environmental risk factors for initiation, dependence and cessation in
two samples. Smoking initiation and cessation was assessed by questionnaire in male and female twins from the Virginia 30, 000 sample. In addition to initiation and cessation, nicotine dependence was assessed by personal
interview in male twins from the population-based Virginia Twin Registry. Results indicated that the liability to start and stop smoking are correlated in the younger sample of the VA30,000, but not in the older (>50 years) sample.
For the male Virginia Twin Registry sample, the correlated liability model fitted best to the data on smoking initiation, nicotine dependence and smoking cessation. Both the causal paths from initiation over dependence to cessation
and directly from initiation to cessation were significant. Genetic factors account for the familial resemblance in smoking initiation and cessation. Excluding genetic risk factors for smoking initiation, the specific familial
aggregation for nicotine dependence cannot be resolved in terms of genetic versus shared environmental factors.
Kristian E. Markon1, Robert F. Krueger1, and Thomas. J. Bouchard1
A number of recent studies have demonstrated substantial relationships between normal and abnormal personality traits. Most of these analyses, however, have been restricted to phenotypic models. Using 128 monozygotic
and dizygotic twin pairs from the Minnesota Study of Twins Reared Apart (MISTRA), genetic and environmental correlations between scales of the MMPI and MPQ were estimated. Results indicate that phenotypic correlations
between normal and abnormal personality are mediated by genetic as well as environmental factors, although the magnitude of genetic covariance tended to be larger overall. Achievement motivation demonstrated genetic and
environmental correlations in opposite directions with a number of scales, demonstrating the importance of distinguishing between phenotypic patterns and their etiological underpinnings. Angela J. Marlow1, Simon E. Fisher1, Clyde Francks1, Joel Talcott2, Alex J. Richardson2, Anthony P. Monaco1, John
F. Stein2, and Lon R. Cardon1
Although several studies have reported evidence for linkage of reading measures to specific chromosomal regions (L. R. Cardon et al., 1994, Science 266, 276-279; S. E. Fisher et al., 1999, Am J Hum
Genet 64, 146-156; J. Gayan et al., 1999, Am J Hum Genet 64, 157-164; E. L. Grigorenko et al., 1997, Am J Hum Genet 60, 27-39), the nature of replication remains unclear
because different studies have analysed different phenotypes from samples ascertained under different criteria. Recently, Fisher et al. (1999) reported replication evidence on chromosome 6p using a sample of 82 sibling pairs.
Analysis of only some reading measures in this study revealed evidence for linkage. Here we conduct some multivariate genetic analyses on these data to examine the extent to which the linkage results are consistent with the
familial correlations. We also describe the ascertainment scheme employed, some properties of the measures and descriptive statistics in this sample. We examine eight measures of reading ability and IQ, including the British
Ability Scales (BAS) tests of word recognition, spelling, similarities and matrices, (C. D. Elliot et al., 1979, NFER, Slough, UK), non word and irregular word reading (A. Castles, and M. Coltheart, 1993, Cognition
47, 149-180), spoonerisms (A. Gallagher, and N. Frederickson, 1995, Educ Child Psychol 12, 53-67) and pseudohomophones (R. Olson et al., 1994, in G. R. Lyon, ed., Frames of reference for the
assessment of learning disabilities 243-277). The phenotypic correlations amongst the measures vary widely, with high correlations between some of the tests (e.g., word recognition and irregular word reading = 0.79, spelling
and pseudohomophones = 0.64) and more modest correlations between the reading tests and specific IQ scales (range 0.28 -0.39). Principal components analysis indicates two factors that appear to reflect general reading ability
(explaining 55% of the variance) and IQ (explaining 13% of the variance). Familial correlations mirror the general trend observed in the phenotypic correlations, with some specific differences. Neilson C. Martin, Lon R. Cardon, and Jonathan Flint
Population-based studies of multifactorial traits provide the opportunity to emply a wide variety of selection schemes to minimize genotyping effort and maximise statistical power to detect individual loci. We have conducted
a population-based survey of 88, 141 individuals in Southern England using the Eysenck Personality Questionnaire (EPQ). The sample includes 52249 males and 35893 females and 26799 unique subling pairs. A subset of
1618 individuals were re-assessed on the questionnaire in order to evaluate measure repeatability in this sample. Sibling correlations amongst the specific items are similar to those obtained from twin studies (e.g., sibling
r(neuroticism)=0.165; sibling r(extraversion)=0.173). Scale repeatability ranged from 0.70 - 0.93. Here we report on the study design, sample demographics, and describe some selection plans to guide genotyping and locus
identification. [Poster] Nicholas G. Martin1, and Katherine M. Kirk1
As part of a study to identify quantitative trait loci for anxiety and depression, extreme concordant and discordant sib pairs for the traits of neuroticism, anxiety and depression were identified via reviewing responses to
questionnaire and interviews conducted during the past 20 years of a large cohort of Australian twins and their family members. Re-interview of the selected sample has provided DSM-IV diagnoses for depression and a range
of anxiety disorders for 2470 individuals in 1091 families, including twins and their siblings, parents and/or children. Results of structural equation modelling of twin and family data on the traits of anxiety and depression
will be presented, using corrections for ascertainment bias (T. Wade, M. C. Neale, R. I. Lake, and N. G. Martin, 1999, Behav. Genet. 29, 1-10). Matt McGue1, and Kaare Christensen2
The Longitudinal Study of Aging Danish Twins (LSADT) began in 1995 with an assessment of all living Danish twins aged 75 years and older. A second wave assessment of all twins aged 73 years and older was completed
in 1997, and a third wave that included all twins aged 70 years and older was completed in 1999. The cognitive assessment at each wave included the Mini Mental State Exam (MMSE) and a composite of five cognitive tests.
This presentation will focus on the three waves of longitudinal data. As expected, cognitive performance declined over successive waves of assessment. For example, the mean MMSE declined from 26.2 (SD=3.2) at the first
wave to 24.5 (SD=4.8) at the third wave. Nonetheless, there were marked individual differences in the amount and direction of cognitive change: The MMSE scores between the first and last assessments declined for 57%
of the twins, remained stable for 14% of the twins, and increased for 29% of the twins. Preliminary analysis suggests that genetic factors had little influence on the direction and degree of cognitive change. For example, rate
of cognitive decline on the MMSE was correlated only .07 in 58 MZ twin pairs and -.02 in 56 DZ twin pairs, suggesting no familial component. Results from a more comprehensive analysis will be presented and discussed
in terms of its relevance to understanding the influence of genetic factors on normative aging processes. T.Momose1, J.Ando2, N.Onoda1, Y.Ono1
Depression and anxiety are not only prevalent but also co-morbid in clinical settings. We conducted a research on the effect of genetic and environmental factors of depression and anxiety, based on the results of HADS(hospital
anxiety depression scale) in Japanese population. The subjects were 218 twin pair's (MZF=91, DZF=38, MZM=42, DZM=22, DZO=25). The univariate genetic analysis suggested that AE models are most fit for both depression
and anxiety. The multivariate genetic analysis showed that a common genetic factor exists between those two phenotypes as well as the phenotype-specific nonshared environment factors. [Poster] Brian S. Mustanski1, Richard J. Viken1, Jaakko Kaprio2, 3, and Richard J. Rose1
Antisociality has been correlated with both alcohol consumption and alcohol problems. Some evidence suggests a stronger connection between antisociality and alcohol problems than alcohol consumption. We explored
the genetic covariance between antisociality and alcohol consumption and between antisociality and alcohol problems. Subjects were 1, 293 alcohol consuming, twin pairs from the population based Finn Twin 16 study.
Antisociality was measured using the MMPI Pd scale at age 16, and Alcohol problems were measured with the Rutgers Alcohol Problem Inventory at age 18 «. Cholesky decomposition models were fit to Pd, alcohol consumption,
and alcohol problems. Results indicted significant heritability for all three variables, as well as suggesting a minor influence from common environmental effects. Comparison of the models indicated a larger genetic covariance
for Pd and alcohol problems than Pd and alcohol consumption (r=.51 vs. .31). Additionally, larger common environmental covariance existed for Pd and alcohol problems than Pd and alcohol consumption (r= .46 vs. .29).
Unshared environmental covariance was low for both models. These results appear to support the hypothesis of a stronger link between antisociality and alcohol problems than antisociality and alcohol consumption. Donald J. Nash and Laura J. Draski
The hotfoot mutation (ho), when homozygous, leads to a severe ataxia characterized by a high-stepping, quick patting motion of the hindfeet and a body tremor at rest. The phenotype is not clinically evident until about the
third postnatal week. The purpose of the present study was to examine neuro-ontogeny and development in hotfoot mice and their normal sibs to determine if neurological abnormalities could be deteted early in postnatal life
prior to the onset of ataxia. Modifications of a standardized battery of reflex, morphological, and behavioral tests first developed by W.M. Fox (1965, Anim. Behav., 13, 234-241) were used. Mice from a total of 17 litters containing
102 pups were tested. Except for body mass, no significant effects or interactions of gender were noted. Overall, ho/ho mice tended to weigh the least at all ages beginning on postnatal day 3. Compared to their normal sibs, ho/ho
mice showed a delayed response for forelimb placing, hindlimb placing, disappearance of pivoting, auditory startle, hindlimb grasp, and eye opening. For some reflexes, maternal genotype also had an influence sometimes
independent of any effect due to genotype of the pup. Although hotfoot mice weighed signficiantly less than phenotypically normal sibs, the age of appearance of a developmental measure did not appear to be related to
within-genotype variations in body mass. While maternal genotype appeared to delay development and inhibit the rate of growth in pups, it is not clear how these effects are related. [Poster] Michael C. Neale1
Full-information maximum likelihood offers a number of advantages for the analysis of ordinal data. First, it is possible to handle missing data in a natural fashion entirely analogous to the analysis of raw continuous
data. Such analyses will be robust to data that are missing completely at random, or that are missing contingent on values of other measured variables. In addition, data that involve contingent steps, for
example, drug dependence can be observed only in those who initiate use of of a drug, are easily accomodated. Second, the analysis of selected samples is quite straightforward, and it is possible to conduct joint analyses
of samples of patient and control samples. Third, using definition variables within Mx, it is also possible to use ordinal or continuous variables as moderators of threshold or covariance parameters, without making
assumptions about their distribution. Thus it is possible to include age or sex as a covariate, to allow genetic or environmental effects to be moderated by other variables, or to conduct joint linkage
and association analyses with ordinal data. Computational demands of the method remain a concern but improvements in hardware, especially parallel processing, suggest that this problem will be short-lived. Jenae M. Neiderhiser1
There are a growing number of studies that demonstrate the important role that genetic factors play in influencing mother-child relationships. These studies include both child-based and parent-based designs, indicating that
both child*s genes and parent*s genes play a role in influencing mothering. Research is currently underway to examine what enduring characteristics of women influence mothering and to identify the impact of her mothering
on adjustment. It is also possible that a woman*s relationship with her child could play an important role in mediating the effect of these factors. The current report will examine mothering as a mediator of the influence of enduring
characteristics, like temperament and self-worth, on adjustment, like depression and anxiety, in the Twin Mothers sample. Preliminary findings indicate that negative mother-child relationships mediate the impact of temperament
and self-worth on depression and that these associations are influenced by genetic factors. It is important to note that nonshared environmental factors also appear to play a prominent role in explaining these associations. A cholesky
model will be employed to more carefully specify the roles of genetic, shared and nonshared environmental factors in explaining these associations. In addition, potential differences in maternal negativity and warmth will be
explored. Naoko Onoda1, Juko Ando2, Yutaka Ono1
To clarify the role of genetic and environmental factors in a type of parenting "affectionless control", PBI(Parental Bonding Instrument)was carried out for 213 twin pairs from 15to27 years old.For maternal affectionless control,
additive genetic factor and specific environmental factor have a substantial influence. On the other hand, not only additive genetic and specific environmental factor but also common environmental factor plays a substantial role
in paternal affectionless control. Heritability of maternal affectionless control is 57% and that of paternal affectionless control is 30%.It is shown that maternal affectionless control is more influenced by genetic factor than paternal
affectionless control. We are now analysing on the relationship between affectionless control and other scores for example depression score and so on. [Poster] Nancy L. Pedersen 1,2, Margaret Gatz 1,2, Samuel F. Posner 3, Samuli Ripatti 1
Estimating heritability of late life disorders such as Alzheimer's disease is complicated by several considerations. Twins may vary widely in their age of onset for the disorder, and twins may die of other causes, leaving
ambiguous whether or not the individual would have become demented. In this presentation, we discuss three different ways of looking at twin similarity for dementia, trying to account for the competing and complementary
aspects of whether one gets the disorder, age of onset, and mortality. One method involves modeling heritability for a categorical trait based on tetrachoric correlations. A second method involves modeling heritability for age
of onset (building on Meyer & Breitner's adaptation of Pickles et al.). The third method uses a frailty approach that takes mortality into account. Results from the different methods will be contrasted, and the strengths and limitations
of each considered. Nancy L. Pedersen1
In the Twin Mom study, a key pathway in the nexus of associations describing influences on women's mental health is that from mothering practices to mid-life adjustment. An obvious research question is whether this pathway
is mediated predominantly by genetic, shared or non-shared influences. We have three assessments of mother-child relationships: mother's report, child's report and ratings of video recordings of the mother-child dyad. Only
mother's self-reports of mothering (negativity and warmth) were associated with her mental health as measured by depressive symptoms, quality of life, and somatic and psychic anxiety. Preliminary analyses indicate that these
associations were predominantly mediated by genetic factors. Given the lack of associations with child's report, one may speculate whether the findings reflect mother's personality or reporting style. This will be expanded upon
in the presentation by Neiderhiser. Robert Plomin
The IQ QTL Project has nearly completed an association genome scan for 'g'. We used a four-stage strategy beginning with DNA pooling to genotype nearly 2000 short-sequence repeat markers (SSRs) at about 1cM intervals
for a group of 101 high 'g' subjects (IQs > 130) and for a group of 101 control subjects of average 'g' (IQs = 90 - 110). Markers that showed a nominally significant specific allelic difference in stage 1 were replicated using DNA
pooling for a sample of 100 super-high 'g' subjects (IQs > 160) and 100 controls. Markers that survived stage 2 were genotyped for each of the 402 subjects and standard QTL analyses were conducted. QTLs that survived the
first three stages were genotyped for 200 parent-child trios to conduct within-family transmission disequilibrium tests (TDTs). The question is whether a genome scan with this power and design can detect any replicable QTLs
associated with 'g'. Of course, much denser maps are needed in order to exclude QTL associations-the hope of the present study is to identify some, certainly not all, QTLs associated with 'g'. We have also obtained DNA from
other samples to replicate and extend these results. For example, we have DNA from an unselected and representative sample of 800 individuals and several other samples in order to replicate results further, assess directly the
effect size of the QTLs, and test other hypotheses such as increasing genetic influence on 'g' during the lifespan. We will also refine the localization of QTLs using saturated SSR and single-nucleotide polymorphism (SNPs) markers.
Finally, in contrast to a bottom-up molecular biological approach to functional genomics, a top-down behavioral genomics approach will be used to begin to investigate how genes affect 'g' by comparing associations for QTLs
across diverse measures of cognitive processes. Carol A. Prescott and Kenneth S. Kendler
This presentation illustrates a method for separating components of change and demonstrates its application to phenotypic and biometric analyses of change in alcohol consumption. Alcohol consumption is strongly associated
with age but it is unclear if this is due to maturation or to factors correlated with age such as birth cohort, legal drinking status, or demographic characteristics. Frequency and quantity of past-year alcohol consumption were collected
on 1-4 occasions over an 8-year interval from 2428 adult female twins from the MCV Stress & Coping Twin Study. Latent growth models were fit to raw data for all available observations. There was substantial heterogeneity
in patterns of change by age. Consumption quantity was highest among women under 30 or over 40. Women of all ages decreased their consumption quantity over time, but young women decreased most rapidly. Change in
frequency of alcohol consumption was more closely associated with year of assessment than with age (e.g., the predicted decline differed for women who were 30 in 1988 vs in 1993). Marital and family status, but not legal status,
were significant predictors of decreased consumption, even after accounting for age or birth year. Results of twin pair analyses indicated for both younger and older women, genetic factors contributed substantially to initial
frequency. Change in frequency was influenced primarily by genetic factors for younger women, but by a combination of genetic and individual-specific factors for older women. For consumption quantity, younger women had
higher means and greater variation than older women, but similar biometric structure with genetic influences accounting for over half the variation in initial level and in decrease over time. For both quantity and frequency the
genetic factors influencing frequency level and change were largely independent. Thomas S. Price1, Philip S. Dale2, Jim Stevenson3, Thalia C. Eley1, and Robert Plomin1
The current study uses a longitudinal design to investigate whether genetic influences on specific cognitive abilities become more unitary between infancy and childhood, with the aim of identifying the developmental origins
of general cognitive ability. Verbal and non-verbal cognitive ability were assessed in a population sample of 3, 608 British twin pairs as part of the Twins Early Development Study (TEDS), using parental report instruments
administered at 2, 3 and 4 years of age. Verbal ability was assessed using vocabulary checklists adapted from the MacArthur Communicative Development Inventory (MCDI), non-verbal ability using a novel measure adapted
for use at each age (PARCA). These measures showed modest heritability at all three ages. MCDI and PARCA measures at successive time points correlated .58-.60, while contemporaneous verbal and non-verbal measures
correlated .41-.45. A well-fitting multivariate genetic model suggested that the genetic influences on cognitive abilities become increasingly molar: that is, verbal and non-verbal cognitive abilities become more highly correlated
genetically with increasing age. These findings are consistent with the developmental emergence of a heritable general cognitive ability factor. In addition, genetic influences on verbal ability at 2 years are more strongly related
to genetic influences on non-verbal ability at 3 years than the converse, suggesting that verbal ability in infancy may be more predictive genetically of later g. S. Purcell1, and P. Sham1
Epistasis has received relatively little treatment in the QTL mapping literature, largely due to its low detectability. QTL mapping approaches have tended to only ever analyse multiple markers sequentially rather than
simultaneously, apparently focusing on additive main effects of single loci rather than the epistatic interactions between loci. Here, we develop and explore a variance components model of QTL linkage incorporating epistasis.
For a range of epistatic models we calculate the expected non-centrality parameter (NCP) per sib pair, under a full model and under nested submodels without epistatic terms. The difference in NCP between the full and submodels
indicates the power to detect epistasis. We demonstrate that for QTL linkage additive main effects and epistatic interactions effects are in fact partially confounded. As a result, variance components under submodels are distorted,
with two main implications. First, the analysis of a single locus can in fact detect a QTL with no main effect that interacts epistatically with another (unmeasured) locus. Second, because the apparent variance components in
submodels soak up a large proportion of variance attributable to epistatic effects under the full model, power to detect epistasis formally is low. Therefore, genome scan approaches that analyse one marker at a time for linkage
are in fact not necessarily precluding the detection of purely epistatically interacting loci. However, generalisations regarding the power to detect epistasis either as a main effect or as an interaction effect in linkage analysis are
difficult due to the large number of possible models of epistasis and the complex influence of allele frequencies on expected variance components. These results remind us that the interpretation of variance estimates is strictly
model-dependent. In this context, the modelling of variances (versus path coefficients) is encouraged as variance components estimated under an incorrect model can theoretically be negative and so it is not necessarily helpful
to constrain them to positive values. David Reiss1, Nancy Pedersen2, Marianne Cederblad3, Kjell Hansson3, Paul Lichtenstein2, Jenae M. Neiderhiser1, Olof
Elthammar3
Gene-environment (GE) correlation and the nonshared environment (NSE) have moved to center stage in developmental theory. With respect to GE correlations, recent work suggests that heritable characteristics in children
evoke specific social responses from intimates such as parents, sibs and friends. These responses, in turn, influence further development of these heritable traits into patterns of competence and psychopathology; thus social
relationships may mediate the expression of genetic influence on a range of behaviors. The Twin Mom study was designed to clarify the important of GE correlations and NSE in women at mid life and is built on three hypotheses
of maternal adjustment. First, mother's heritable traits may influence the quality and process of her marriage which in turn influences her mid-life adjustment. Second, genetic influences may shape how mother's remember their
own experiences of being parented; these memories shape both their current marital and parenting practices and then her adjustment. Third, influences on mothers of father's personality, marital interaction styles and parenting
constitutes an important component of systematic NSE influence on her adjustment. Papers presented in this symposium explore facets of these three hypotheses. The study used a Swedish, population based sample of 150 MZ
and 175 DZ pairs of twin mothers, their husbands and their adolescent children and deployed a range of measures of heritable characteristics, social relationships including coded videotape records of in-home family interaction
and the assessment of competence and psychopathology in the mothers. Chandra Reynolds
Age, education, psychosocial and health-related traits have been shown in previous research to predict cognitive decline (e.g., Albert et al., 1995; Schaie, 1989). The sources of covariance contributing to putative predictors
and cognitive decline were investigated utilizing a longitudinal sample of 638 individuals aged 50 years and older from the Swedish Adoption /Twin Study of Aging (SATSA). A battery of cognitive tests tapping multiple domains
were administered on multiple occasions over a six-year period. Both genetic and environmental factors were important for cognitive decline for verbal, spatial, memory and perceptual speed domains, though the relative magnitudes
varied dependent on the growth model utilized. Of the predictors considered, educational attainment and health-related traits such as pulmonary function were most strongly related to decline across cognitive domains and across
method of examining change. Implications of various growth models to the resolution of sources of variation and covariation on decline will be discussed. Soo Hyun Rhee1, John K. Hewitt1, Robin P. Corley1, and Michael C. Stallings1
Knowledge regarding the cause of comorbidity between two disorders has a significant impact on research regarding the classification, treatment, and etiology of the disorders. Neale and Kendler (1995, Am. J. Hum.
Genet. 57, 935-953) provided the most comprehensive description of the possible causes of comorbidity between two disorders, explaining 13 alternative comorbidity models. Many studies have used the family
study method (i.e., examination of the prevalence of disorders in probands and their relatives) to test 3 of the 13 Neale and Kendler models: the alternate forms model (the two comorbid disorders are alternate manifestations
of a single liability distribution), the correlated liabilities model (the liabilities for the two disorders are correlated), and the three independent disorders model (a separate liability distribution for the comorbid disorder). We
identified 38 studies that tested these models by conducting one or more of 30 separate analyses examining the prevalence of specific disorders in relatives of different classes of probands (18 analyses with a specific expected
result for either the alternate forms model or the correlated liabilities model and 12 analyses with a specific expected result for the three independent disorders model). In order to test the validity of these analyses, we conducted
all 30 analyses on 13 datasets simulated under the assumptions of the Neale and Kendler models. If an analysis is valid, one should obtain the expected result only when the analysis is conducted on data simulated for the tested
model. Five of the 18 analyses testing the alternate forms model were valid tests of the alternate forms model, but none of the analyses were valid tests of the correlated liabilities model or the three independent disorders model.
These results suggest that past family studies may have made misleading conclusions regarding the etiology of comorbidity between the disorders examined in the studies. Kristin Riggins-Caspers1, Remi Cadoret1, John Knutson2
Using an adoption paradigm, Bronfenbrenner and Ceci's (Bronfenbrenner , U., & Ceci, S., 1994, Psychological Bulletin, 101, 568-586) Bioecological Model was evaluated by concurrently testing for
gene-environment interaction and evocative gene-environment correlation (Plomin, R., DeFries, J.C., & Loehlin, J.C., 1977, Psychological Bulletin, 84, 309-322). A sample of 150 adult adoptees (ages: 18 45)
provided retrospective reports on harsh adoptive parent discipline. Biological psychopathology was determined by the presence of alcoholism, drug abuse, antisocial personality, and/or criminality in the birth parent of the adoptee.
Adolescent aggressive and conduct-disordered behavior was determined from retrospective adoptee and adoptive parent reports. Finally, a contextual environmental risk factor was created from adoptive parent reports on the
presence of psychopathology (e.g., anxiety, depression, legal problem) in either adoptive parent. A cutoff of 2 or more adoptive parent diagnoses was used to determine low versus high environmental risk. Analyses were conducted
in two steps. First, evocative gene-environment correlation was evaluated for the entire sample using the criteria for mediation (Baron, R. M., & Kenny, D. A., 1986, Journal of Personality and Social Psychology,
51, 1173-1182). Adoptee adolescent behavior was found to mediate the genetic association between birth parent psychopathology and harsh parental discipline thereby providing support for evocative gene-environment
correlation. Second, the moderation of evocative gene-environment correlation by environmental risk was determined by testing for the former for adoptees from low risk versus high-risk adoptive homes. The evocative process
was found only when two or more risk factors were present in the adoptive home. These findings provide preliminary support for the Bioecological Model of development (Bronfenbrenner & Ceci, 1994). F.V. Rijsdijk and P.C. Sham
Variance components models for QTL linkage analysis have been developed for sib pairs and extended to pedigrees. Recently, ananalytic formulae were derived for the power of variance components QTL linkage analysis
using sibships of varying sizes (P.C. Sham, S.S. Cherny, S. Purcell and J.K. Hewitt, 2000, Am.J.Hum.Genet. in press). It was shown that the non-centrality parameter (NCP) for the linkage test is approximately proportional
to the squares and product of the additive and dominance QTL variance components, and the number of possible sib pairs in the sibship. We have now extended the power analysis to general pedigrees. This involved the derivation
of a first order approximation: the total NCP of a pedigree is approximately the sum of NCP contributions from all possible pairs of relatives in the pedigree. Using an exact formula and this first order approximation, we compared
the NCPs of two different types of extended pedigrees to those of sib-pairs, sib-trios, and sib-quads, under a range of genetic models. Overall, sib-quads have greater efficiency than smaller sibships or extended pedigrees. However,
in the absence of dominance at the QTL, extended pedigrees are also reasonably efficient. In particular cases where large sibships are generally unavailable, extended pedigrees beyond nuclear families could, at least in principle,
provide a method of increasing power. Joseph Lee Rodgers1, Hans-Peter Kohler2, Kirsten Kyvik3, and Kaare Christensen3
In this paper we document the existence of systematic genetic influence on human fertility. Our data come from 1620 same-sex Danish MZ and DZ twin pairs born between 1953 and 1959 who have virtually completed
childbearing. Two different fertility measures were defined, Age at First Attempt to Get Pregnant (FrstTry) and Number of Children (NumCh). Biometric models were fit using SEM and DF Analysis, which tested for several
different domains of influence on fertility: shared environmental influence, genetic additivity, genetic dominance, bivariate influences from FrstTry to NumCh, differential influence by gender, and differential influence in low
and high fertility. A consistent medium-level additive genetic influence was identified for NumCh, equal across genders, and a stronger additive genetic influence was identified for FrstTry, greater among females than among
males. Heritability estimates were also converted to genetic coefficients of variation, and results re-interpreted. Our findings combine with others to provide explanatory support for both contemporary and historical models of
human fertility and the fertility transition. David C. Rowe1, Michael Gilson1, and Cathy B. Hunt2
A research design that expands the sibling design to include friends of each sib permits a test of the determinants of friends' behavioral similarity. Under a selection hypothesis in which friends choose one another for their
phenotypic traits, friend 1 and friend 2, of sibling 1 and 2, respectively, should possess little behavioral resemblance, although the friend-sib pairs are alike behaviorally. Social homogamy processes, on the other hand, predict
that all four individuals should share the same average level of behavioral resemblance. We tested these predictions in theNational Longitudinal Study of Adolescent Healthusing self-reported delinquency and verbal
IQ. The structural equation model of delinquency was run only on full siblings because of sample size limitations. The model of delinquency yielded results strongly in support of peer selection. In contrast, the verbal IQ model
indicated that social homogamy processes dominated. We will provide further examples of the model's application. Kimberly J. Saudino1, Lee A. Thompson2, and Jeffrey R. Gagne1
Few behavioral genetic studies have examined genetic and environmental influences on temperament in adolescence. None have used objective measures. The present study examines the etiology of individual differences
in activity level (AL) in a sample of adolescent twins (46 pairs MZ , 30 pairs DZ; mean age=14.6 years) participating in the Western Reserve Twin Project. AL was assessed using parent ratings, self ratings, and mechanical motion
recorders (actometers) attached one per limb for a 48-hour period. All measures were significantly correlated (r acto-parent=.43; r acto-self=.19; r parent-self=.40). For all measures, intraclass correlations
for MZ twins exceeded those for DZ twins, suggesting a genetic influence. However, the problem of too low DZ correlations emerges for both rating measures (Parent: MZr=.54, DZr=.01; Self: MZr=.52,
DZr=.00) suggesting that contrast effects may be operating. When AL is mechanically measured, both MZ and DZ twins display significant co-twin resemblance (MZr=.75, DZr=.42). Multivariate
model-fitting analyses reveal significant genetic and nonshared environmental influences for all measures of AL (Parent h2=.53, Self h2=.42, Actometer h2=.38). Although not significant
in our small sample, shared environmental influences accounted for a third of the variability in actometer scores (c2=.34). The best-fitting model was one that included a common genetic factor, unique genetic
influences on actometer AL, and unique nonshared environmental influences on each measure. Thus, there was significant genetic covariance between all measures. Genetic correlations ranged from .76 to .90. These results
suggest that although parent and self ratings of AL might be prone to contrast effects, they tap the same genetic effects as objective measures of AL. [Poster] Stephanie Schmitz1, Robin P. Corley1, and John K. Hewitt1
Personality measures were collected from a sample of young adults (19 and 20 years of age) via questionnaires, namely the TPQ (Cloninger, C. R., 1987, The Tridimensional Personality Questionnaire. St. Louis, MO:
Washington University School of Medicine) and a short form of the EPQ (Floderus-Myrhed, B., Pedersen, N. and Rasmuson, I., 1980, Behavior Genetics, 10(2), 153-162). In the young adult sample, the personality
dimensions were quite stable over time (correlations of .50 to .80 over periods of one to four years); however, the TPQ dimensions correlated slightly but significantly with each other and were thus not as orthogonal as postulated
by Cloninger. The correlations between the TPQ dimensions of Harm Avoidance, Novelty Seeking, and Reward Dependence and the Extraversion and Neuroticism scales of the EPQ replicated the findings of Stallings et al. from
a sample of 50- to 96-year olds. (Stallings, M.C., Hewitt, J.K., Cloninger, C.R., Heath, A.C., and Eaves, L.J., 1996, Journal of Personality and Social Psychology, 70(1), 127-140). Additionally, their rearing parents
completed the same questionnaires when the young adults were 17 years old plus the 16PF (Cattell, R. B., Eber, H. W. and Tatsuoka, M. M., 1970, Handbook for the Sixteen Personality Factor Questionnaire. Champaign,
IL: Institute for Personality and Ability Testing) and the EASI (Buss, A. H. and Plomin, R., 1975, A temperament theory of personality development. New York: Wiley-Interscience) before the young adults were born
or about one year old. Parent-offspring correlations were of the expected magnitude (.10 to .15) and thus non-significant with a sample size of about 80 mothers and fathers, each for the adoptive and non-adoptive sample.
Interestingly, harm avoidance in the young adults correlated significantly negatively with the parent's sociability scores from 20 years ago, for both non-adoptive parents and biological parents. [Poster] Nancy L. Segal1, and Alec Roy2
Family resemblance for suicidal behavior has been interpreted by some researchers as reflecting extreme grief following loss. This view anticipates a higher frequency of attempted suicide among bereaved MZ than DZ twins
(regardless of cause of death), given their increased social closeness. Alternatively, support for a genetic influence on suicidal behavior has been provided by findings of greater concordance between MZ co-twins than DZ co-twins,
and between pairs of biological than adoptive relatives. Our earlier study attempted to reconcile these views by comparing the frequency of attempted suicide in 166 MZ twins and 79 DZ twins whose co-twins' deaths were
non-suicides (N.L. Segal and A. Roy, 1995, Pers. and Indiv. Diffs.19, 937-940). Suicidal attempts (during the first two months following the loss) were recalled by 3 MZ twins (1.8%) and by 3 DZ twins (3.7%),
a difference that was not significant. This finding supported the view that concordance for suicide among family members reflects a shared genetic predisposition. In contrast, suicidal ideation was indicated by a greater number
of MZ than DZ twin survivors, consistent with more severe bereavement response among surviving MZ than DZ twins (N.L.Segal, 1999, Entwined Lives, Dutton, New York). The current study presents a replication
and elaboration of the earlier analysis, based on 289 bereaved MZ twins and 150 bereaved DZ twins. Again, surviving MZ and DZ twins whose co-twins' deaths were non-suicides indicated low and equal frequencies of suicidal
attempts shortly following the loss. However, suicidal ideation occurred with equal frequencies among the two twin groups. Specifics personality or temperamental characteristics, partly genetically based, may predispose some
individuals to engage in suicidal thoughts following various life events. [Poster] Leo A. Sirota, Dean H. Hamer
The optimal design of candidate gene association studies often depends on conditions and parameters that are unknown or poorly estimated prior to the beginning of sample collection. The risk of false positives due to population
stratification in case-control population-based studies and the lack of power of linkage analysis are two well-known limitations. We compared power to detect a true candidate gene and ability to resist population stratification
for four different designs: population based association (measured genotypes), within-sibship association (the sib-paired t-test), parent-child trios (the TDT), and sib-pair linkage analysis (Haseman-Elston method). Power was
analyzed as a function of heritability due to the locus, allele frequency, sibling phenotypic correlation, and degree of dominance. Two different models of data confounding due to population admixture were used for Monte-Carlo
comparisons of design robustness. The results indicate that in most practical situations, the sib-pair based association design gives the best combination of power and robustness. The ANOVA-based test proposed by Allison
is a natural generalization of the sib-paired t-test that can accommodate larger sibships and multiple alleles(D. B. Allison et al., 1999, Am. J. Hum. Genet.64, 1754-1764). [Poster] Erica L. Spotts1
> Previous research has found evidence for genetic and environmental influences on measures of parenting in child- and parent-based designs (e.g. Kendler, K. S., 1996, American Journal of Psychiatry, 153, 11-20;
Plomin, R., 1994, Genetics and Experience, Sage Publications: Thousand Oaks, CA). The current report extends these findings by exploring possible sources of genetic and environmental influences on mothering using
a parent-based design. Borrowing from the ecological perspective (Bronfenbrenner, U., 1989, In R. Vasta (Ed.), Greenwich, CT: JAI Press), three levels of influence on positive and negative parenting are hypothesized:
within-parent (e.g. personality, temperament), intrafamilial (e.g. marital relationship, child characteristics, family environment), and extrafamilial (e.g. SES, life events). The current report focuses on only the first level, the
association between mothering and within-parent characteristics, using the Twin Mothers sample. Preliminary analyses indicate moderate to strong phenotypic correlations between all three levels of influence, and positive and
negative parenting. Cross-correlations of the bivariate associations between influences and parenting suggest large amounts of nonshared environment with hints of genetic and shared environmental influences. Model-fitting
will allow for simultaneous estimation of the influence of one predictor of parenting above and beyond other predictors, as well as depicting the pattern of genetic and environmental influences on predictors of both positive and
negative parenting. Michael C. Stallings
Genetic structure of visual / verbal working memroy and its relationship with the ERP parameters
1Faculty of Letters, Keio University, Tokyo, Japan. 2National Institute of Media Education, Chiba, Japan. 3Graduate School of Arts and Sciences, University of Tokyo
, Tokyo, Japan. 4School of Medicine, Keio University, Tokyo, Japan
Address: J. Ando, Department of Education, Faculty of Letters, Keio University, 2-15-45, Mita, Minatoku, Tokyo, 108-8345, Japan Telephone: +81 3 3453 4511 Facsimile: +81 3 3798 7480 E-mail:
juko@msa.biglobe.ne.jp
Genetic structure of personality: Relationship between TCI and NEO
1Faculty of Letters, Keio University, Tokyo, Japan. 2School of Medicine, Keio University, Tokyo, Japan
Address: J. Ando, Department of Education, Faculty of Letters, Keio University, 2-15-45, Mita, Minatoku, Tokyo, 108-8345, Japan Telephone: +81 3 3453 4511 Facsimile: +81 3 3798 7480 E-mail:
juko@msa.biglobe.ne.jp
Genetic correlations between P300 and EEG power spectrum3
1Dept. of Psychiatry, Washington University School of Medicine, St.Louis, MO 63108. 2Dept. of Biological Psychology, Vrije Universiteit Amsterdam, The Netherlands.
3Supported by a grant from the Van Coeverden Adriani Stichting, grant 575-65-052 from the Netherlands Organization for Scientific Research (NWO) and grant DA-07261 from the National Institute of Drug Abuse
Address: A.P.Anokhin, Dept. of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway Suite 1, St.Louis, MO 63108. Tel: (314)286-2201; FAX: (314)286-2213; E-mail: andrey@matlock.wustl.edu
Candidate genes for frontal EEG asymmetry: preliminary results of a case-control study 2
1Washington University School of Medicine, St.Louis, MO 63108, USA. 2Supported in part by grants AA-008401-3 from the National Institute on Alcohol Abuse and Alcoholism
and DA-07261 from National Institute on Drug Abuse
Address: A.P.Anokhin, Dept. of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St.Louis, MO 63108, USA. Tel: (314)286-2201; FAX:(314)286-2213; E-mail:
andrey@matlock.wustl.edu
Longitudinal Genetic Analyses of Intelligence at 5, 7, 10, and 12 years of age
1Department of Biological Psychology, Vrije Universiteit, De Boelelaan 1111, 1081 HV Amsterdam, The Netherlands
Address: Department of Biological Psychology, Vrije Universiteit, De Boelelaan 1111, 1081 HV Amsterdam, The Netherlands Telephone: +31 (0)20 4448812 Fax: +31 (0)20 4448832 E-mail: m.bartels@psy.vu.nl
Effects of prenatal cocaine exposure upon a sequence of aggression situations in mice
Department of Biology, William Paterson University, Wayne, NJ 07470
Address: Department of Biology, William Paterson University, Wayne, NJ 07470. Telephone: 973 720 2480 Fax: 973 720 2338 E-mail: HahnM@wpunj.edu
Immunological disorders in transgenic mice for Down Syndrome Region
CNRS UPR 9074, GNC, Orléans, France
Address: Génétique, Neurogénétique, Comportement, CNRS, UPR 9074, 3B rue de la Férollerie, 45071 Orléans Cedex 02, France, Telephone: (33) 2 38 25 79 63 Fax:
(33) 2 38 25 79 79 E-mail: bichler@cnrs-orleans.fr
Assessment of possible alterations of cholinergic basal forebrain in YAC polytransgenic mice: a mouse model of Down syndrome
CNRS UPR 9074, GNC, Orléans, France
Address: CNRS UPR 9074, Génétique Neurogénétique Comportement, 3b Rue de la Ferollerie, 45071 Orléans, France. E-mail: migliore@cnrs-orleans.fr
Alcohol dependence and depression in a national sample of Australian twins4
1Missouri Alcoholism Research Center, Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63108. 2Missouri Alcoholism Research Center,
Department of Psychology, University of Missouri-Columbia, Columbia, MO. 3Queensland Institute of Medical Research, Brisbane, Queensland, Australia. 4Supported by NIH Grant AA10249
Address: Dept. of Psychiatry, Washington U. Schl of Med, 40 N. Kingshighway, Ste 2, St Louis MO 63108 Telephone: 314 286 2284 Fax: 314 286 2213 Email: kkb@matlock.wustl.edu
An examination of the associations between DRD4 and personality traits4
1Department of Psychology, University of Minnesota, Minneapolis, MN 55455. 2Department of Psychology, University of Minnesota, Minneapolis, MN 55455.
3Department of Psychology, University of Minnesota, Minneapolis, MN 55455. 4Supported in part by NIH Grants DA05147, AA09367, AND AA00175
Address: Department of Psychology, Elliott Hall University of Minnesota Tel: (612) 874-8821 75 East River Road Email: burt0105@tc.umn.edu Minneapolis, MN 55455-0344
[beta]-2 Adrenergic Receptor Gene Variations and Blood Pressure under Stress In Normal Twins
1Franz Volhard Clinic. 2Max Delbrueck Center
Address: Franz-Volhard-Klinik, 13125 Berlin, Germany Telephone: +49-30-94172277 Fax: +49-30-94172335 E-mail: busjahn@fvk-berlin.de
Behavioral and cognitive performances of trangenic mice for Down Chromosomal Region (DCR)
1UPR 9074 CNRS, Genetics, Neurogenetics, Behavior, 3b rue de la Férollerie, 45071 Orléans Cedex 2, France. 2University of Orléans, BP 6749, 45067
Orléans cedex 2. 3Supported by a grant of Fondation pour la Recherche Médicale. Supported by CNRS, University of Orléans, Ministry for research and technology, DRRT, Conseil de la
Région Centre
Address: UPR 9074 CNRS, Genetics, Neurogenetics, Behavior, 3b rue de la Férollerie, 45071 Orléans Cedex 2, France. Telephone: 33 2 38 28 79 63 Fax: 33 2 38 25 79 79, chabert@cnrs-orleans.fr
Heritability of the Gender Identity Disorder3
1Psychology Department, University of Colorado at Colorado Springs, Colorado Springs, CO 80933-7150. 2Institute for Behavioral Genetics, University of Colorado, Boulder, CO
80309
Address: Frederick L. Coolidge, Ph.D., Psychology Department, University of Colorado at Colorado Springs, P. O. Box 7150, Colorado Springs, CO 80933-7150 Telephone: 719 262 4146 FAX: 719 262 4166 E-mail:
fcoolidg@hotmail.com
Longitudinal and developmental analysis of general cognitive ability and school performance: A sibling study2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0447. 2Supported by NICHD grant HD-10333, NIMH grant MH-43899, and NIDA grants DA-05131
and DA-11015
Address: IBG, Campus Box 447, University of Colorado, Boulder, Boulder, CO 80309-0447. Phone: 303-492-5189, FAX #: 303-492-8063, E-mail: corley@colorado.edu
Behavioral and Neural Phenotype of a Mouse Model of Down Syndrome3
Department of Pediatrics1and Psychiatry2, University of Colorado School of Medicine, Denver, CO 80262. 3Supported by NIH grants HD-04024, HD-17449 and MH
15442
Address: 4200 E. 9th Ave. Box C233, Denver, CO 80262 Telephone: 303 315 7212 Fax: 303-315-8080 Email: Linda.Crnic@UCHSC.edu
Demographic risk factors and moderators of genetic influence in separation anxiety disorder3
1Department of Psychology, University of Missouri-Columbia, Columbia, MO 65211. 2Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63108.
3Supported by NIH grants AA00264, AA09022, AA07728, DA00272
Address: Nikole Cronk 210, McAlester Hall, University of Missouri-Columbia, Columbia, MO 65211 Telephone: 573 882 8251 E-mail: nikole@taxa.psyc.missouri.edu
Sex differences in the genetic influences on motivations for drinking
1Department of Psychology, University of Richmond, Richmond, VA 23173. 2Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College
of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0126. 3Department of Psychology, University of Southern California, Los Angeles, CA 90089
Address: VIPBG, MCV/VCU, P.O. Box 980126, Richmond VA 23298-0126 telephone: (804)828-5968; fax (804) 828-1471; email: cprescott@hsc.vcu.edu
Differential genetic etiology of reading disability as a function of rapid automatized naming and phonological decoding2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309. 2Supported by program project and center grants from the National Institute of Child Health and
Human Development (HD-27802) to J. C. DeFries. This report was prepared while C. J. Davis was supported by NIMH training grant MH-16880 and V. S. Knopik was supported by NICHD training grant HD-07289
Address: Institute for Behavioral Genetics Campus Box 447 University of Colorado Boulder, CO 80309 Telephone: 303-492-7362 Fax: 303-492-8063 E-mail: davisc@colorado.edu
Are Opposite-Sex Twins Sex-Atypical?
Northwestern University, Evanston, IL, and Queensland Institute of Medical Research, Brisbane, Queensland, Australia
Address: Department of Psychology, Northwestern University, 2029 Sheridan Road, Evanston, IL 60208. E-mail: khytam@nwu.edu
The mapping of Down syndrome phenotypic features
CNRS UMR 8602, Faculte Necker-Enfants Malades, Paris
Address: Delabar@necker.fr
Exploring Gene-Environment Interactions: Moderating Influences on Alcohol Use4
1Department of Psychology, Indiana University, Bloomington, IN 47405. 2Department of Public Health, University of Helsinki, FIN 00014, Finland. 3Department of
Public Health and General Practice, University of Oulu, 90220, Finland. 4Supported by NIAAA with grants AA08315, AA00145, and AA07611, and by a National Science Foundation Fellowship awarded to the
first author
Address: Indiana University, Department of Psychology, 1101 E. 10th St., Bloomington, IN 47405 Telephone: (812) 855-4101 Fax: (812) 855-4691 E-mail: ddick@indiana.edu
Murine models with different expression levels of genes relevant to Down syndrome: a tool for understanding the role of single genes in neurophatological traits
Down Syndrome Research Group, CGMM-IRO, Hospital Duran i Reynals, 08907-L'Hospitalet de Llobregat, Barcelona. 1Dept. Pharmacology, University of Cantabria, 39011 Santander. Spain
Address: Down Syndrome Research Group, CGMM-IRO, Hospital Duran i Reynals, 08907-L'Hospitalet de Llobregat, Barcelona. TEL: 00 34 932607775 FAX: 00 34 932607776 EMAIL: mdierssen@iro.es
Genetic influences on aggression in preschoolers: Preliminary analyses2
1Department of Psychiatry, Southern Illinois University School of Medicine, Carbondale, IL 62901-6517. 2Supported by grants from Southern Illinois University Carbondale and
the SIUC School of Medicine. I would like to thank all the families who volunteer for this project and the students who have helped with data collection
Address: Department of Psychiatry, Southern Illinois University School of Medicine, Carbondale, IL 62901-6517 Telephone: 618 453 1855 Fax: 618 453 1859 E_mail: ldilalla@siu.edu
Partitioning the intergenerational transmission of parental smoking and child birth weight: The role of the children of twins methodology
1Psychology Department, University of Virginia, Charlottesville, VA 22904-4400. 2Virginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University,
Richmond, VA 23298-0003. 3The Institute of Medical Genetics, University of Oslo, Oslo, Norway
Address: Psychology Department, University of Virginia, PO Box 400400, Charlottesville, VA 22904-4400, Phone: 804-982-4750, Email: briand@virginia.edu
The structure of anxiety in 4-year-olds: A genetic analysis
1Social, Genetic and Developmental Psychiatry Research Centre, and. 2Department of Psychology, Institute of Psychiatry, Kings College, London, SE58AF. Supported by MRC
Grant G9426437
Address: Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, Kings College, London, SE58AF. Telephone: +44 (0)20 848 0873 Fax: +44 (0)20 848 0863 Email: t.eley@iop.kcl.ac.uk
A study of the genetic and environmental etiology of stuttering in a selected twin sample4
1Department of Speech-Language Pathology, Duquesne University, Pittsburgh, PA 15282. 2Queensland Institute of Medical Research and Joint Genetics Program, The University
of Queensland, Brisbane, Australia. 3Virginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University, Richmond, VA 23298. 4The sceening phase of this study was supported
by NIH grants (AA07535 and AA07728) and the interview phase by an NIH grant to SF (DC 03776-01). Dr Neale's development of Mx is supported by NIH grant MH 01458. The Australian Twin Registry is supported by the
National Health and Medical Research Council
Address: Department of Speech-Language Pathology, 600 Forbes Avenue, Duquesne University, Pittsburgh, PA 15282, Telephone: 412 396 4205 Fax: 412 396 4196 E-mail: felsenfeld@duq.edu
Contributions of Perceptual and Motor Speed to Heritability of Cognition in Late Adulthood 1
Department of Psychology, Indiana University Southeast. 1 Supported by National Institute on Aging Grant No. R03-AG15211
Address: E-mail: DFinkel@IUSMail.IUS.Indiana.EDU
Everyone Recalls the Same Items From a Word Recall Task2
1Division of Social Sciences, Indiana University Southeast, New Albany, IN 47150. 2MTSADA is supported by NIA grant AG06886
Address: Division of Social Sciences, Indiana University Southeast, 4201 Grant Line Road, New Albany, IN 47150 Telephone: 812 941 2668 Fax: 812 941 2591 E-mail: dfinkel@ius.edu
Maternal sensitivity and measured common environmental factors: a twin study4
1Research Unit on Children s Psychosocial Maladjustment, University of Montreal, Montreal, Canada, H3T 1J7. 2Research Unit on Children s Psychosocial Maladjustment, University
of Quebec at Trois-Rivières, Trois-Rivières, Canada, G9A 5A7. 3Research Unit on Children s Psychosocial Maladjustment, Laval University, Quebec City, Canada, G1K 7P4. 4Supported
by grants to D. Perusse from the Medical Research Council of Canada, the National Health Research and Development Program/Health Canada, The Social Sciences and Humanities Research Council of Canada, the Fond de
la recherche en sante du Quebec and the Quebec Ministry of Health and Social Services. Nadine Forget-Dubois is supported by a fellowship from the Social Sciences and Humanities Research Council of Canada
Address: Centre de recherche Fernand-Seguin, 7331 Hochelaga, Montreal, Canada, H1N 3V2. E-mail: forgetdubois@sympatico.ca. Phone: (514) 251-4015. Fax: (514) 251-2617
Genetic and Environmental Contributions Common And Specific to Suicidality: A Multivariate Analysis6
1Missouri Alcoholism Research Center, Washington University School of Medicine, St. Louis, MO 63108. 2University of Illinois School of Public, Chicago, IL. 3Harvard
Medical School, Department of Psychiatry at the Brockton/West Roxbury VAMC and Department of Psychology, Boston University. 4Menlo Park VA Medical Center, Menlo Park, CA. 5St. Louis
University School of Public Health, St. Louis, MO 6308. 6Supported by NIH grants: AA07728, AA10339, AA11667, AA11822, AA11998, DA04604, MH37685, & MH31302
Address: Washington University, 40 N. Kingshighway Blvd., Suite 2, St. Louis, MO 63108
Longitudinal analyses of teacher-rated temperament in early adolescence
1Boston University, Department of Psychology, Boston, MA 02215
Address: Boston University, Department of Psychology, 64 Cummington Street, Boston, MA 02215 Telephone: 617 353 1102 Fax: 617 353 6933 E-mail: gagnej@bu.edu
The nature of attachment3
1Department of Psychology, George Washington University, Washington, DC 20052. 2Center for Family Research, George Washington University, Washington, DC 20037.
3Supported by NIMH Grant R01MG54610
Address: > Department of Psychology, George Washington University, Washington, DC 20052 Telephone: 202 994 7571 Fax: 202 994 1602 E-mail:ganiban@gwu.edu
Direction of causation modeling between personality, measures of perceived parenting and recently experienced psychiatric symptoms
1Queensland Institute of Medical Research, Brisbane, Australia This work was supported by NIH grants AA04535, AA07728, and AA10249 and NHMRC (Australia) grants 941177, and 971232.
We thank the twins, who were drawn from the Australian NH&MRC Twin Registry for their cooperation
Address: Nathan A. Gillespie Queensland Institute of Medical Research Post Office, Royal Brisbane Hospital Brisbane QLD 4029 Telephone: (61) 7 3362 0228 Fax: (61) 7 3362 0101 E-mail: nathanG@qimr.edu.au
Assortative mating for DSM-IV alcohol dependence: Evidence from the Australian Twin Study3
1Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63108. 2Queensland Institute of Medical Research, Brisbane, Australia. 3Supported
by: AA10249, AA07728, DA07261, DA00272, AA11998
Address: Department of Psychiatry, Washington University School of Medicine, 40 N. Kingshighway, Suite 1, St. Louis, MO 63108. Telephone: (314) 286-2299 FAX: (314) 286-2213 email: julie@matlock.wustl.edu
Canine Kaspar Hausers. A film by John L. Fuller on the effects of isolation on the behavior of dogs
Department of Biology, William Paterson University, Wayne, NJ 07470
Address: Department of Biology, William Paterson University, Wayne, NJ 07470. Telephone: 973 720 2480 Fax: 973 720 2338 E-Mail: Hahnm@wpunj.edu
Genetic influences on ERP slow wave measures of working memory in adolescent twins
1Queensland Institute of Medical Research, Brisbane, Australia. 2Cognitive Psychophysiology Laboratory, School of Psychology and Department of Psychiatry, University of
Queensland, Brisbane, Australia. 3School of Psychology, University of Queensland, Brisbane, Australia
Address: Epidemiology, Queensland Institute of Medical Research, Royal Brisbane Post Office, Brisbane, QLD 4029, Australia. Telephone: +617 33620299 Fax: +617 33620101 E-mail: narelleH@qimr.edu.au
Effects of prenatal cocaine exposure upon maternal retrieval behavior in mice
Department of Biology, William Paterson University, Wayne, NJ 07470
Address: Department of Biology, William Paterson University, Wayne, NJ 07470. Telephone: 973 720 2480 Fax: 973 720 2338 E-mail: HahnM@wpunj.edu
A population-based twin study of generalized anxiety disorder in men and women
1 Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia, Commonwealth University, Richmond, VA 23298. 2
Department of Human Genetics, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA 23298
Address: Dept of Psychiatry, MCV/VCU, P.O. Box 980710, Richmond, VA 23298-0710, Telephone: 804-828-8592 Fax: 804-828-1471 E-mail: jhettema@hsc.vcu.edu
A Biometric Analysis of Personality Traits and Externalizing Disorders
Department of Psychology, University of Minnesota, MN 55455-0344 The Minnesota Twin Family Study is supported in part by USPHS grants AA00175, AA09367, and DA05147
Address: Department of Psychology, University of Minnesota, Elliott Hall, 75 E. River Rd., Minneapolis, MN 55455-0344 Telephone: 651 628 0714 Fax: 612 626 2079 Email: hick0131@tc.umn.edu
The heritability of evolutionarily acquired mental mechanisms: A study on the Selection task with twin design5
1Graduate School of Arts and Scinces, The University of Tokyo, Tokyo, Japan. 2JPSP research fellow, Tokyo, Japan. 3Faculty of Letters, Keio University, Tokyo, Japan.
4Faculty of Medicine, Keio University, Tokyo, Japan, 153-8902. 5Supproted by a Grant-in-Aid for JPSP Fellows No.11-10333 from Japanese Ministry of Education, Keio University Special Grant-in-Aid
Innovative Collaborative Resarch Project, and Human Frontier Science Program
Address: Department of Life Sciences (Psychology), Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo, Japan. Telephone: +81 3 5454 4332 Fax: +81 3 5454 6266
E-mail: kai@darwin.c.u- tokyo.ac.jp
Sex Differences in the Genetic and Environmental Influences on the Development of Antisocial Behavior
1Virginia Institute for Psychiatric & Behavioral Genetics; MCV/VCU
Address: 800 E Leigh Street, PO Box 980126; Richmond, Va 23298-0126. Phone: 804 828 8126.
Fax: 804 828 1471. E-mail: jacobson@physio.vipbg.vcu.edu
Sources of Structure: Genetic, Environmental, and Artifactual Influences on the Covariance of Personality Traits
1Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada. 2 Gerontology Research Center, National Institute on Aging, NIH, Baltimore, MD.
3Department of psychology, Universit t Bielefeld, Bielefeld, Germany
Address: Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada. V6T 2A1. Telephone: (604) 822-7895; Facsimile: (604) 822-7756; E-mail: kjang@unixg.ubc.ca
Understanding smoking patterns across adolescence: Genetically informative analyses of trajectories of smoking and covariance with drinking4
1Department of Public Health, University of Helsinki, FIN 00014, Finland. 2Department of Public Health and General Practice, University of Oulu, 90220, Finland.
3Department of Psychology, Indiana University, Bloomington, IN 47405. 4Supported by NIAAA with grants AA08315, AA00145, and AA07611, and by Academy of Finland
Address: Department of Public Health, University of Helsinki, FIN 00014, Finland Telephone: +358 9 191 27 595 Fax: +358 9 191 27 600 E-mail: jaakko.kaprio@helsinki.fi
Depression and anxiety disorders in a selected sample of Australian twins and their families: Methodology
1Queensland Institute of Medical Research, Brisbane, QLD 4029 Australia. 2World Health Organization Collaborating Centre for Mental Health and Substance Abuse, St. Vincent's
Hospital Sydney, Darlinghurst, NSW 2010 Australia
Address: Queensland Institute of Medical Research, Post Office Royal Brisbane Hospital, Brisbane QLD 4029 Australia. Telephone: +61 7 3362 0272 Fax: +61 7 3362 0101 E-mail: kathE@qimr.edu.au
Change and stability of self-reported life satisfaction among adult twins - a 15 year follow-up5
1The Finnish Twin Cohort Study, Department of Public Health, University of Helsinki, FIN 00014, Finland. 2Department of Public Health, University of Turku, Finland.
3Department of Psychiatry, University of Kuopio, Finland. 4Department of Public Health and General Practice, University of Oulu, FIN 90220, Finland. 5Supported by the Academy of
Finland
Address: Department of Public Health, University of Helsinki, PO Box 41, FIN 00014 University of Helsinki, Finland. Telephone: +358 9 1911 Fax: +358 9 191 27 600 E-mail: markku.koskenvuo@pp.inet.fi
Phenotypic, Genetic and Environmental Parallels in the Structure of Personality: Evidence from the Minnesota Twin Registry
1Department of Psychology, University of Minnesota, Minneapolis, MN, USA
Address: Department of Psychology, University of Minnesota, Minneapolis, MN, USA, 55455. Telephone: 612 624 8204 Fax: 612 626 2079 E-mail: krueg038@tc.umn.edu
Gender Differences and Interactive Effects in the Etiology of Early Adolescent Substance Use
University of Minnesota, Minneapolis, MN 55455. Supported in part by NIH Grants MH17069, DA05147, and AA09367
Address: Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN 55455. E-mail: llegrand@tfs.psych.umn.edu
Defining the Nicotine Dependence Phenotype3
1Washington University School of Medicine, St. Louis, MO 63110. 2Queensland Institute of Medical Research, Brisbane, Australia. 3University
of Missouri, Columbia, MO 65211
Address: 40 N. Kingshighway, Suite 1, St. Louis, MO 63108, Phone: 314-286-2298, Fax: 314-286-2213, E-mail: christina@matlock.wustl.edu
Spontaneous stereotypy in an animal model of Down syndrome (Ts65Dn mice)4
1Departments of Psychiatry & Neuroscience, University of Florida, Gainesville, FL 32610. 2Department of Pediatrics, University of California, San Francisco, San Francisco, CA.
3Departments of Psychiatry & Pediatrics, University of Colorado, Denver CO. 4Supported by NIH Grants MH56163, HD04024 and HD17449
Address: Department of Psychiatry, P.O. Box 100256, University of Florida, Gainesville, FL, 32610-0256, Telephone: 352 294 0415, FAX: 352 392 2579, e-mail: mlewis@college.med.ufl.edu
The etiology of genetic and environmental influences of marital relationships2
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. 2Supported by NIMH grant MH-54610
Address: Box 281, SE-171 77 Stockholm. Email: paul.lichtenstein@mep.ki.se, Phone 46 8 728 7424, Fax: 46 8 314 975
The influence of genetic factors on choice response time and delayed response tasks
1Queensland Institute of Medical Research, Brisbane, Australia. 2Cognitive Psychophysiology Laboratory, University of Queensland, Brisbane, Australia. 3Department
of Psychology, University of Queensland, Brisbane, Australia
Address: Queensland Institute of Medical Research, Royal Brisbane Hospital Post Office, Brisbane, QLD 4029 Australia. Telephone: +61 7 3362 0218 Fax: +61 7 3362 0101 E-mail: michelLu@qimr.edu.au
Differential deficit in working memory, not attention, associated with liability to schizophrenia: a sibling study of the expectancy AX-CPT
University of Pittsburgh, Departments of Psychology and Psychiatry
Address: 604 Old Engineering Hall, Pittsburgh, PA 15260; Telephone 412 383 2174; Email angus3+@pitt.edu
Heritability of Heavy Smoking in Adult Twins3
1Washington University School of Medicine, St. Louis, MO, 63110. 2Universities of Helsinki and of Oulu, Helsinki and Oulu, Finland. 3Karolinska Institutet, Stockholm,
Sweden. 4Queensland Institute of Medical Research, Brisbane, Australia. 5Supported by NIH grants DA00272, DA12540, AA07535, AA11998 and AA07728
Address: 40 N. Kingshighway, Suite #2, St. Louis, MO 63108; Phone: (314) 286-2286; Fax: (314) 286-2213; E-Mail: pam@matlock.wustl.edu
Genetic analyses of smoking initiation, nicotine dependence, and smoking cessation2
1Virginia Institute for Psychiatric & Behavioral Genetics, Department of Human Genetics and Psychiatry, Virginia Commonwealth University, Richmond VA 23298. 2 Supported
by NIH grants HL60688, MH45268, AG04954, GM30250, GM32732, AA06781, AA07728, AA07535, MH40828, RR08123 and MH01458
Address: VIPBG, MCV/VCU, P.O. Box 980003, Richmond VA 23298-0003. Tel 804 828 8145; Fax 804 828 8801; hmaes@vipbg.vcu.edu; http://www.vipbg.vcu.edu
Genetic and environmental relationships between normal and abnormal personality
1Department of Psychology, University of Minnesota, Minneapolis, MN, 55455
Address: Department of Psychology Elliott Hall University of Minnesota Minneapolis MN 55455 Telephone: 612.626.8221 Email: mark0060@tc.umn.edu
Familial correlations between reading measures in a U.K. sib-pair cohort3
1Wellcome Trust Centre for Human Genetics, University of Oxford. 2Department of Physiology, University of Oxford. 3Supported by The Wellcome Trust
Address: The Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Headington, Oxford, OX3 7BN, UK. Telephone: +44 1865 287598 Fax: +44 1865 764276
E-mail:angela@well.ox.ac.uk
Population based survey of the EPQ in Southern England
Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford
Address: University of Oxford, The Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford, OX3 7BN, United Kingdom. Telelphone: (+44) 01865 287597 Fax: (+44) 01865 287664 E-mail:
neilson@well.ox.ac.uk Web address: http://www.well.ox.ac.uk/bioinformatics
Depression and anxiety disorders in a selected sample of Australian twins and their families: Models of family resemblance
1Queensland Institute of Medical Research, Brisbane, QLD 4029 Australia
Address: Queensland Institute of Medical Research, Post Office Royal Brisbane Hospital, Brisbane QLD 4029 Australia. Telephone: +61 7 3362 0278 Fax: +61 7 3362 0101 E-mail: nickM@qimr.edu.au
Genetic and Environmental Influences on Late-life Cognitive Decline3
1Department of Psychology, University of Minnesota, Minneapolis, MN 55455. 2Odense University Medical School, Odense Denmark. 3Supported by National Institute
on Aging grant P01- AG08761
Address: Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN 55455 Telephone: 612-625-8305 Fax: 612-626-2079 E-
Address: { HYPERLINK mailto:mmcgue@tfs.psych.umn.edu }mmcgue@tfs.psych.umn.edu
Japanese twin study of co-morbidity of the depression and anxiety, and the effect of genetic and environmental factors
1Depertment of Psychiatry, Keio University, School of Medicine, 35 Shinanomachi, shinjyuku-ku , Tokyo 160-8582. 2Department of Education, Keio University Faculty of Letters,
Mita, Minato-ku, Tokyo 180-8345
Address: Department of Psychiatry, Keio University, School of Medicine, 35 Shinanomachi, shinjyuku-ku , Tokyo 160-8582 Telephone: 3 3353 1211 (62453) FAX: 3 5379 0187 E-mail: momose@med.keio.ac.jp
Genetic and environmental correlations among antisociality, alcohol consumption, and alcohol problems4
1Department of Psychology, Indiana University, Bloomington, IN 47405. 2Department of Public Health, University of Helsinki, FIN 00014, Finland. 3Department
of Public Health and General Practice, University of Oulu, 90220, Finland. 4Supported by NIAAA (AA08315) and The Academy of Finland (44069)
Address: Indiana University Department of Psychology 1101 East 10th St. Bloomington, IN 47405 Telephone: 812.855.9232 Fax: 812.856.4544 E-mail: bmustans@indiana.edu
Neuro-ontogeny and development in the ataxic mouse mutant, hotfoot
Department of Biology, Colorado State University, Fort Collins, CO 80523
Address: Department of Biology, ColoradoState University, Fort Collins, CO 80523 Telephone: 970 491 5481 Fax: 970 491 0649 Email: dnash@lamar.colostate.edu
Genetic analysis of multivariate ordinal data2
1Virginia Institute for Psychiatric & Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond VA 23298. 2 Supported by NIH grants
RR-08123 and MH-01458
Address: VIPBG, MCV/VCU, P.O. Box 980126, Richmond VA 23298-0126. 804/828-3369(phone); 804/828-1471(fax); neale@vipbg.vcu.edu; http://www.vipbg.vcu.edu
Genetic and environmental contributions to the associations between personality characteristics and adjustment in twin women: The role of mothering as a mediator2
1The Center for Family Research, The George Washington University, Washington, DC. 2This project is supported by grant RO1MH54610 from the National Institutes of Mental
Health
Address: Center for Family Research, The George Washington University, 2300 I St. NW Room 613, Washington, DC 20037 Telephone: 202.994.2212 Fax: 202.994-4812 E-mail: cfrjmn@gwumc.edu
Genetic and environmental influences on "affectionless control" in Japanese population
1Department of Neuropsychiatry, Keio University School of Medicine. 2Department of Education, Faculty of Letters, Keio University
Address: Department of Neuropsychiatry, Keio University 35 Shinanomachi Shinjuku Tokyo Telephone:03 3353 1211 (62453) Fax:03 5379 0187 E-mail:naoko-o@med.keio.ac.jp
Finding a Satisfactory Solution to Influences on Age at Onset in Dementia4
1 Karolinska Institutet. 2 University of Southern California. 3 Centers for Disease Control. 4 Supported by National Institute on Aging Grant No.
R01-AG08724
Address: E-mail: Nancy.Pedersen@mep.ki.se
Mothering as an Influence on the Mothers Own Mental Health
1Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden and Department of Psychology, University of Southern California. 2Supported by NIMH grant
MH-54610
Address: Box 281, SE-171 77 Stockholm. Email: paul.lichtenstein@mep.ki.se, Phone +46 8 728 7418, Fax: +46 8 314975
A genome scan for QTLs associated with general cognitive ability ('g')
Social, Genetic and Developmental Research Centre, Institute of Psychiatry, King's College London. Supported by NIH Grant HD27694
Address: Social, Genetic and Developmental Research Centre, Institute of Psychiatry, King's College London, DeCrespigny Park, Denmark Hill. London SE5 8AF. UK Telephone: +44 207 848 0894 Fax: +44
207 848 0866 E-mail: r.plomin@iop.kcl.ac.uk
Separating the influences of age, and age-related variables in the analysis of change in alcohol consumption among female twins
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond VA, USA. Supported by NIH Grants
R01-MH/AA-49492, R01-AA/DA-09095 and K01-AA-00236. We thank Linda Corey and Lenn Murrelle, directors of the Mid-Atlantic Twin Registry, and Patsy Waring, Lisa Halberstadt, and Barbara Brooke who supervised
data collection
Address: VIPBG, MCV/VCU, P.O. Box 980126, Richmond VA 23298-0126 telephone: (804) 828-5968; fax: (804) 828-1471; email: cprescott@hsc.vcu.edu
A longitudinal twin study of specific cognitive abilities in preschool children
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, England. 2Department of Communication Science and Disorders, University of
Missouri-Columbia. 3Centre for Research into Psychological Development, University of Southampton, England. The Twins Early Development Study is funded by the Medical Research Council
Address: Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, 111 Denmark Hill, London SE5 8AF, England. Telephone: +44 (0) 207 848 0961 Fax: +44 (0) 207 848 0866 E-mail:
T.Price@iop.kcl.ac.uk
Epistasis in QTL linkage analysis: interaction or main effect?2
1Social, Genetic & Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, United Kingdom. 2Supported by MRC grant G9700821, NIH grant
EY-12562 and Wellcome Trust grant 055379
Address: 111, Denmark Hill, Denmark Hill, London SE5 8AF, United Kingdom. Telephone + 44 (0) 207 848 0924. Fax +44 (0) 207 848 0866. E-mail s.purcell@iop.kcl.ac.uk
The Twin Mothers Project4
1Center for Family Research, George Washington University, Washington, DC 20037. 2Karalinska Institut, Stockholm, Sweden. 3Lund University, Lund, Sweden.
4Supported by grant R01MH54610
Address: > Center for Family Research, George Washington University, 2300 Eye St., N.W., 613 Ross Hall, Washington, DC 20037 Telephone: 202 994 2623 Fax: 202 994 4812 E-mail:cfrdxr@gwumc.edu
Age, Education, and Bio-markers Associated with Cognitive Decline in Swedish Twins1
Department of Psychology, University of Southern California . 1Supported by National Institute on Aging Grant No. R01-AG10175 and a grant from the Turken Family Foundation
Address: E-mail: reynold@rcf.usc.edu
A review of family studies examining the etiology of comorbidity between two disorders2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309. 2Supported by NIDA Center DA-11015
Address: Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder, CO 80309 Telephone: (303) 492-4631 Fax: (303) 492-8063 E-mail: soo.rhee@colorado.edu
Gene-Environment Interaction and Evocative Gene-Environment Correlation: Contributions of Harsh Discipline and Parental Psychopathology to Problem Adolscent Behaviors3
1Department of Psychiatry, University of Iowa, Iowa City, IA 52242. 2Department of Psychology, University of Iowa, Iowa City, IA 52242. 3Data collection for this
project was supported by grant R01 DA05821 from the National Institute on Drug Abuse awarded to the second author. Preparation of the poster was supported by a National Research Scientist Award (T32MH14620) presented
to the first author
Address: Kristin Riggins-Caspers, Ph.D., Psychiatry Research/MEB, College of Medicine, University of Iowa, Iowa City, IA 52242 Telephone: (319) 353-3932. FAX: (319) 353-3003. E-mail: kristin-caspers@uiowa.edu
Effects of Pedigree Structure and Genetic Model on the Power of QTL Linkage Analysis
Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, London
Address: SGDP Research Centre, Institute of Psychiatry, 111 Denmark Hill, Denmark Hill, London SE5 8AF, England. Telephone: +44 (0)207 848 0890 Fax: +44 (0)207 848 0866 E-mail: spjgfvr@iop.kcl.ac.uk
Behavior Genetic Modeling of Human Fertility: Findings from a Contemporary Danish Twin Study
1Department of Psychology, University of Oklahoma, Norman OK 73019. 2Max Planck Institute for Demographic Research. 3Institute of Public Health, and the Danish
Twin Registry, Odense University
Address: Joseph Lee Rodgers, Department of Psychology, University of Oklahoma, Norman OK 73019 Telephone: 405-325-4591 Fax: 405-325-4737 e-mail: JRODGERS@OU.EDU
The Friends of Siblings: A Test of Social Homogamy vs. Peer Selection
1School of Family and Consumer Resources, Campus Box 210033, University of Arizona, Tucson, AZ 85721. 2Department of Psychology, Campus Box 210033, University of Arizona,
Tucson, AZ 85721
Address: 1School of Family and Consumer Resources, Campus Box 210033, University of Arizona, Tucson, AZ 85721 Telephone: 520 621-7127 Fax: 520 621-3401 E-mail: dcr091@ag.arizona.edu
Genetic influences on activity level in adolescence: Do the same genetic effects operate on parent ratings, self ratings and mechanical measures?
1Boston University, Department of Psychology, Boston, MA 02215. 2Case Western Reserve University, Department of Psychology, Cleveland, OH 44106
Address: Boston University, Department of Psychology, 64 Cummington Street, Boston, MA 02215 Telephone: 617 353 3679 Fax: 617 353 6933 E-mail: ksaudino@bu.edu
Personality structure in young adults and their parents2
1Institute for Bahavioral Genetics, University of Colorado, CO 80309. 2Supported by a grant from the W. T. Grant Foundation and NIH grants HD10333, DA11015, and DA05131
Address: Institute for Bahavioral Genetics, Campus Box 447, University of Colorado, CO 80309; Telephone: (303) 492-0835; Fax: (303) 492-8063; email: schmitzs@colorado.edu
Twin Study of Suicidal Behavior: Replication and Extension3
1Psychology Department, California State University, Fullerton, California 92834. 2Department of Psychiatry, School of Medicine & Dentistry of New Jersey, Newark, NJ 07103.
3Supported by a faculty research award from California State University, Fullerton
Address: Psychology Department, California State University, Fullerton, California 92834. 714-278-2142, 714-278-4843, nsegal@fullerton.edu
Power and robustness of candidate gene study designs
Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
Address: Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, bldg. 37, rm. 4a13, Bethesda, MD 20892 Telephone: 301 496 1747 Fax: 301 402 5565 E-mail: lsirota@helix.nih.gov
An ecological exploration of factors influencing the parenting of adolescents using behavioral genetic techniques2
1The Center for Family Research, The George Washington University, Washington, DC. 2This project is supported by grant RO1MH54610 from the National Institutes of Mental
Health
Address: Center for Family Research, The George Washington University, 2300 I St. NW Room 613, Washington, DC 20037 Telephone: 202.994.2404 Fax: 202.994-4812 E-mail: elspotts@gwu.edu