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 | 2000-2001 | 2001-2002 |
| President President-Elect Past President Secretary Treasurer Member-at-Large Member-at-Large Member-at-Large | John Hewitt Matt McGue Richard Rose Hermine Maes Pam Madden Irwin Waldman Jennifer Harris Carol Prescott | Matt McGue Nancy Pedersen John Hewitt Michael Pogue-Geile Pam Madden Jennifer Harris Carol Prescott Caroline Van Baal |
MEETING INFORMATION
The 31st Annual Meeting of the Behavior Genetics Association will be held at Peterhouse College, a college of the University of Cambridge. Paper, poster and plenary sessions will be held throughout the day on the 9th, 10th and 11th of July. The opening reception is scheduled to begin at 6:00 PM on Sunday July the 8th. The banquet will be held on Wednesday the 11th.
Peterhouse College Situated in the heart of picturesque Cambridge, beside the peaceful river Cam, Peterhouse College was founded in 1284 and its Hall, constructed between 1286 and 1290, was the first collegiate building in Cambridge. The variety and charm of its interior derive from the 19th century stained glass, wall tiles and decoration by William Morris, Edward Burne-Jones and Ford Maddox-Brown. The college theatre, where the majority of the conference will be held, with its curving auditorium and gallery was converted from a Victorian lecture room. Cambridge itself needs no introduction. One of England's most elegant and historical town centre is only a short stroll away from the conference venue.
Sanger Centre This genome research centre was set up in 1992 by the Wellcome Trust and the Medical Research Council in order to further our knowledge of genomes, and in particular to play a substantial role in the sequencing and interpretation of the human genome. The Centre is situated on the Wellcome Trust genome Campus at Hinxton Hall, a 55-acre parkland site 15 minutes south of the university city of Cambridge. More information on the Centre can be obtained from the website: www.sanger.ac.uk. The visit will include a tour of the laboratories followed by a brief talk and discussion session.
Local Host: Dr. Thalia Eley
SGDP Research Centre
Institute of Psychiatry
111 Denmark Hill
London SE5 8AF UK
Tel: +44 (0) 20 7848 0863
Fax: +44(0) 20 7848 0866
Email: t.eley@iop.kcl.ac.uk
| 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 | Ronald Johnson | Martine Thomis | Tony Vernon -Toronto, Canada |
| 1998 | Norman Henderson | Stephen Maxson | Javier Gayán & Alexander Weiss | N Pedersen - Stockholm, Sweden |
| 1999 | Richard Rose | Lindon Eaves | Danielle Posthuma & Danielle Dick | Kerry Jang, Vancouver, Canada |
| 2000 | John Hewitt | Pierre Roubertoux | Brian D'Onofrio & Nathan Gillespie | James Hudziak, Burlington, Vermont |
BEHAVIOR GENETICS ASSOCIATION
31st ANNUAL MEETING
Peterhouse College, Cambridge, England
July 8-11, 2001
SUNDAY JULY 8
| 2:00 - 6:00
| REGISTRATION
| 4:00 - 5:00
| EXECUTIVE COMMITTEE MEETING
| 6:00 - 8:00
| WELCOME RECEPTION
| MONDAY JULY 9
| Monday July 9th
| 9:00 - 11:00 PAPER SESSION I
| Cognitive Ability Chair: Michael F. Pogue-Geile 9:00 - 9:15
| Functional analysis of genes included in the Down syndrome chromosomal region-1 (DCR-1) with transpolygenic mice
| Caroline Chabert, Ameziane Cherfouh, Vincent Duquenne and Pierre L. Roubertoux 9:15 - 9:30
| General Cognitive Ability (g) in Mice as the basis of a Functional Genomics Model of Cognitive Abilities and Disabilities
| Michael J. Galsworthy, Jose L. Paya-Cano, Lin Liu, Santiago Monleon and Robert Plomin 9:30 - 9:45
| Modularity and genetic correlation in cognitive development: A study of pre-school age twins (T)
| Tom S. Price, P.S. Dale, T.C. Eley and Robert Plomin 9:45 - 10:00
| Genetics of electroencephalographic coherence and intelligence in young twins
| G. Caroline M. van Baal, Dorret I. Boomsma and Eco J.C. de Geus 10:00 - 10:15
| Socioeconomic status modifies heritability of intelligence in impoverished children
| Eric Turkheimer, Andreana Haley, Brian D'Onofrio, Mary Waldron, Robert E. Emery and Irving I. Gottesman 10:15 - 10:30
| Cognitive Function and Dopamine Transporter (DAT) Genetic Polymorphisms: A Twin and Genetic Association Study
| Michael F. Pogue-Geile, Stephen Manuck, Robert Ferrell and Thomas Debski 10:30 - 10:45
| Are faster brains also smarter? (T)
| Danielle Posthuma, Dorret I. Boomsma, G. Caroline C. van Baal and Eco J.C. de Geus 10:45 - 11:00
| Association between APOE and ACE genotypes and cognitive decline
| Chandra A. Reynolds, Lars Feuk, Margaret Gatz, Ulf de Faire, Anthony Brookes and Nancy L. Pedersen Monday July 9th
| 9:00 - 11:00 PAPER SESSION II
| Childhood Psychopathology and Neurological Disorder Chair: Maricela Alarcón 9:00 - 9:15
| Genetic analysis of DSM-oriented scales in 3 year-old Dutch twins
| Dorret Boomsma, Toos van Beijsterveldt, Caroline van Baal, Therese Stroet, Tinca Polderman, Alexia Groot, Jolande van der Valk, Frank Verhulst, Tom Achenbach and Jim Hudziak 9:15 - 9:30
| Daytime Basal Cortisol and Common Childhood Psychopathology
| Meike Bartels, E.J.C. de Geus, C. Kirschbaum, M.J.H. Rietveld and D.I. Boomsma 9:30 - 9:45
| Shared environmental effects are important for stability and genetic effects for change in fears and phobias in the transition from childhood to early adolescence
| Paul Lichtenstein and Peter Annas 9:45 - 10:00
| Neonatal seizures, M-channels, and retigabine
| V. Elving Anderson 10:00 - 10:15
| Linkage Analysis of Language Traits in Autistic Families
| Maricela Alarcón, Rita M. Cantor, AGRE Consortium and Daniel H. Geschwind 10:15 - 10:30
| Intergenerational Transmission of ADHD and Associated Psychopathologies
| Florence Levy, David A. Hay, Michael McStephen and Nicholas G. Martin 10:30 - 10:45
| Modelling the relationship of Inattention and Hyperactivity/Impulsivity in ADHD
| Michael McStephen, David A. Hay and Florence Levy 10:45 - 11:00
| 11:00 - 11:30
| TEA
| Monday July 9th
| 11:30 - 12:30 PLENARY ADDRESS
| The John/Joan case and implications for behavior Genetics Milton Diamond 12:30 - 1:30
| LUNCH
| Monday July 9th
| 1:30 - 3:30 SYMPOSIUM I
| Developmental approaches to the genetics of antisocial behaviour and adjustment problems Organizer and Chair: Thalia Eley Discussant: Terrie Moffitt
| Longitudinal genetic analysis of aggressive and non-aggressive antisocial behavioural symptoms
| Thalia C. Eley and Paul Lichtenstein
| Does Parenting Really Matter? A Test of the Nurture Assumption
| Jenae M. Neiderhiser and Alison Pike
| Examining sex and cohort differences in the etiology of conduct disorder: A study of 6,342 adult twin pairs
| Wendy S. Slutske, Andrew C. Heath, Kathleen K. Bucholz, Pamela A. F. Madden, Dixie Statham and Nicholas G. Martin
| Behavioral Genetic Confirmation of a Life-Course Perspective on Antisocial Behavior: Can We Believe the Results?
| Kristen C. Jacobson, Michael C. Neale, Carol A. Prescott, and Ken S. Kendler Monday July 9th
| 1:30 - 3:30 SYMPOSIUM II
| Laterality: Genetic and evolutionary approaches Organizer and Chair: Pierre L. Roubertoux Discussant: Stephen Maxson
| Non-human primate patterns of manual laterality
| Jacques Vauclair and Eric Damerose
| ProtocadherinXY as a candidate for the Homo sapiens speciation gene
| Tim Crow, Nic A Williams, Maria Giouzeli, Norman Ross, Patricia Blanco, Carole A Sargent and Nabeel A Affara
| Familial study and partial genome scan for degree of laterality
| Anne-Lise Doyen, Thierry Dufour, Laetitia Prut and Michele Carlier
| Analysis of quantitative trait loci for behavioral laterality in mice
| Pierre L. Roubertoux, Isabelle Le Roy, Danièle Migliore-Samour and Améziane Cherfouh
| Genetic, neuroanatomical and behavioural approaches to studying CNS asymmetries in zebrafish
| Anukampa Barth, Miguel Concha, Claire Russell and Steve Wilson 3:30 - 4:00
| TEA
| Monday July 9th
| 4:00 - 5:15 PAPER SESSION III
| Methodology Chair: Stacey Cherny 4:00 - 4:15
| The analysis and statistical power of data collected from screened samples of twins
| Michael C. Neale and Kenneth S. Kendler 4:15 - 4:30
| The role of the Children of Twins design in highlighting genetic and environmental pathways between parental and child characteristics
| Brian M. D'Onofrio, Eric Turkheimer, Linda A. Corey, Robert E. Emery, Mary Waldron and Lindon J. Eaves 4:30 - 4:45
| A measurement error explanation of the biased QTL effect estimates when pi-hat is used as the IBD probability for untyped sib pairs
| A. Leo Beem and Dorret I. Boomsma 4:45 - 5:00
| Gene-by-environment interaction in twin and sib-pair analysis (T)
| Shaun Purcell 5:00-5:15
| Bayesian approaches to modeling deveopment in twins
| Lindon J. Eaves and Al Erkanli Monday July 9th
| 4:00 - 6:00 VISIT to SANGER CENTER
| limited places only - please sign up at the registration desk Monday July 9th
| 5:30 - 7:00 POSTER SESSION I
| 1
| Genetic analysis of DSM-oriented scales in 3 year-old Dutch twins as a function of parental Socio-economic status
| Tinca Polderman, Toos van Beijsterveldt, Caroline van Baal, Therese Stroet, Alexia Groot, Jolande van der Valk, Frank Verhulst, Tom Achenbach, Jim Hudziak and Dorret Boomsma 2
| Genetic and environmental influences on sex-typed behavior in pre-school children: A study of 1,973 twin pairs at 3 and at 4 years of age (T)
| Alessandra C. Iervolino, Melissa Hines, Susan Golombok, John Rust, Thalia Eley and Robert Plomin 3
| Continuous and Discontinuous Cognitive Development (T)
| Marjolein J. H. Rietveld, G. Caroline M. van Baal, Meike Bartels and Dorret I. Boomsma 4
| Genetic and environmental contributions to continuity and change of behaviors at ages 3 to 7 (T)
| Jolande C. van der Valk, Edwin J.C.G. Van den Oord, Frank C. Verhulst and Dorret I. Boomsma 5
| Heterogeneity of childhood aggression and anti-social behavior: A twin study
| Laura A. Baker, Jennifer K. Johnson, Dora I. Lozano and Adrian Raine 6
| Genetic and contrast effects on temperamental difficulty and unadaptability in infancy and early childhood (T)
| Kathryn S. Lemery, Nicole L. Schmidt and H. Hill Goldsmith 7
| Common and unique genetic and environmental influences on EAS temperament dimensions in childhood (T)
| Amber L. Gahagan and Irwin D. Waldman 8
| Shared environmental transmission of culture: Methodology and findings
| Juko Ando and Yutaka Ono 9
| Genetic and environmental contributions of TCI subscales
| Juko Ando, Naoko Onoda, Yoshimura Kimio and Yutaka Ono 10
| Presence of mammary tumor virus alters the body odor of mice
| Kunio Yamazaki, Gary K. Beauchamp, Judith Bard and Edward A. Boyse 11
| Genetic variation for circadian activity rhythm period among eight inbred mouse strains
| Bernard P. Possidente, Jennifer Wishnow, Felicia Gomez and Susan Kur 12
| Quantitative Trait Loci (QTL) Analysis of Body Weight in F2 and Recombinant Inbred Mice
| Holly A. Mack, Michael D. Grant, Tara K. Kerin, Jose R. Fernandez, George P. Vogler, David J. Vandenbergh and Gerald E. McClearn 13
| Genetic control of skeletal maturation during growth
| Martine A.I. Thomis, Hermine H.M. Maes, Maarten Peeters, Ruth Loos, Roeland Lysens, Albrecht L. Claessens, Bavo Vanden Eynde, Robert Vlietinck and Gaston Beunen 14
| Evolution of genetic and environmental influences on regional fat distribution from early adolescence to young adulthood (T)
| Maarten W. Peeters, Hermine H.M. Maes, Martine A. Thomis, Ruth Loos, Albrecht L. Claessens, Roeland Lysens, Bart Vanden Eynde, Robert Vlietinck and Gaston P. Beunen 15
| Studies of Chromosome Sensitivities in Twin Children (T)
| Kazuko Nakashima and Kanehisa Morimoto 16
| Assessment of Stratification in Linkage and Association Samples
| Neilson C. Martin, Goncalo R. Abecasis and Lon R. Cardon 17
| An overview of regression methods of linkage analysis in selected samples
| Jeffrey M. Lessem, Stacey S. Cherny, Goncalo R. Abecasis, Pak C. Sham and Shaun Purcell 18
| Triton Survey Designer: A software package for the design, administration, and analysis of surveys
| Ian L. Cesa, Michael King, Mo Zheng, Tina Lee, Jennifer K. Johnson and Laura A. Baker 19
| Family history influences on adopted adolescents' substance experimentation
| Sally-Ann Rhea and Robin P. Corley 20
| Candidate Gene Studies in Substance-Dependent Adolescents, their Siblings, and Controls
| Susan E. Young, Andrew Smolen, Michael C. Stallings, Robin P. Corley, Thomas J. Crowley and John K. Hewitt 21
| Genetic and Environmental Transmission of Attitudes toward Alcohol Consumption
| Richard J. Viken, Richard J. Rose, Jaakko Kaprio and Markku Koskenvuo 22
| Genetic and environmental influences on the covariation between sensitivity and tolerance to alcohol
| Jennifer K. Johnson, Richard J. Viken and Richard J. Rose 23
| Common Genetic and Environmental Vulnerability for Alcohol and Tobacco Use in a Volunteer Sample of Older Female Twins
| Christian J. Hopfer, Michael C. Stallings and John K. Hewitt 24
| Continuity or Discontinuity between Substance Experimentation, Regular Use, and Dependence Symptoms in Adolescence: Twin and Adoption Results
| Robin P. Corley, Michael C. Stallings, John K. Hewitt and Susan E. Young 25
| Reading performance at 7, 12 and 16 years of age in the Colorado Adoption Project: Parent-offspring analyses
| Sally J. Wadsworth, Robin Corley, John K. Hewitt, Robert Plomin and John C. DeFries TUESDAY JULY 10
| Tuesday July 10th
| 8:30 - 10:30 PLENARY SYMPOSIUM, PART I
| New Molecular Techniques of Behavioral Genetics Organizers and Chairs: Ian Craig and Robert Plomin
| Human genome: Facts and fallacies
| Ian Craig
| Genetic markers: Mileposts and maps
| David Bentley
| Trawling the DNA bases: How to make sense of sequence
| Mark Ross
| The highs and lows of genome screens
| Simon Fisher 10:30 - 11:00
| TEA
| Tuesday July 10th
| 11:00 - 1:00 PLENARY SYMPOSIUM, PART II
| New Molecular Techniques of Behavioral Genetics Organizers and Chairs: Ian Craig and Robert Plomin
| What's new with linkage and association approaches to identifying QTLs
| Pak Sham
| Theory and practice of DNA pooling
| Michael Owens
| Looking for polymorphisms that affect gene regulation
| Mick O'Donovan
| Mouse models for human behavior
| Lee Schalkwyk 1:00 - 2:00
| LUNCH
| Tuesday July 10th
| 2:15 - 3:30 PAPER SESSION IV
| Personality Chair: Katherine Kirk 2:15 - 2:30
| Genetic simplex modeling of personality in adolescent twins
| Nathan A. Gillespie and Nicholas G. Martin 2:30 - 2:45
| Longitudinal analysis of measures of anxiety and depression in adult twins
| Katherine M. Kirk and Nicholas G. Martin 2:45 - 3:00
| Anxious genes and the EDAC design
| Andrew J. Birley, Michael C. Neale, Katherine M. Kirk and Nicholas G. Martin 3:00 - 3:15
| Multivariate analysis of level and lability of self-esteem
| Michelle B. Neiss, Elizabeth F. Gramzow, Constantine Sedikides and Jim Stevenson 3:15 - 3:30
| DRD4, psychopathology, and personality: preliminary findings from the Dunedin multidisciplinary health and development study
| Jonathan S. Mill, Joseph L. McClay, Karen Sugden, Philip J. Asherson, Richie Poulton, Terrie E. Moffitt and Avshalom Caspi Tuesday July 10th
| 2:15 - 3:30 PAPER SESSION V
| Smoking Chair: Pamela Madden 2:15 - 2:30
| Relative risk of smoking parents and smoking siblings on smoking status (T)
| Jacqueline M.Vink and Dorret I. Boomsma 2:30 - 2:45
| Genetic and environmental influences on smoking initiation: An extended twin kinship analysis
| Hermine H. Maes, Andrew C. Heath, Nicholas G. Martin, Michael C. Neale and Lindon J. Eaves 2:45 - 3:00
| Smoking Progression Among Adolescents: A sibling study
| George D. Papandonatos, Richard Rende, Ray Niaura and Elizabeth E. Lloyd 3:00 - 3:15
| Toward characterization of adolescent nicotine dependence
| Christina N. Lessov, Pamela A.F. Madden, Kathleen K. Bucholz, Wendy S. Slutske and Andrew C. Heath 3:15 - 3:30
| The DRD4 VNTR Polymorphism Influences Reactivity to Smoking Cues
| Kent E. Hutchison, Heather LaChance, Raymond Niaura, Angela D. Bryan and Andrew Smollen 3:30 - 4:00
| TEA
| Tuesday July 10th
| 4:00 - 5:15 PAPER SESSION VI
| Alcohol Chair: Andrew Heath 4:00 - 4:15
| Parental Alcohol Dependence and Suicidal Behavior in Adolescent Female Twins (T)
| Anne L. Glowinski and Andrew C. Heath 4:15 - 4:30
| Latent Growth Curve Analyses of Drinking Trajectories Across Adolescence
| Danielle M. Dick, Richard J. Viken, Jaakko Kaprio and Richard J. Rose 4:30 - 4:45
| Genetics of Alcohol Dependence: Controlling for other heritable risk factors
| Valerie S. Knopik, Andrew C. Heath, Pamela A. F. Madden, Kathleen K. Bucholz, Elliot C. Nelson and Nicholas G. Martin 4:45 - 5:00
| Sources of covariance between alcoholism and motivations for drinking
| Carol A. Prescott, Rebecca Cross, John L. Horn and Kenneth S. Kendler 5:00 - 5:15
| Modeling the familial transmission of alcohol dependence symptom counts in clinical and control family pedigrees
| Michael C. Stallings, John K. Hewitt, Jeff M. Lessem, Susan E. Young, Robin P. Corley, Susan K. Mikulich and Thomas J. Crowley Tuesday July 10th
| 4:00 - 6:00 VISIT to SANGER CENTER
| limited places only - please sign up at the registration desk Tuesday July 10th
| 5:30 - 7:00 POSTER SESSION II
| 1
| Genetic and environmental relationships between eating disorder and personality in the Japanese female twin sample
| Hiroko Maekawa, Juko Ando and Yutaka Ono 2
| Indirect effects of the DRD4 VNTR polymorphism on sexual desire
| Angela D. Bryan, Kent E. Hutchison and Andrew Smolen 3
| Is Prolonged Fatigue in Children & Adolescents Heritable? (T)
| Tom A Fowler, Anita Thapar and Ann Farmer 4
| Genome scan for quantitative traits involved in cardiovascular disease in three independent populations
| M. Beekman, B.T. Heijmans, N. Lakenberg, E. Suchiman, G.P. Vogler, N.G. Martin, J.B. Whitfield, N.L. Pedersen, C. Kluft, G.J.B. van Ommen, R.R. Frants, P. de Knijff, E. Slagboom and D.I. Boomsma 5
| Genetics of the contingent negative variation in migraine
| Michael S. Siniatchkin and Wolf-Dieter Gerber 6
| 24-hour saliva cortisol measurements in twins and siblings selected to be at high or low genetic risk for anxious depression (T)
| Mireille van den Berg, Eco de Geus, Dorret I. Boomsma, Conor V. Dolan and Clemens Kirschbaum 7
| A Longitudinal Study of Japanese Adolescents' Depression and Received Parenting
| Naoko Onoda, Juko Ando and Yutaka Ono 8
| Extreme Depressive Symptoms in Children and Adolescents (T)
| Frances J Rice, Gordon T Harold and Anita Thapar 9
| A Twin Study of the Genetics of Fear Conditioning
| John M. Hettema, Peter Annas, Michael C. Neale, Mats Fredrikson and Kenneth S. Kendler 10
| Heritability of Depression Symptomatology in the Second Half of Life: Evidence from Danish Twins over 45 (T)
| Wendy Johnson, Matt McGue, David Gaist, James W. Vaupel and Kaare Christensen 11
| Reading difficulties and rapid naming: Bivariate twin and genetic linkage analyses(T)
| Chayna J. Davis, Javier Gayan, Valerie S. Knopik, Shelley D. Smith, Lon R. Cardon, Bruce F. Pennington, Richard K. Olson and John C. DeFries 12
| Differential genetic etiology of reading disability as a function of processing speed (T)
| Rebecca J. Cross, Javier Gayan, John C. DeFries and Richard K. Olson 13
| Sensory deprivation and predatory behavior in mice
| Donald J. Nash, Alan Schell, Brooke Quigley, Jake Adams and Bryan Hill 14
| Aggression and Mating in Sex Reversed Mice (T)
| Andrew Canastar and Stephen C. Maxson 15
| Factor analyses of phenotypic correlations of animal behaviors assessed in multiple test events are often not informative
| Norman D. Henderson 16
| A review of QTL and knock-out studies for emotionality in mice
| Rens de Groot, Nico Lakenberg, Eline Slagboom, and Dorret Boomsma 17
| East-West, home's best: rewarding properties of the home-cage of laboratory mice
| David A Blizard, Rachel Cohen, Laura Cousino-Klein and Gerald E. McClearn 18
| Investigating Age Differences in the Genetic and Environmental Structure of the TPQ in Later Adulthood (T)
| Noa Heiman, Michael C. Stallings, John K. Hewitt and S.M. Hofer 19
| Analysis of Twin Data of Adult Attachments
| Masaki Fujimoto, Toshimitsu Kamakura, Hisako Itoi, Yuko Kobori, and Kunii Suzuki 20
| Social Closeness and Familiarity in MZA and DZA Twin Pairs
| Nancy L. Segal and Sara Arad 21
| Genetic and environmental influences on self-esteem in a sample of middle-aged twins in Japan
| Toshimitsu Kamakura, Masaki Fujimoto, Hisako Itoi, Kunitake Suzuki and Yuko Kobori 22
| Genetic and environmental influences on 'theory-of-mind' in Japanese adult twins ()
| Atsushi Senju, Juko Ando, Yutaka Ono, Toshikazu Hasegawa and Mariko Hiraiwa-Hasegawa 23
| Is giving up smoking on the nicotine patch related to genotype?
| Patricia Yudkin, Kate Hey, Sarah Roberts, Sarah Welch, Elaine Johnstone, Michael Murphy, Sian Griffiths, Lesley Jones and Robert Walton 24
| Failed Smoking Cessation: Nicotine Withdrawal and Genetic Vulnerability
| Hong Xian, Jeffrey Scherrer, Pamela AF Madden, Michael Lyons, Ming Tsuang, William R True and Seth A Eisen 25
| The Fagerstrom Test for Nicotine Dependence in a Twin-family Study (T)
| Jacqueline M.Vink and Dorret I Boomsma 26
| The Genetic Basis for Tobacco Dependence: A Systematic Review
| Marcus Munafo, Robert Walton, Elaine Johnstone, Patricia Yudkin, Michael Murphy, Lindsay Stead and Lon Cardon 27
| A Twin and Sibling Study of Cigarette Smoking in the National Longitudinal Study of Adolescent Health
| David C. Rowe and Kristen C. Jacobson WEDNESDAY JULY 11
| Wednesday July 11th
| 9:00 - 11:00 SYMPOSIUM III
| Organizer and Chair: Stacey Cherny and Pak Sham Discussant: Lon Cardon
| The effects of genotype errors on mapping complex traits: Detection and treatment
| Stacey S. Cherny, Lon R. Cardon1 and Gonzalo R. Abecasis
| Optimal Selection Strategies for QTL Mapping using Pooled DNA Samples
| Ansar Jawaid, Shaun Purcell, Stacey S. Cherny and Pak Sham
| An index of multipoint polymorphism information content (MPIC)
| Frøhling Rijsdijk and Pak Sham
| Equivalence between Haseman-Elton and variance-components methods for sib-pair quantitative trait linkage analysis (T)
| Shaun Purcell and Pak Sham Wednesday July 11th
| 9:00 - 11:00 SYMPOSIUM IV
| Tools for identifying sources of nonshared environment Organizer and Chair: Erica L. Spotts Discussant: Eric Turkheimer
| Genetic and environmental mechanisms underlying the association between marriage and depressive symptoms (T)
| Erica L. Spotts and David Reiss
| The experiential context of parenting
| Jody M. Ganiban
| Differential Parental Negativity: Objective Reality or in the Eye of the Beholder?
| Alison Pike and Jenae M. Neiderhiser
| A meta-analytic review of bivariate nonshared environment (T)
| Mary Waldron and Eric Turkheimer 11:00 - 11:15
| BREAK
| Wednesday July 11th
| 11:15 - 12:30 BUSINESS MEETING
| 12:30 - 1:30
| LUNCH
| Wednesday July 11th
| 1:30 - 3:30 SYMPOSIUM V
| Molecular Genetic Studies of Dopamine Genes and ADHD Organizer and Chair: Irwin Waldman Discussant: Robert Plomin
| Association and linkage studies of DAT1, DRD4 and other dopamine system genes in ADHD2
| Philip Asherson, Sarah Curran, Jon Mill and Eric Taylor
| QTL association analysis of the DRD4 exon 3 VNTR polymorphism in a population sample of children screened with a parent rating scale for ADHD symptoms
| Sarah Curran, Jon Mill, Pak Sham, Fruhling Rijsdijk, Katja Marusic, Eric Taylor and Philip Asherson
| Evidence of Association between DRD4 and ADHD with conduct disturbance
| Anita Thapar, Jane Holmes, Anthony Payton, Jenny Barrett, Richard Harrington, Peter McGuffin, Michael Owen, William Ollier, Michael Gill, Aiveen Kirley, Ziarih Hawi, Michael Fitzgerald, Philip Asherson, Sarah Curran, John Mill, Alison Gould, Eric Taylor, Lyndsey Kent, Nick Craddock and Jane Worthington
| Association of DRD4 and measures of executive functions relevant to ADHD
| Irwin D. Waldman, Yuki Hadeishi, David C. Rowe, Craig Stever, L. Nicole Giedinghagen, Jaime M. C. Gard, Jennifer H. Mohr, Stephanie Sherman and Ann Abramowitz Wednesday July 10th
| 1:30 - 3:00 PAPER SESSION VII
| Developmental Chair: Richard Rose 1:30 - 1:45
| A Longitudinal Study of Common Childhood Psychopathology (T)
| Marjolein J. H. Rietveld, Toos van Beijsterveldt, Jolande C. van der Valk, F. C. Verhulst and Dorret I. Boomsma 1:45 - 2:00
| Attention Problems and Emotionality at Ages 7 and 12
| Stephanie Schmitz 2:00 - 2:15
| Genetic and Environmental Influences on Pubertal Development in Males and Females
| Brian S. Mustanski, Richard J. Viken, Jaakko Kaprio, Lea Pulkkinen and Richard J. Rose 2:15 - 2:30
| Drosophila Kin Recognition
| Yong-Kyu Kim 2:30 - 2:45
| The nature of shared environmental influence on adolescent Behavioral deviance: Parent versus sibling effects
| Matt McGue and William G. Iacono 2:45 - 3:00
| Shared Environmental Effects on Behavior: Distinguishing Familial from Non-Familial Sources with Data from Twins and their Classmate Controls
| Richard J. Rose, Richard J. Viken, Danielle M. Dick, Lea Pulkkinen and Jaakko Kaprio 3:30 - 4:00
| TEA
| Wednesday July 11th
| 4:00 - 5:00 PAPER SESSION VIII
| Comorbidity Chair: Soo Hyun Rhee 4:00 - 4:15
| The etiology of comorbidity between substance dependence and conduct disorder in adolescents
| Soo Hyun Rhee, John K. Hewitt, Susan E. Young, Robin P. Corley, Thomas J. Crowley and Michael C. Stallings 4:15 - 4:30
| Covariation among childhood externalizing disorders: Identifying shared environmental contributions(T)
| S. Alexandra Burt, Robert F. Krueger, Matthew K. McGue and William G. Iacono 4:30 - 4:45
| The Relationship between Attention-Deficit/Hyperacitvity Disorder, Reading Disorder, and Communication Disorder Symptomatology (T)
| Erika Hagemann, David A. Hay and Catherine L. Taylor 4:45 - 5:00
| The association between depressive symptoms and common variance among metabolic risk factors for cardiovascular disease: results from the NHLBI twin study (T)
| Jeanne McCaffery, Raymond Niaura, John Todaro, Dorit Carmelli and Gary Swan Wednesday July 11th
| 4:00 - 6:00 VISIT to SANGER CENTER
| limited places only - please sign up at the registration desk Wednesday July 11th
| 5:00 - 6:00 EXECUTIVE COMMITTEE MEETING
| Wednesday July 11th
| 7:00 BANQUET
| PRESIDENTIAL ADDRESS: Substance dependence and antisocial behavior in adolescence: the Colorado studies John K. Hewitt THURSDAY JULY 12
| Thursday July 12th
| 10:00 - 12:00 VISIT to SANGER CENTER
| limited places only - please sign up at the registration desk | |||||
Maricela Alarcón1, Rita M. Cantor2, AGRE Consortium, and Daniel H. Geschwind1
Autism is a neuropsychiatric disorder with complex inheritance that affects about 1 in 1000 children and is characterized by deficits in language and social skills, and repetitive behaviors. Although
linkage analyses of the autism diagnosis have been performed, none have focused on the behavioral traits associated with this disorder. To investigate the language component of autism, a nonparametric genome scan
analysis was performed to identify quantitative trait loci (QTL) for this trait in a subset of families collected by the Autism Genetic Resource Exchange (AGRE). The AGRE families were recruited for the presence of at least
two children with autism spectrum disorders using the Autism Diagnostic Interview (ADI-R; C. Lord, M. Rutter, and A. Le Couteur, 1994, J. Aut. and Dev. Dis. 24, 659-685) which was administered to the
parents by pediatric neurologists to confirm the children's diagnoses and to clinically characterize them. Parents and offspring were genotyped for 335 markers and mutipoint linkage analyses were conducted using the
Genehunter (L. Kruglyak, M. J. Daly, M. P. Reeve-Daly, and E. S. Lander, 1996, Am. J. Hum. Genet. 58, 1347-1363) software. The strongest evidence of linkage to a measure of language development, the
ADI-R item'age at first word', was observed on chromosomal region 7q (Z = 2.98), about 25 cM away from the SPCH1 locus (S. E. Fisher, F. Vargha-Khadem, K. E. Watkins, A. P. Monaco, and M. E. Pembrey, 1998,
Nat. Genet. 18, 168-170) and only 3 cM away from previously reported results for the autism diagnosis (International Molecular Genetic Study of Autism Consortium, 1998, Hum. Mol. Genet.
7,571-578). These findings suggest that the putative susceptibility region on chromosome 7 may be a QTL for language traits associated with autism. V. Elving Anderson The recent convergence of three independent lines of research has made it possible to trace the pathways connecting a seizure disorder, a physiological mechanism and a therapeutic agent. (1) Benign
familial neonatal convulsions (BFNC) are characterized by autosomal dominant inheritance of seizures that have onset usually in the first week of life and that stop by the fourth month with some later exceptions. One gene
was mapped to chromosome 20 in 1989 and a second to chromosome 8 soon thereafter. Early in 1998 two research groups reported these to be potassium ion channel genes, KCNQ2 and KCNQ3. (2) Later
that year the two gene products were recognized as the major subunits of M-channels that are important in determining the excitability of neurons. When potassium leaves or chloride enters a cell, the cell interior becomes
more negative, and thus less excitable. Joint expression in Xenopus oocytes of both genes yields potassium currents 11-fold higher than with either gene alone. BFNC involves mutations in either KCNQ2 or KCNQ3 that
reduce the current amplitude without affecting other properties of the channels. (3) Retigabine is an anticonvulsant that recently was found to have a marked effect on KCNQ2/3 currents, causing the channels to open sooner
and slowing the rate of channel closing. When mutant KCNQ2 is expressed together with normal KCNQ3, retigabine stabilizes the cells. Thus retigabine may be the first anticonvulsant to target the cause of an epilepsy
syndrome by compensating the deficit of a specific channelopathy. Pharmaceutical researchers now are using KCNQ2/3 channels to identify other drugs that are selective channel openers. Conclusions: These findings show
how the identification of epilepsy susceptibility genes provides new approaches to basic neurophysiological studies and to drug development. They may have implications for other disorders that affect neuronal
excitability. Juko Ando1, and Yutaka Ono2 In traditional behavioral genetics studies, it is widely recognized that shared environmental effects are negligible in general psychological traits like personality, intelligence after adolescent and
psychopathology. However, it is reasonable to think that substantial shared environmental contribution would be found in cultural domains like reading, musical, athletic, artistic, and academic activities. In order to show
specific shared environmental cultural transmission, the following conditions should be met: 1) one's specific cultural activity (e.g. the amount of books one reads in a week) shows shared environmental contribution, 2) a
specific cultural environment related to this activity (e.g. how often one's parents recommend him/her to read books) shows shared environmental contribution, 3) this specific cultural activity (=1) is phenotypically
correlated with this specific cultural environment (=2), 4) this correlation is mediated by shared environment of (1) and (2). In the present study, for example, boys' involvement of reading books (=1) and their fathers'
preference of reading books (=2) showed shared environmental contributions (49% and 78%), and were significantly correlated (.17; p<.05). Multivariate analysis revealed that this correlation was mediated by shared
environment (.11) more than by nonshared environment (.05). Juko Ando1, Naoko Onoda2, Yoshimura Kimio3, and Yutaka Ono
2 TCI (Temperament and Character Inventory, Cloninger et al., 1993, Archives of Genetic Psychiatry 50, 975-990) contains 25 subscales with seven higher-order dimensions (four for
Temperament and three for Character). Univariate genetic analyses were conducted at subscale level with the Japanese twin sample (184 pairs of MZ and 112 pairs of DZ). CE models yielded the best fit in two subscales
(NS1 and NS4)out of four in Novelty Seeking (NS), one (RD4) out of three in Reward Dependence (RD), one (SD2) out of five in Self-Directedness, and two (CO2 and CO5) out of five in Cooperativeness. For all the
subscales in Harm Avoidance and Self-Transcendence, AE models were the best fit. An average contribution of additive genetic effects was .31 (range: .09-.43) whereas that of shared environment was .21 (range:
.16-.34). Philip Asherson1, Sarah Curran1, Jon Mill1, and Eric Taylor1 Molecular genetic studies in attention deficit hyperactivity disorder (ADHD) have focused on candidate genes within the dopamine system, which is thought to be the main site of action of stimulant
drugs. Of particular interest are findings with the dopamine transporter gene (DAT1), since stimulant drugs interact directly with the transporter protein. To date, there have been eight published association studies of ADHD
with a 480 base-pair allele of a variable number tandem repeat (VNTR) polymorphism in the 3'-untranslated region of the gene, five that support an association and three against. We have analysed the same VNTR marker in
a dataset of UK Caucasian children and an independent dataset of Turkish Caucasian children with DSMIV ADHD, using the transmission disequilibrium test (TDT). Results from the UK (x2=8.97, p=.0.01, OR=1.95), but
not the Turkish sample (x2=0.93, p=0.34) support association and linkage between genetic variation at the DAT1 locus and ADHD. When considered alongside evidence from other published reports, there is only modest
evidence for the association, consistent with a very small main effect for the 480-bp allele (x2=3.45, p=.06, OR=1.15), however we find significant evidence of heterogeneity between the combined dataset (x2 = 22.64, df=8,
p=.004). Another association of interest is between ADHD and the 7-repeat allele of a VNTR in exon 3 of DRD4. Using a case (n=132) vs. control (n=189) design we provide evidence for the putative association with
7-repeat allele (c2=6.17, 1 d.f., OR=1.73, 95% CI=1.11-2.71). A total of 85 complete trios were available for within family tests of association and linkage. TDT analysis in this subset did not confirm the association (29
transmitted versus 23 non-transmitted, c2 =0.69). We conclude that the case-control findings may be falsely positive, but can not rule out the alternative explanations of low power and gene-environment correlation. Data
from other dopamine system genes (DRD5, SNAP-25, DBH) will also be presented. Laura A. Baker1, Jennifer K. Johnson1, Dora I. Lozano1, and Adrian Raine1 Previous studies have found only moderate agreement between parent and child reports of children's behavior. We propose that this may be due to the global nature of the measures and inclusion of
behaviors for which the parents may have little knowledge. We have begun a large scale, longitudinal twin study to address just such issues. Several measures of aggression and delinquency have been included in order to
examine possible subtypes and to investigate parent-child agreement for behaviors more likely to be known to the parents. Preliminary analyses will address agreement between child self-report and parent report of
children's aggressive and delinquent behavior. Constructs measured include reactive and proactive aggression, relational aggression, physical and verbal aggression, conduct and oppositional defiant disorders, and
delinquency (which includes a wide range of rule-breaking behaviors). We will also examine the extent to which autonomic arousal (both cardiac and electrodermal) may show differential associations with various measures
of aggression. Sex differences among different subtypes of aggressive behavior will then be explored. We will investigate the existence of mean level sex differences in physical and relational aggression. Finally, twin
correlations will assess the degree to which different subtypes of aggressive and delinquent behavior are familial and will be used to estimate the relative influence of genetic and environmental factors on these
behaviors. Meike Bartels1, E.J.C. de Geus1, C. Kirschbaum2, M.J.H. Rietveld1, and D.I. Boomsma1 Individual variation in cortisol levels plays a prominent role as a possible explanatory variable in studies on childhood psychopathology. For instance, high and low basal cortisol levels have been
associated with externalizing and internalizing problem behavior, respectively, suggesting a disturbed functioning of the hypothalamic-pituitary adrenocortico (HPA)-axis in the pathogenesis of these behavioral disorders.
The aim of this study is to determine whether variation in cortisol and problem behavior share the same genetic source. Toward this end, basal cortisol levels (4 samples per day on two consecutive days) and common
childhood psychopathology (as assessed by the Child Behavior Checklist; CBCL) were assessed in a large sample of twelve-year-old children. The results show that heritabilities of daytime cortisol vary from weak right after
awakening (h2=. 32), to moderate (h2=. 43) during the afternoon to strong (h2=. 71) during the morning peak (within an hour after awakening). Further, we
observed a trend towards a negative association between cortisol and externalizing problem behavior. Whether problem behavior is a consequence of HPA-axis disregulation or a causing factor, or whether an underlying
genetic defect independently gives rise to both problem behavior as well as HPA-axis disregulation, remains to be investigated. Bivariate modeling of cortisol and problem behavior could resolve this issue of the etiology
causality.
Anukampa Barth1, Miguel Concha1, Claire Russell1, and Steve Wilson1 One of the research interests within our group is to understand the genetic pathways that lead to the establishment of differences between the left and the right sides of the brain. To achieve this, we are
using a variety of neuroanatomical, genetic and behavioural approaches. In terms of neuroanatomy, we have focused upon asymmetries within the dorsal diencephalon and have shown that the photoreceptive parapineal
nucleus is located on the left side of the brain and that axons from this nucleus project to the left habenular nucleus which is larger than the right nucleus. In collaboration with Becky Burdine and Alex Schier, we have
shown that the Nodal pathway regulates the laterality of these asymmetries. In collaboration with Jenny Watkins, Adam Miklosi and Richard Andrew, we are now trying to determine whether the laterality of
neuroanatomical asymmetries is correlated with lateralised behaviours in young zebrafish fry. To facilitate these studies, we are developing and characterising transgenic lines in collaboration with Miranda Gomperts,
Enrique Amaya and Darren Gilmour. The aim of the transgenic studies is to generate fish in which GFP is used to reveal neuroanatomical asymmetries in living fish that can subsequently be used in behavioural assays.
Finally, we are attempting to isolate novel mutations that disrupt CNS laterality. The best characterised of these lines is htr u28 in which affected fry show randomisation of situs. Affected fry also show reversal of some
lateralised behaviours. These observations suggest that an event that determines the laterality of all embryonic tissues (endoderm, mesoderm). M. Beekman The genetic basis of cardiovascular disease (CVD) is highly complex. One strategy to dissect this is to study less complex intermediate phenotypes instead of clinical endpoints. For CVD, such
intermediate phenotypes include blood pressure, plasma levels of cholesterol, apolipoproteins and triglycerides, of which more than 50% of the variation is attributable to genetic factors. The aim of our study is to map and
identify genes with a major effect on these intermediate phenotypes in the general population. We are performing a genome-wide scan in population-based samples of healthy Dutch, Swedish and Australian twin pairs. We
designed 80 multiplex PCR reactions randomly typing markers, with an average spacing of 18 cM, in sets of 3 to 5 chromosomes, thereby enabling statistical analyses of chromosomes during the search. Intermediate
phenotypes for CVD were determined in all the twin pairs. We calculated multipoint maximum-likelihood scores using GENEHUNTER 2.0 on the data of the first scanned chromosomes. Suggestive linkage was found with
total cholesterol with a maximum LOD score of 2.8 in the Dutch twin population (N=199 pairs). In the Swedish (N=53 pairs) and Australian (N=263 pairs) twin populations maximum LOD scores of respectively 1.6 and 1.0
were found in the same chromosomal region. These linkage results provide support for the presence of one locus contributing to variation of total cholesterol levels in three independent populations. It is explored how the
power and QTL localisation are influenced by simultaneously analysing the populations and by genotyping parents and additional markers. A. Leo Beem1, and Dorret I. Boomsma1 In variance components models for QTL linkage analysis, the IBD status of sib pairs can be modeled by a mixture (or weighted likelihood) approach or by using pi-hat, the estimated expected proportion
of alleles shared IBD. As QTL effects are often quite small and resources limited, marker data are mostly obtained for a selected sample of sib pairs, which are extreme concordant, discordant or both. Results from analyses
that do not take the selection into account will usually be invalid. Several methods have been proposed for the analysis of such data (P.C. Sham, J.H. Zhao, S.S. Cherny and J.K. Hewitt, 2000, Genet. Epidemiol.
19, S22-S28). The analyses may include only the subjects for which marker data are available or both subjects with and without marker data. If the mixture approach is used in the full sample, the weights for the
untyped subjects are the a priori probabilities for IBD zero, one and two. With the pi-hat approach, the a priori expected number of alleles shared IBD is substituted for the untyped subjects. The latter approach, which is
attractive because of its simplicity, has been shown in simulations to give seriously biased estimates of the QTL effect (C.V. Dolan, D.I. Boomsma and M.C. Neale, 1999, Am. J. Hum. Genet. 64, 268-280).
However, the reason for this bias remained unclear. Here the imputation of IBD probabilities will be approached as a measurement problem, in which true IBD status is estimated with various amounts of error. Obtaining
consistent estimators then requires corrections for attenuation (as it is called in psychometrics). It will be demonstrated that the pi-hat approach yields the wrong correction for attenuation. David A Blizard1, Rachel Cohen1, Laura Cousino-Klein1,2 and Gerald E. McClearn1,2 Organic deficits (e.g. food or water deprivation) or noxious stimuli (e.g. electric shock or escape from water) which are used to motivate maze learning in mice often have effects on performance which are
unequally distributed across genotype and age. Thus, group differences in error scores in a maze often cannot be unambiguously attributed to variation in cognition. In the present experiment we explored the ability of a
reward (return to home-cage; RHC), which does not involve manipulation of organic deficits or escape from stimuli which are clearly noxious (tissue-damaging), to motivate performance of mice in the Lashley III maze. A
2 X 2 independent groups experimental design was used to compare acquisition and retention of performance in the Lashley III maze under two reward conditions (RHC and food reward, FR) in two genetically
heterogeneous groups (HS and Swiss) of male mice. The striking and unexpected finding was that RHC (N=20, Mean +/-S.E.=11.2 +/- 0.91) was as powerful a motivator of acquisition (criterion: 3 consecutive trials with
one error or less per trial) as FR (N=19, 11.90 +/-0.84; RHC Vs FR, P<0.44). Furthermore, HS (9.55+/-0.57) reached criterion in fewer trials than Swiss (13.63+/-0.90;P<0.0001; no Reward X Motivational group
interaction). Retention of performance after 2 weeks was excellent for most mice and did not differ significantly between reward or genetic groups. A new motivational paradigm is therefore presented which has great
potential for the investigation of genetic and age-related differences in cognition. The fact that return to home-cage does not involve manipulation of organic deficits or use of noxious stimuli provides experimenters with an
animal-friendly protocol that largely avoids many of the obvious confounds (e.g. differential impact of food-deprivation, differential threshold to electric shock) which are inherent in the use of the most commonly used
motivators. Dorret Boomsma1, Toos van Beijsterveldt1,2, Caroline van Baal1, Therese Stroet1, Tinca Polderman1, Alexia
Groot1, Jolande van der Valk1,2, Frank Verhulst2, Tom Achenbach3, and Jim Hudziak3 We collected parental ratings of behaviOral and emotional problems with the Child Behavior Checklist (CBCL2-3) in a large sample of 3-year old Dutch twins (N = 6522 pairs). Mother's ratings of the
twins' behavior was used to obtain the empirically-based CBCL syndrome scales. In addition, the recently developed scoring algorithm to obtain DSM-oriented scales was applied to the data (Achenbach & Rescorla: Manual
for the ASEBA Preschool Forms & Profiles. Burlington, VT: Univ Vermont, Dept Psychiatry, 2000). The following DSM-oriented scales were constructed: affective and anxious problems, pervasive developmental problems
and oppositional and overactive behavior. Results show high heritabilities for these DSM-oriented scales. For overactive behavior, genetic dominance is suggested; for the other scales there are small contributions of shared
family environment.
Angela D. Bryan1, Kent E. Hutchison2, and Andrew Smolen3 There appears to be a reliable association between the DRD4 VNTR polymorphism and cue-elicited craving for tobacco and alcohol, and this effect seems specifically related to dopamine
neurotransmission. An incentive sensitization model posits that dopamine function is a critical factor in the appetitive characteristics of drugs of abuse in general, as well as naturally appetitive stimuli including sex
(Berridge & Robinson, 1998, Brain Res Brain Res Rev 28, 309-369). We conducted a pilot test assessing the generality of the effect of the DRD4 on appetitive motivation by examining its association with
desire for sexual activity. We posited that the DRD4 might express its relationship to sexual desire indirectly, through personality characteristics associated with sensation/novelty-seeking. College students (N=104, 62%
male) completed measures of sensation/novelty-seeking and sexual desire. Participants who were homozygous or heterozygous for the 7 repeat (or longer) allele were classified as DRD4 L and all other participants were
classified as DRD4 S. A structural equation modeling analysis of the indirect effect of the DRD4 on sexual desire in EQS 5.7b indicated that the DRD4 was reliably associated with a latent sensation-seeking personality
factor, and the personality factor was reliably associated with a latent measure of sexual desire. Model fit was adequate, [chi]2 (8) = 6.284, ns , CFI=1.0, RMSEA=.00 and the adaptation of the Sobel test (Sobel,
1982, in S. Leinhardt, ed., Sociological Methodology 1982, Jossey-Bass, San Francisco, CA, USA) suggested that the indirect effect of the DRD4 on sexual desire was marginally significant, p = .10. The
results did not differ when gender was included in the model. These findings are suggestive of a more general association of the DRD4 with appetitive motivation not only for drugs of abuse but for naturally occurring
appetitive stimuli. S. Alexandra Burt1, Robert F. Krueger1, Matthew K. McGue1, and William G. Iacono1 The current study aims to expand on a previous study by Burt, Krueger, McGue, & Iacono (submitted for publication), in which we fit a biometrical model to the combined parent-child symptom counts of
three common childhood disorders, specifically Attention Deficit-Hyperactivity Disorder (ADHD), Oppositional Defiant Disorder (ODD), and Conduct Disorder (CD). The results revealed that while genetic factors
appeared to comprise a substantial amount of the variance within each disorder, the covariance among ADHD, ODD, and CD appeared to stem primarily from a single common environmental factor. Moreover, the shared
environmental correlation was 1.0 between each pair of disorders, indicating that the same shared environmental factor influenced the presence of each of these disorders. This study hopes to directly measure this specific,
shared environmental factor via measures of family functioning. Specifically, we examined the FACES-III (Olson, Portner, & Lavee, 1985, Family Adaptability and Cohesion Scale-3rd Edition (FACES-III). St.
Paul: University of Minnesota), a measure of the family's perceptions of overall family functioning, and the Parental Environment Questionnaire (PEQ), a scale developed for use within the Minnesota Twin Family Study
(MTFS) in which both parents and adolescents report on their parent-child relationships. The sample consists of 11 year-old male and female twins assessed as part of the ongoing MTFS (ndz=430 and
nmz=844). Preliminary analyses suggest that certain aspects of the family environment, (i.e. Cohesion, as indexed by the FACES-III questionnaire, and Conflict and Regard, as indexed by the PEQ) may be
contributing to the shared environmental factor that is common to ADHD, CD, and ODD. Andrew Canastar1, and Stephen C. Maxson1 There are effects of the male specific part on the Y chromosome on variation in aggressive and mating behaviors of mice (S. C. Maxson, 1996, Behav. Genet 26, 471-476). There are also
sex differences in these behaviors. It has been suggested that these sex differences may be in part due to the presence of this part of the Y in males and not in females (S.C. Maxson, 1997, Biomed. Rev. 7,
85-90). To test this hypothesis, these behaviors were assessed in XX females and XY females of the C57BL/6JEiYPOS strain and XY males of the C57BL/6J strain. The XY males and females are congenic. The Y of the
C57BL/6JEiYPOS strain derives from Mus poschiavinus, and the Y of the XY males derives from Mus musculus. The poschiavinus Y in the C57BL/6 background results in mice with either ovaries or ovatestes. Only
those with ovaries were tested. These XY females appear to be endocrinologically similar to XX females (A. J. Stavnezer, C. S. McDowell, L. A. Hyde, H. A. Bimonte, S. A. Balogh, B. J. Hoplight, V. H. Denenberg, 2000,
Behav. Brain Res. 112, 135-143). Mice were tested four times for aggression against a genotype-matched opponent in an instigation paradigm (E. W. Fish. S. Faccidomo, K. A. Miczek, 1999,
Psychophar. 146, 391-399). The XY males were more aggressive than the XY and XX females; there was no difference between the XX and XY females for aggression. Mice were then tested twice for
mating behaviors against a C57LBL6JEi female in hormonally induced estrus. The XY males differed from both the XX and XY females in male copulatory behaviors; there was no difference between the XX and XY
females for these behaviors. We suggest that although the male specific part of the Y is involved in variation among males for these behaviors, it has no effect on the sex differences in them other than in the differentiation of
the primordial gonad into a testis. Ian L. Cesa1, Michael King1, Mo Zheng2, Tina Lee2, Jennifer K. Johnson2, and Laura A. Baker2 This poster demonstrates the application of a powerful software package for designing and administering surveys used in the collection of data. The Triton Survey Designer is a highly flexible HTML
based program that allows construction and computerized administration of surveys of varying degrees of complexity. The program interfaces with several statistical packages, including SPSS, SAS, and SPLUS,
automatically providing syntax and data files for each survey. This system combines administration with data entry, therefore minimizing errors and yielding data files of improved integrity. Surveys can be easily
administered by trained interviewers or respondents themselves, and can be implemented on desktops, laptops, or handheld computing devices. Thus, data collection can be done in a laboratory or in the field, or via the
internet. A Triton demonstration is provided, based on interviews from the Twin Study of Social and Moral Development at USC. Caroline Chabert1,3, Ameziane Cherfouh1, Vincent Duquenne
1, and Pierre L. Roubertoux1,2 Down syndrome is characterized by several disorders (central nervous system, immune functions, heart). It is the main source of mental retardation (one out of 700 births). This syndrome is due to an extra
copy of chromosome 21. Partial 21 trisomies have shown that patients carrying an extra chromosomal fragment of the 21q22.2-21q22.3 region was associated with most of the signs that define the syndrome (J. M. Delabar,
D. Theophile, ..., and P. M. Sinet, 1993, European Journal of Human Genetics 1, 114-124). This region has been thus labeled DCR-1 (Down Chromosomal Region-1). Syntenies between chromosome 16 in
mice and chromosome 21 in humans are very well documented. Ed Rubin's group has taken advantages of theses syntenies to develop transgenic mice for four chromosomal fragments covering DCR-1 (D. J. Smith, Y. Zhu,
and E. M. Rubin, 1997, Nature Genetics 16, 28-36). These fragments of chromosome 21 were inserted into yeast artificial chromosomes, then incorporated into mice genome. Theses incorporations have
created partial trisomy for the integrated chromosomal segment. Only the region encompassing the markers 21ES0203-21ES0291 appeared to be involved in cognitive impairments observed in these transgenic mice.
Processes implicated in behavioral plasticity are particularly impaired. This region is, moreover, implicated in hind limb motor incoordinations. Neuroanatomical examinations of partial trisomic mice did not show
hippocampal alterations or modifications that could be directly linked with cognitive disorders that we reported in these mice. Observations in progress could suggest that motor and cognitive disorders may have a common
cerebellar origin. Stacey S. Cherny1, Lon R. Cardon1, and Gonzalo R. Abecasis1 The lack of success in mapping complex traits is a result of many factors. One potential cause is the presence of (random) errors in genotypes, which has been shown to reduce power for linkage, in some
cases, quite dramatically. The robustness of a study to the effects of error depends on the sample ascertainment strategy and the method of analysis. For linkage studies, imposing random genotypes on one per cent of the
assays in an unselected sample results in only a modest reduction in power, while in an affected pairs study this same error rate, which is one that would be considered low by most labs, can have the effect of transforming an
otherwise adequately powered study into one which has virtually no power to detect linkage to a disease locus. Given that, it is imperative that we do our best to detect errors in our data and correct them. We discuss the
effects of genotype errors on studies of linkage and association and explore the efficacy of methods for detection of errors in recovering the power lost as a result of errors, for a variety of study designs. R. P. Corley1, M. C. Stallings1, J. K. Hewitt1, and S. E. Young1 Heath and colleagues (A.C. Heath, J. Meyer, L. J. Eaves, and N.G. Martin, 1991, J. Stud. Alc. 52, 345-352) have suggested that abstinence from consumption is qualitatively distinct from
quantity and frequency dimensions of alcohol use in adults. In adolescent substance use, it is harder to distinguish between abstinence and still-pending initiation because assessments are made during the transitional age of
risk. This may result in substantial overlap between liability dimensions for experimentation, regular use, and dependence. Data on adolescent substance use has been collected from a Colorado twin sample and participants
in the Colorado Adoption Project using interview and questionnaire instruments. For a measure of substance dependence that includes alcohol, tobacco, marijuana, and other drugs, adjusted for the number of substances
tried, and corrected for age within gender, the correlation for 297 MZ twin pairs was 0.64, for 268 DZ twin pairs was 0.39, for 140 non-adopted sibling pairs was 0.35, and for 131 adopted sibling pairs was 0.21. We used
the multiple threshold approach for ordinal data implemented in Mx to examine whether the dependence dimension could be distinguished from dimensions of use and experimentation. Rebecca J. Cross1, Javier Gayan1, John C. DeFries1, and Richard K. Olson1 There is strong evidence from Behavioral genetic studies for a significant genetic etiology in reading disability at the group level (J.C. DeFries and M. Alarcon, 1996, Mental Retardation and
Developmental Disabilities Research Reviews 2, 39-47). However, genetic influence may vary in kind and amount for different individuals. In the present analyses, we show that genetic influences on reading
deficits are relatively low in disabled readers who are slow in three processing speed measures: matching of target pictures to one of 5 choices (Identical Pictures), rapid naming of letters and numbers presented in rows
across a page (Rapid Naming), and speed in matching strings of 4 unrelated letters and numbers to the identical string among 3 foils (Colorado Perceptual Speed). 242 MZ and 171 DZ twin pairs age 8-18 years were
ascertained to have at least one member with a school history for reading disability. Probands' reading scores (a composite measure of reading recognition, reading comprehension, and spelling subtests of the Peabody
Individual Achievement Test) were at least 1.5 SD below the mean of a normal-twin comparison group. The interaction between the genetic etiology of reading deficits (h2g) and probands'
processing speed was tested with an extension of the DeFries and Fulker (J.C. DeFries and D.W. Fulker, 1985, Behav. Genet. 15, 467-473) basic model for assessing the group heritability of extreme scores
(h2g). Interactions between speed scores and h2g for reading disability were tested with groups above and below the proband medians for speed, and with individual
scores on the continuous processing-speed dimensions. The interactions were significant with the high and low speed groups for all but the Rapid Naming measure. For the composite speed measure,
h2g = .31 for the slow speed group, and .86 for the high speed group (interaction p = .001). When continuous speed dimensions were employed, interactions were significant (p < .05) between
h2g for reading disability and the speed dimension for all three speed measures and their composite score. Tim Crow1, Nic A Williams1, Maria Giouzeli11, Norman Ross1, Patricia Blanco2,Carole A
Sargent2, and Nabeel A Affara2. Asymmetry is the characteristic that distinguishes the brain of Homo sapiens, as a possible correlate of language, from that of the chimpanzee. Degrees of asymmetry are a determinant of cognitive ability
including the acquisition of words. On the basis of observations of the deficits associated with sex chromosome aneuploidies there is a substantial case that the relevant gene is in the class that is present in homologous form
on the X and Y chromosomes. Such a location is consistent with the sex differences for handedness and verbal ability that may be correlates of faster brain growth in females. The Xq21.3/Yp11.2 region of homology was
generated by a translocation that occurred after the separation of the chimpanzee and hominid lineages and was subject to a subsequent paracentric inversion. Within this region a gene (protocadherinXY) has been located
that belongs to a class of cell adhesion molecules that are expressed in brain and may be expected to influence axonal growth towards its target tissue. The gene sequence on the Y differs from that on the X in part as a result
of chromosomal events that occurred after the translocation. Such differences could account for sex differences in cerebral asymmetry and the development of verbal ability. ProtocadherinXY is thus a candidate for the the
characteristic of cerebral asymmetry that defines the species and allowed language to evolve. Sarah Curran1 , Jon Mill1, Pak Sham1, Fruhling Rijsdijk1, Katja Marusic1, Eric Taylor1and2, Philip
Asherson1 Current developments in molecular genetics has led to a rapid increase in research aimed at the identification of genetic variation that influences complex human phenotypes. One such phenotype that has
aroused a great deal of interest is the behavioural trait hyperactivity and the related clinical disorder attention deficit hyperactivity disorder (ADHD). The driving force behind the molecular genetic research in this area is the
overwhelming evidence from quantitative genetic studies, that show high heritablility (h2 = 0.7- 0.9) for the behaviours characterising the diagnosis of ADHD whether the disorder is viewed as the extreme of a normally
distributed trait (i.e. categorical entity) or a continuous trait. To date, molecular studies have aimed at identifying susceptibility genes for ADHD, defined using operational diagnostic criteria, and have focused on variation
within genes that regulate dopamine neurotransmission. Several studies have reported ADHD to be associated with the 7 repeat of a 48 base pair variable number tandem repeat polymorphism (VNTR) in exon 3 of the
dopamine receptor 4 gene (DRD4). In this study, we take a dimensional perspective of ADHD and examine the relationship of the DRD4.7 polymorphism, in a sample of children selected from the general population on the
basis of high and low scores on the 5 ADHD items of the strengths and difficulties questionnaire (SDQ) as rated by their parents. We found a significant relationship between DRD4-7 and high scoring individuals (Chi-
Squares test = 8.63, p = 0.003; Odds ratio = 2.09 (95% C.I. 1.24< OR < 3.54), F statistic of 7.245, p =. 008). Chayna J. Davis1, Javier Gayan1, Valerie S. Knopik2, Shelley D. Smith3, Lon R. Cardon4, Bruce F. Pennington5,
Richard
K. Olson1, and John C. DeFries1 Children with reading deficits perform more slowly than normally-achieving readers on speed of processing measures, such as rapid automatized naming (RAN). While RAN is a well-estabilished
correlate of reading performance, and the heritable nature of both reading difficulties and RAN have been supported by previous research, few studies have attempted to assess the etiology of their covariation (C. J. Davis et
al., Annals of Dyslexia, submitted). Measures of RAN (numbers, colors, pictures, and letters subtests), phonological decoding, orthographic choice, and a composite variable (discrm) derived from the reading
recognition, reading comprehension, and spelling subtests of the Peabody Individual Achievement Test were obtained from a total of 550 twin pairs with a positive school history of reading problems. Basic DeFries and
Fulker (DF) multiple regression models for the analysis of selected twin data (J. C. DeFries and D. W. Fulker, 1985, Behav. Genet. 15, 467-473) confirmed the heritable nature of phonological decoding
(h2g = .68), orthographic choice (h2g = .67), and discrm (h2g = .57). Bivariate DF models were employed to examine
the extent to which deficits in these three reading measures covary genetically with RAN. Significant bivariate heritability estimates for each of the reading measures with RAN composites (numbers and letters; colors and
pictures; and total) were also obtained. Subsequently, univariate sib-pair linkage analyses confirmed the presence of a QTL on chromosome 6p21.3 for phonological decoding, orthographic choice, and discrm deficits.
Bivariate linkage analyses were then conducted to test the hypothesis that this QTL for reading difficulties is also a susceptibility locus for slower performance on RAN tasks. Although the results obtained from these
analyses do not provide evidence that the QTL for reading difficulties found on chromosome 6p21.3 has significant pleiotropic effects on RAN, larger samples will be necessary for adequate power to conclude that the
genetic correlation between reading deficits and RAN is not due in part to the 6p QTL for reading. Rens de Groot1, Nico Lakenberg2, Eline Slagboom2, and Dorret Boomsma1 Anxiety-related behaviour in mice called "emotionality" has been studied extensively. We reviewed mouse QTL and knock-out studies for emotionality and combined the results with the latest knowledge
of mouse and human homology (www.informatics.jax.org). Results of 24 mouse studies were ordered and used for creating maps in which the locations of QTL's and knock-out genes are shown both at mouse and human
chromosomes. The combination of these two sources gives an good overview of candidate regions for emotionality in humans based on mouse studies. Mouse chromosomes 1, 10, 12, and 15 show regions with replication
and are therefore candidates for further investigation. We present an overview of the literature and four mouse-human homolgy maps of the most promising regions. Danielle M. Dick1, Richard J. Viken1, Jaakko Kaprio2, and Richard J. Rose1 Adolescence is characterized by dramatic changes in alcohol use. At age 16, the average adolescent reports drinking about once every two months; by age 18, drinking frequency has increased to a couple
of times per month. We employed latent growth curve analyses to study drinking trajectories across this age range in a population-based sample of Finnish twins, Finntwin16. With genetically informative data,
latent growth curve analyses permit one to investigate the extent to which variations in (1) the intercept, or mean level of drinking, and (2) the slope, representing change in the trait over time, are due to genetic and
environmental influences. We applied these models to data from >1200 same-sex twin pairs from Finntwin16who were concordantly drinking at age 16. The slope for both males and females was positive,
indicating that individuals with higher levels of drinking at 16 also had a steeper increase in drinking across time. In both males and females, genetic factors largely accounted for variation in mean levels of drinking, with
no evidence of common environmental effects. However, in females, environmental factors were primarily responsible for changes in drinking trajectories, while genetic factors were more influential in males' changes across
time. These findings support developmental theories proposing that girls are more sensitive to environmental pressures than are boys. Extensions of these analyses, such as the inclusion of other traits and environmental
factors, will be discussed. Brian M. D'Onofrio1, Eric Turkheimer1, Linda A. Corey2, Robert E. Emery1, Mary Waldron1, and Lindon J.
Eaves2 Most studies examining the relationship between parents and children rely only on correlational data, but simple epidemiological correlations may represent a multitude of different underlying pathways.
The Children of Twins (COT) design helps distinguish between the possible intergenerational pathways by delineating the associations into those due to common genetic factors, common shared environmental factors, and
common nonshared environmental factors. Common intergenerational genetic factors, an example of passive gene-environment correlation, and common shared environmental factors are non-causal pathways. Only the
common nonshared environmental pathway, which includes the measured parental variable, suggests a causal relationship between the two variables. Therefore, the COT design provides a powerful study of parental
influences on children by controlling for genetic and shared environmental effects which hinder correlational studies of parents and children. The current study utilizes the COT design to investigate the relationship between
parental smoking and child birth weight in samples of same-sex twins from Norway and the United States. Multiple children from each family are included in order to increase the power of estimating the intergeneration
coefficients and to test for familial influences that effect birth weight but not parental smoking. Limitations of the COT design and future directions will also be discussed. Anne-Lise Doyen1, Thierry Dufour2, Laetitia Prut1, and Michele Carlier1 We undertook a study to determine chromosomal regions involved in degree of laterality in Human. We recruited 94 informative families on the following criteria: they included at least two self-professed
left-handers or ambidextrous either in two generations or in the same generation (having a genetic proximity of 50 %). Laterality was assessed with four tools: a reaching card task, a pegmoving task, the Purdue Pegboard
and a manual preference questionnaire (for metric qualities see A.-L. Doyen and M. Carlier, In press in Laterality). Families were then proposed to participate to the genetic study, giving blood samples or buccal
cells: 52 among 94 agreed to follow the molecular study. Familial resemblance was estimated in the whole sample by intraclass correlation coefficients and regression analyses: quantitative genetics showed a large
father/child resemblance for the degree of laterality. This may indicate an implication of the homologous region of X and Y chromosomes in laterality (S. H. Laval, J. C. Dann, ..., and T. J. Crow, 1998, Am. J. Med.
Genet. 81, 420-427). Four STSs (DXS8030, DXS1217, DXS1203 and DXS8034) were used to mark out this region. A link between the degree of laterality and DXS1203 marker was found (p< .05) and will be
confirmed with a larger sample. In the same time we focused on another chromosomal region, synthenic between murine and human genomes, following previous results obtained in mice in the lab. Thalia, C. Eley1, and Paul Lichtenstein2 Recent theories on the development of antisocial behaviour (ASB) in children and adolescents suggest greater genetic influence on aggressive ("life-course persistent") as compared to non-aggressive
("adolescent limited") ASB (e.g. T. E. Moffitt, 1993, Psych. Rev. 100, 674-701). Recent twin studies including previous analyses from this study confirmed higher heritability for aggressive as compared to
non-aggressive ASB symptoms, especially in girls (T. C. Eley, P. Lichtenstein, and, J. Stevenson, 1999, Child Dev. 70, 155-681). Data are now available from a second time point which replicate and extend
these results. The Child Behavior Checklist was completed by the parents of over 1000 Swedish twin pairs aged 7-9 years and again at age 13-14 years. Aggressive ASB showed greater continuity from time 1 to time 2 as
compared to non-aggressive ASB. Genetic factors had a greater influence on aggressive ASB than non-aggressive ASB at both time points. Shared environment influences were significant for non-aggressive ASB. There
were also significant sex differences in the etiology of non-aggressive antisocial behavior at both time points. Continuity in aggressive antisocial behavior symptoms from time 1 to time 2 was largely mediated by genetic
influences at both time points, whereas continuity in non-aggressive antisocial behavior was mediated by the shared environment for boys, and largely by genetic influences in girls. These data provide further support for the
hypothesis that aggressive ASB is a stable heritable trait as compared to non-aggressive behavior which is more strongly influenced by the environment and shows less stability over time. Tom A Fowler1, Anita Thapar1, and Ann Farmer2 Disabling Fatigue in children is a cause of serious concern, with epidemiological research showing that up to 15% of referrals to paediatric infectious disease centres (B.D. Carter & G.S. Marshall, 1995,
Current Problems in Pediatrics 25, 281-93) and 42% of all medically certified long-term sickness absence from school (E.G. Dowsett & J. Colby, 1997, Journal of Chronic Fatigue Syndrome
3, 29-41) is due to fatigue. Previous work (A. Farmer, J Scourfield, N. Martin, A. Cardno & P. McGuffin, 1999, Psychol. Med. 29, 279-282) provides evidence that disabling fatigue is familial, but
could not significantly differentiate between an AE model a CE model. A questionnaire on fatigue was sent to the main carer's of twins, aged 8-17 years, in 2 population based twin registries. Data were collected for 557
monozygotic (MZ) and 789 dizygotic (DZ) pairs. The results concurred with previous research in that disabling fatigue in childhood of more than a few days is highly familial. Using model fitting an AE model provided the
most acceptable explanation of the variation in the twin population. For fatigue lasting over a month, a CE model was the most acceptable model, however the role of additive genetics could not be conclusively rejected.
Member Masaki Fujimoto The purpose of the present study is to examine the mechanism of Attachment in genetic and environmental influences using Japanese twin sample. We apply Behavioral genetic analyses to the
corresponding covariance data examining genetic and environmental influences on Adult Attachment in Japanese twin. The development of Attachment, as the relationship between self and others, influences on shaping
personality. Bartholomew and Holowitz (1991) have generated a four-group taxonomy based on a 2 classification of self positive or negative) and others ( positive or negative). Many Behavioral genetic studies have done to
examine the genetic and environmental influences on self and other cognition. We elucidate the mechanism of Adult Attachment in genetic and environmental influences using Japanese twin sample. Amber L. Gahagan1, and Irwin D. Waldman1 Behavior genetic studies have consistently revealed genetic influences on childhood temperament. Because of difficulties in obtaining self-reports from young children, these studies have relied primarily
on parental reports. Parental reports may lead to biases in the results of these studies, however. For example, contrast effects have been implicated in parent ratings of temperament. Using the most widely used measure of
childhood temperament, Buss and Plomin's Emotionality, Activity, and Sociability (EAS) scale, we collected data on 844 twin pairs (54% DZ, 46% MZ) born in Georgia. Our sample is 49% male and 51% female, and 82%
of the twin pairs are Caucasian, 11% African American, 1% Hispanic and 6% of mixed ethnicity. The twins were on average 10.6 (range 4.5-17.85) years old when twins were rated by their parents on the 20-item EAS
questionnaire. We first performed univariate behavior genetic analyses of the four temperament dimensions (Emotionality, Activity, Sociability, and Shyness) to examine the pattern and magnitude of genetic and
environmental influences, taking into account potential contrast effects. We then conducted multivariate behavior genetic analyses of the temperament dimensions to examine whether the EAS scales share common genetic
and environmental underpinnings. Significant positive phenotypic correlations between the Emotionality and Shyness scales and the Activity and Sociability scales suggest common genetic or environmental influences may
account for these relations. It has been suggested that temperament dimensions may be differentially predictive of later outcomes, thus understanding more explicitly the influences on each dimension and the relations
among the dimensions may have implications for understanding the specific relations between temperament dimensions and later outcomes. Michael J. Galsworthy1, Jose L. Paya-Cano1, Lin Liu1, Santiago Monleon2 and Robert Plomin1 One of the best-documented facts about human cognitive abilities is that diverse abilities intercorrelate, indicating that many learning and memory processes are general (molar) rather than specific
(modular). What such diverse tests have in common is termed general cognitive ability (g). In the human species g accounts for about 40% of the variance across diverse cognitive processes from IQ tests to working memory
tasks and cognitive reaction time measures. Quantitative genetic research has shown that g is substantially heritable, and QTLs associated with general and specific cognitive function are already being nominated. Recent
work by ourselves and collaborators indicates the presence of a general cognitive ability in mouse as well as man, which opens the opportunity for a functional genomics model of g. We have developed an efficient battery of
measures that will make it possible to assess g in large samples of mice needed for genetic analysis while controlling for variables such as motor activity and emotionality. We are using heterogeneous stock (HS) mice,
outbred for over 60 generations from eight inbred strains, in order to capture greater genetic variability and to provide finer resolution for QTL mapping than possible with the use of inbred strains. In our first studies of 40
HS mice, we found our cognitive tasks intercorrelated on average 0.2 and all loaded positively on a first factor that accounted for over 30% of the variance, indicating the presence of g. Our ongoing work aims to greatly
increase the sample size in order to confirm these preliminary results and to begin QTL analyses of 'g' in mice. Our QTL analyses will focus on polymorphisms in candidate genes nominated by human QTL and mouse
knockout literature. Jody M. Ganiban 1 This study explored the experiential determinants of parenting. We hypothesized that non-shared environmental contributions to mothers' warmth and negativity towards their adolescent children are
explained by the women's marital relationships, and by their children's characteristics. Participants included 326 pairs of adult female Swedish twins (MZ=150; DZ=176), their partners and one adolescent child.
Questionnaires were mailed to female participants prior to a home visit. During the home visit, mothers were observed during separate 10-minute interactions with their children, and with their husbands. Trained observers
rated marital warmth, marital conflict, maternal warmth, and maternal negativity during the problem solving interactions. Children's characteristics were rated by their mothers and fathers. Preliminary analyses suggest that
the emotional quality of the women's marital relationships and their children's characteristics partially explain non-shared environmental contributions to maternal warmth and negativity. Nathan A. Gillespie1, and Nicholas G. Martin1 We investigated the relative stability and magnitude of genetic and environmental effects underlying major dimensions of personality across time. As part of an ongoing study of nevus risk factors and
cognitive development, the Junior Eysenck Personality Questionnaire was administered to around 600 twin pairs at ages 12, 14 and 16. Data was analyzed using genetic simplex modeling which explicitly takes into account
the nature of longitudinal data. Results and limitations of the methodology are discussed.
Anne L. Glowinski1, and Andrew C. Heath1 As noted in a comprehensive review of research findings by J. Johnson and M. Leff (1999, Am. Acad. Pediat. 103, 1085-1099. Supplement to Pediatrics, Part 2 of 2, May 1999) the
documentation of poor outcomes and increased risk for psychopathology in Children of alcoholics (COAs) has been done by many, yet studies allowing the examination of both genetic and environmental effects on these
outcomes were scant till recently. Data from 3418 Missouri female adolescent twins with a mean age of 15.5 at assessment (947 MZ and 692 DZ pairs) and at least one of their parents were analyzed to examine the
relationship between parental alcoholism (alcohol dependence or AD) and offspring suicidal behavior (defined as persistent suicidal ideation or a suicide attempt). These subjects were interviewed with a telephone version
of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) (which includes a separate section for the assessment of lifetime suicidal behavior) for the Missouri Female Adolescent Twin Study (MOAFTS), a
population-based prospective twin-family study of alcohol use and problems and psychiatric comorbidity in young females. With logistic regression analyses, major predictors of suicidal behavior included Major Depressive
Disorder (MDD), a history of childhood abuse, AD and parental AD ( with 46.1% of the subjects reporting a suicide attempt having at least one alcohol dependent parent). When twin pairs were stratified by parental history
of alcoholism, we found significantly elevated heritability of suicidal behavior: 54% (95%CI: 42.6-62.9) compared to families with no parental alcoholism: 27.1% heritability (95%CI: 15.6-36.2). These results imply
important genotype x environment interaction effects with the underlying genetic vulnerability particularly likely to lead to suicidal behavior, in the adverse environments (which include an increased risk of childhood abuse
and other traumatic events) more commonly found in association with parental alcoholism.
Erika Hagemann1, David A. Hay1, and Catherine L. Taylor1 Although Attention-Deficit/Hyperactivity Disorder (AD/HD) is recognised as the most common childhood onset behavioural disorder affecting up to 10% of children and adolescents (M.L. Wolraich, J.N.
Hannah, T.Y. Pinnock, A. Baumgaertel, and J. Brown, 1996, J. Am. Acad. Child Adolesc. Psychiatry 35, 319-324), many issues are yet to be clarified in regards to symptomatology, gender, age and
co-development with other disorders. This twin study explored the relationship of Reading Disorder and Communication Disorder symptomatology to the DSM-IV subtypes of AD/HD. Participants for this study were
recruited from the Western Australian (WA) Twin Register, a population-based register of families with multiple birth children born in WA between 1980 and 1992. Following exclusion of known significant physical,
sensory, or intellectual handicap, or birth defects in one or more of the twins, a sample of 449 families with twins born between 1981 and 1984, and 1988 and 1989, were approached for this study. At least one full sibling,
closest in age to the twin pair, and one of the twin pairs' biological parents were also ascertained and included in the study. Self report and parent report questionnaire data of symptomatology of AD/HD, Reading Disorder,
and Communication Disorder were obtained. For validation, a sub-sample of families who participated in this questionnaire survey received individual follow-up assessment. Taking both twin-singleton and age effects into
account, a series of bivariate and multivariate genetic and environmental structural equation models investigated underlying mechanisms for the co-occurrence and co-development of AD/HD, Reading, and Communication
Disorder symptomatology. Of particular interest in the models was whether the dimensions or subtypes of DSM-IV AD/HD actually represented discrete subtypes with specific causes and comorbidity patterns. As the
symptomatology of the disorders investigated are more frequent in twins than singletons and differ between genders, significant issues arise in determining models most appropriate for the general population.
Noa Heiman1, Michael C. Stallings1, John K. Hewitt1, and S.M. Hofer2 Although there is considerable literature examining the development of personality constructs from childhood to adulthood, there is a paucity of research investigating age-related personality changes in
later adulthood. In this study we examined cross-sectional age differences in means, phenotypic covariance structure, and the underlying genetic and environmental structure of four personality constructs from Cloninger's
personality system (C.R. Cloninger, 1986, Psych. Dev. 3, 167-226): Novelty Seeking (NS), Harm Avoidance (HA), Reward Dependence (RD), and Persistence (PS). Study participants were 2770 same-sex
female twins between the ages of 50 and 96 (626 MZ twin pairs plus 480 singletons; 307 DZ twin pairs plus 424 singletons), drawn from the American Association of Retired Persons (AARP) twin sample. Personality
assessments were obtained through mail-out questionnaire surveys. Age differences were examined by comparing younger (age 50-66) and older (age 67+) cohorts (based on a median split of the sample), as well as
estimating model parameters as linear and quadratic functions of continuous age. Results of cohort comparisons indicated modest, but significant (approximately 15-20% of a SD), declines in mean levels for NS, RD and
PS. No significant mean difference was found for HA. Phenotypic variances were equivalent across age cohorts for all of the personality dimensions except NS, which showed a 15% decline in the older cohort. The relative
proportions of phenotypic variance accounted for by genetic and environmental influences were also equivalent across the two age cohorts for HA, RD and PS. Only NS showed significantly higher heritability in the older
cohort, while shared environment made a greater contribution in the younger cohort. Analyses using age as a continuous moderator variable confirmed the cohort comparison findings. In sum, with the exception of NS, the
genetic and environmental architecture of Cloninger's personality dimensions showed minimal age differences across this age range. Norman D. Henderson1 Since the 1930's, animal researchers have been factor analyzing phenotypic correlation matrices of Behavioral measures assessed in multiple test events either test batteries or repeated tests in the same
apparatus. It has been a steady but only marginally successful enterprise. Results using multiple measures from each of two or more test situations frequently produce "instrument factors" that account for most of the factor
variance. Similarly, factor analyses of multiple measures obtained repeatedly from the same apparatus often suggest that the test apparatus is measuring different constructs in the repeated sessions. Covariance among
Behavioral measures taken during a test event can be ascribed to genetic influences, pre-test environmental (i.e., rearing and treatment) history and unique test environment factors. Covariance created by genetic and pre-test
environment can exist across different test events, whereas unique test environment covariance cannot. Using environmental correlations among 90 measures obtained within genetically homogenous mouse strains, we found
that unique test environment covariance can often be the dominant contributor to phenotypic covariance among measures taken simultaneously, whereas this contribution is necessarily zero across different test events. As a
result, factor analyses of phenotypic correlation matrices can be highly misleading in situations where genetic variation and/or the effects of pre-test environmental treatments are not substantial on the behaviors
examined. John M. Hettema1, Peter Annas2, Michael C. Neale1, Mats Fredrikson3, and Kenneth S. Kendler1 Phobias represent one of the most common psychiatric disorders, and the relationship between fears and phobias has long been a subject of psychiatric study. Fear conditioning via aversive learning is one
well-established model for the acquisition of fears and phobias. Also, Behavioral treatment paradigms are based on the related processes of habituation and extinction, yet little is known regarding their underlying genetic
structure. A unique sample of classical fear conditioning data has been obtained from 90 monozygotic and 83 dizygotic same-sex twin pairs. Sequences of evolutionary fear-relevant (snakes and spiders) and fear-irrelevant
(circles and triangles) pictorial stimuli served as conditioned stimuli paired with a mild electric shock serving as the unconditioned stimulus. The outcome measure is the electrodermal skin conductance response. We used
univariate and multivariate structural equation modeling of the three conditioned phases of habituation, acquisition, and extinction to determine the extent to which genetic and environmental factors are responsible for and
shared between these three processes. Christian J. Hopfer1, Michael C. Stallings2, and John K. Hewitt2 Objective: We report patterns of genetic and environmental correlations for alcohol and tobacco use in a volunteer sample of older, Caucasian, female twins using three different levels of severity for
alcohol use and smoking. The levels of severity for alcohol use and smoking were: ever drank, weekly drinking, problematic drinking; ever smoked, daily smoking of a half-pack or more, and daily smoking of at least 1 pack
or more. Procedures: A community-based sample of 1,926 female twins aged 50 to 96 were recruited through advertisements in the journal of the American Association of Retired Persons. Subjects were asked to rate alcohol
and tobacco use over their lifetime. Analyses: Twin correlations for alcohol and tobacco use measures were fit using Mx. Results:
Neonatal seizures, M-channels, and retigabine
Division of Epidemiology and Institute of Human Genetics, University of Minnesota, Minneapolis, MN
Address: University of Minnesota, MMC 197, 420 Delaware St SE, Minneapolis MN 55455
Phone: 612 625 3281 Fax: 612 625 8950 Email: ander087@umn.edu
Shared environmental transmission of culture: Methodology and findings3
1Faculty of Letters, Keio University, Mita Tokyo
2School of Medicine, Keio University, Shinanomachi Tokyo
3Supported by a Grant-in Aid for Scientific Research (C) from the Ministry of Education, Science, Sports and Culture
Address: Faculty of Letters, Keio University, 2-15-45, Mita, Minatoku, Tokyo, 108-8345, Japan
Phone: 81 3 3453 4511 Fax: 81 3 5427 1578 Email: juko@msa.biglobe.ne.jp
Genetic and environmental contributions of TCI subscales4
1Faculty of Letters, Keio University, Mita Tokyo
2School of Medicine, Keio University, Shinanomachi Tokyo
3Cancer Information and Epidemiology Division, National Cancer Research Institute, Chiyodaku Tokyo
4Supported by a Grant-in Aid for Scientific Research (C) from the Ministry of Education, Science, Sports and Culture
Address: Faculty of Letters, Keio University, 2-15-45, Mita, Minatoku, Tokyo, 108-8345, Japan
Phone: 81 3 3453 4511 Fax: 81 3 5427 1578 Email: juko@msa.biglobe.ne.jp
Association and linkage studies of DAT1, DRD4 and other dopamine system genes in ADHD2
1Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, London, UK, SE5 8AF
2Research supported by UK MRC
Address: Social Genetic Developmental Psychiatry Research Centre (SGDP), Institute of Psychiatry, London, UK, SE5 8AF
Phone: +44 207 848 0859/0319/0951 Fax: +44 207 848 0407 Email: p.asherson@iop.kcl.ac.uk
Heterogeneity of childhood aggression and anti-social behavior: A twin study2
1Department of Psychology, University of Southern California, Los Angeles, CA
2Supported by MH 58354
Address: University of Southern California, Department of Psychology, 3620 S. McClintock Ave #501, Los Angeles, CA 90089-1061
Phone: 213 740 2255 Fax: 213 746 9082 Email: lbaker@usc.edu
Daytime Basal Cortisol and Common Childhood Psychopathology3
1Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands
2Institute of Physiological Psychology II, University of Dsseldorf, Universitaetsstrasse 1, D-40225 Dsseldorf, Germany
3This work was financially supported by The Netherlands Organization for Scientific Research (575-25-012)
Address: Department of Biological Psychology, Vrije Universiteit, room 1F 57, van der Boechorststraat 1, 1081 BT, Amsterdam, The Netherlands
Phone: +31 20 4448812 Fax: +31 20 4448832 Email: m.bartels@psy.vu.nl
Genetic, neuroanatomical and behavioural approaches to studying CNS asymmetries in zebrafish
1Department of Anatomy and Developmental Biology, University College London
Address: Department of Anatomy and Developmental Biology, University College London, Gower St. London C1E 6BT
Phone: +44 20 7679 7349 Fax: +44 20 7679 3348 Email: s.wilson@ucl.ac.uk
Genome scan for quantitative traits involved in cardiovascular disease in three independent populations
1TNO Prevention and Health, Gaubius Laboratories, Dept of Vascular and Connective Tissue Research; Leiden, The Netherlands
2Dept of Human Genetics Leiden University Medical Centre; Leiden, The Netherlands 3Dept of Medical Statistics, Leiden University Medical Centre; Leiden, The Netherlands
4Center for Special Populations and Health, Pennsylvania State University; Pennsylvania, PA, USA
5Queensland Institute for Medical Research; Brisbane, Australia
6Royal Prince Alfred Hospital; Sydney, Australia
7Dept of Medical Epidemiology, Karolinska Institute; Stockholm, Sweden
8Dept of Psychology, Free University of Amsterdam; Amsterdam, The Netherlands
Address: TNO Prevention and Health, PO Box 2215 2301 CE Leiden, The Netherlands
Phone: +31 71 5181403 Fax: +31 71 5181904 Email: m.beekman@pg.tno.nl
A measurement error explanation of the biased QTL effect estimates when pi-hat is used as the IBD probability for untyped sib pairs2
1Department of Biological Psychology, Free University, Amsterdam, The Netherlands
2Supported by NWO Grant 904-61-090
Address: Afdeling Biologische Psychologie, Vrije Universiteit, Van der Boechorststraat 1, 1081 BT Amsterdam, The Netherlands
Phone: +31 20 4448811 Fax: +31 20 4448832 Email: AL.Beem@psy.vu.nl
East-West, home's best: rewarding properties of the home-cage of laboratory mice
1Center for Developmental and Health Genetics
2Department of Biobehavioral Health, College of Health and Human Development, Pennsylvania State University, University Park, PA 16802
Address: 201, Research Building D, Pennsylvania State University, University Park, PA 16802
Phone 814 865 3429 Fax:814 863 787 Email: dab22@psu.edu
Genetic analysis of DSM-oriented scales in 3 year-old Dutch twins4
1Vrije Univ, Department Biological Psychology, Amsterdam
2Erasmus Univ, Sophia Kinderziekenhuis, Rotterdam
3Univ of Vermont, College of Medicine, Burlington, Vermont
4Supported by Sophia Foundation SSWO 165, NWO-904-57-94 and NIH-R01 MH58799
Address: VU, Dept of Biological Psychology, Van der Boechorststraat 1, 1081 BT Amsterdam The Netherlands
Phone: +31 20 444 8789/8786 Fax: +31 20 444 8832 Email: dorret@psy.vu.nl
Indirect effects of the DRD4 VNTR polymorphism on sexual desire4
1Department of Psychology/Institute of Behavioral Science, University of Colorado, Boulder, CO 80309
2Department of Psychology, University of Colorado, Boulder, CO 80309
3Institute for BehaviOral Genetics, University of Colorado, Boulder, CO 80309
4Supported by grants from NCI (CA81637) to the second author and from NIAAA (RO3 AA12925-01) to the first author
Address: Angela D. Bryan, Department of Psychology CB 345, University of Colorado, Boulder, CO 80309-0345
Phone: 303 735 1587 Fax: 303 492 6924 Email: angela.bryan@colorado.edu
Covariation among childhood externalizing disorders: Identifying shared environmental contributions
5
1Department of Psychology, University of Minnesota, Minneapolis, MN 55455
2Supported in part by NIH Grants DA05147, AA09367, AND AA00175
Address: Department of Psychology, Elliott Hall University of Minnesota, 75 East River Road, Minneapolis, MN 55455-0344
Phone: 651 645 9354 Email: burt0105@tc.umn.edu
Aggression and Mating in Sex Reversed Mice2
1BioBehavioral Sciences Graduate Degree Program, The University of Connecticut, Storrs, CT
2Supported by The Inbred Mouse Fund and the Research Foundation of The University of Connecticut
Address: BioBehavioral Sciences Graduate Degree Program, U-154, The University of Connecticut, Storrs, CT 06269-4154
Phone: 860 486 2455 Fax: 860 486 3827 Email: lippachenko@hotmail.com
Triton Survey Designer: A software package for the design, administration, and analysis of surveys 3
1Horizon Research Corporation, Los Angeles, CA
2Department of Psychology, University of Southern California, Los Angeles, CA
3Supported by NIMH 58354 MAIL: University of Southern California, Department of Psychology, 3620 S. McClintock Ave #501, Los Angeles, CA 90089-1061
Phone: 213 740 2255 Fax: 213 746 9082 Email: lbaker@usc.edu Internet: http://www-rcf.usc.edu/~lbaker/
Functional analysis of genes included in the Down syndrome chromosomal region-1 (DCR-1) with transpolygenic mice
1FRE 2134 CNRS, Génétique, Neurogénétique Comportement, 45071 Orléans Cedex 2, France
2Universite d'Orléans, BP 6749, 45067 Orléans cedex 2
3Supported by the Fondation pour la Recherche Médicale
Address: FRE 2134 CNRS, Génétique, Neurogénétique Comportement, 3b rue de la Ferollerie, 45071 Orléans Cedex 2, France
Phone: 33 2 38 25 79 69 Fax: 33 2 38 25 79 79 Email: chabert@cnrs-orleans.fr
The effects of genotype errors on mapping complex traits: Detection and treatment2
1Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, United Kingdom
2Supported by NIH Grant EY-12562
Address: Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, United Kingdom
Phone: +44 1865 287590 Fax: +1 786 551 8340 Email: cherny@qtl.well.ox.ac.uk URL: http://qtl.well.ox.ac.uk/
Continuity or Discontinuity between Substance Experimentation, Regular Use, and Dependence Symptoms in Adolescence: Twin and Adoption Results2
1Institute for Behavioral Genetics, University of Colorado, Boulder CO
2Supported by grants DA-05131 and DA-11015, HD-10333, and MH-43899
Address: Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder CO 80309-0447
Phone: 303 492 5189 Fax: 303 492 8063 Email: Robin.Corley@colorado.EDU
Differential genetic etiology of reading disability as a function of processing speed2
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309
2This work was supported in part by program project and center grants from the National Institute of Child Health and Human Development (HD-11681 and HD-27802) to J.C. DeFries. This report was
prepared while R.J. Cross was supported by NIMH training grant MH-16880.
Address: Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder, CO
80309
Phone: 303 492 2817 Fax: 303 492 8063 Email: rebecca.cross@colorado.edu
ProtocadherinXY as a candidate for the Homo sapiens speciation gene
1University Department of Psychiatry, Warneford Hospital, Oxford OX3 7JX2University Department of Pathology, University of Cambridge
Address: University Department of Psychiatry,Warneford Hospital, Oxford OX3 7JX, United Kingdom
Phone: +44 1865 226474 Fax: +44 1865 244990 Email: tim.crow@psychiatry.oxford.ac.uk
QTL association analysis of the DRD4 exon 3 VNTR polymorphism in a population sample of children screened with a parent rating scale for ADHD symptoms
1Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, London, UK
2Department of Child and Adolescent Psychiatry, GKT Medical School, London, UK
Address: Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, De Crespigny Park, London, UK, SE5 8AF
Phone: +44 207 848 0745 Fax: +44 207 919 0407 Email: s.curran@kcl.iop.ac.uk
Reading difficulties and rapid naming: Bivariate twin and genetic linkage analyses6
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO
2Department of Psychiatry, Washington University School of Medicine, St. Louis, MO
3Center for Human Molecular Genetics, Munroe Meyer Institute, University of Nebraska Medical Center, Omaha, NE
4Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
5Department of Psychology, University of Denver, Denver, CO
6Supported 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.
Address: Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder, CO 80309
Phone: 303 492 7362 Fax: 303 492 8063 E-mail: davisc@colorado.edu
A review of QTL and knock-out studies for emotionality in mice
1Vrije Universiteit, Department Biological Psychology, Amsterdam
2Gaubius Laboratory, TNO Prevention and Health, Leiden
Address: VU, Dept of Biological Psychology, Van der Boechorststraat 1, 1081 BT Amsterdam, The Netherlands
Phone: +31 20 444 8789/8786 Fax: +31 20 444 8832 Email: dorret@psy.vu.nl
Latent Growth Curve Analyses of Drinking Trajectories Across Adolescence3
1Department of Psychology, Indiana University
2Department of Public Health, University of Helsinki
3FinnTwin16 is supported by NIAAA (AA 08315 and AA 00145), and by the Academy of Finland (44069)
Address: Department of Psychology, Indiana University, 1101 E. 10th St., Bloomington, IN 47405
Phone: 812 855 4101 Fax: 812 855 4691 Email: ddick@indiana.edu
The role of the Children of Twins design in highlighting genetic and environmental pathways between parental and child characteristics
1Psychology Department, University of Virginia,, Charlottesville, VA 22904-4400
2Virginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University, Richmond, VA 23298-0003
Address: Psychology Department, University of Virginia, 102 Gilmer Hall, PO Box 400400, Charlottesville, VA 22904-4400
Phone: 804 982 4750 Email: briand@virginia.edu
Familial study and partial genome scan for degree of laterality
1FRE 2134 CNRS, Génétique, Neurogénétique Comportement, 45071 Orléans cedex 2, France
2Service de Neurochirurgie, Centre Hospitalier Regional d'Orléans, 45067 Orléans cedex 2, France
Address: FRE 2134 CNRS, Génétique, Neurogénétique Comportement, 3B rue de la Ferollerie, 45071 Orléans cedex 2, France
Phone: +33 238 257972 Fax: +33 238 257979 Email: al-doyen@cnrs-orleans.fr
Longitudinal genetic analysis of aggressive and non-aggressive antisocial behavioural symptoms
1Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College, London UK
2Department of Medical Epidemiology, Karolinska Institute, Sweden
3This study was funded by the Swedish Council for Social Research (project F0129/1999). Thalia Eley is supported by a UK Medical Research Council Fellowship.
Address: Social, Genetic and Developmental Psychiatry Research Centre, 111 Denmark Hill, Institute of Psychiatry, De Crespigny Park, London SE5 8AF
Phone: +44 20 7848 0863 Fax: +44 20 7848 0866 E-mail: t.eley@iop.kcl.ac.uk
Is Prolonged Fatigue in Children & Adolescents Heritable?
1Department of Psychological Medicine, University of Wales College of Medicine, Cardiff, Wales
2Social, Genetic & Developmental Research Centre, Institute of Psychiatry, London, England
3Supported by PPP Healthcare Medical Trust Grant 1206/192
Address: Department of Psychological Medicine, University of Wales College of Medicine, Cardiff, Wales, CF14 4XN
Phone: +44 29 20742201 Fax: +44 29 20747839 Email: fowlerta@cf.ac.uk
Analysis of Twin data of Adult Attachments
1Faculty of Humanity, Tokyo Seitoku University
2Faculty of letters, University of Chiba
3Department of Psychology, Tokyo Gakugei University
4Department of Psychology, Tokyo Gakugei University
5Graduate Course, Tokyo Metropolitan University
Address: Hisako Itoi Department of Psychology, Tokyo Gakugei University
Phone: +81 422 51 4458 Fax: +81 422 51 4458 Email: itoi@u-gakugei.ac.jp
Common and unique genetic and environmental influences on EAS temperament dimensions in childhood
1Department of Psychology, 532 N. Kilgo Circle, Emory University, Atlanta, GA 30322
Address: mailing address - Department of Psychology, 532 N. Kilgo Circle, Emory University, Atlanta, GA 30322
Phone: 770 986 7715 Fax: 404 727 0372 Email: agahaga@emory.edu
General Cognitive Ability (g) in Mice as the basis of a Functional Genomics Model of Cognitive Abilities and Disabilities
1SGDP, Institute of Psychiatry, King's College London, UK
2Facultad de Psicolog¡a, Avda. Blasco Ib ¤ez, Valencia, Spain
Address: SGDP, 111 Denmark Hill, London, UK, SE5 8AF
Phone +44 20 7848 0407 Fax: +44 20 7848 0866 Email: m.galsworthy@iop.kcl.ac.uk
The experiential context of parenting2
1Department of Psychology, George Washington University,Washington DC,20052
2 Twin Mom Study NIMH RO1MH54610
Address: 2125 G St NW, Washington, DC 20052
Phone 202 994 7571 Fax: 202 994 1602 Email: ganiban@gwu.edu
Genetic simplex modeling of personality in adolescent twins
1Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, QLD, Australia
Address: Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Post Office, Royal Brisbane Hospital, Brisbane QLD 4029, Australia
Phone: +61 7 3362 0226 Fax: +61 7 3362 0101 Email: nathanG@qimr.edu.au
Parental Alcohol Dependence and Suicidal Behavior in Adolescent Female Twins2
1Department of Psychiatry, Washington University, St. Louis, Missouri, 63108
2Supported in part by NIH grants AA-11998, AA-09022, AA-07728, AA-07580 and the Klingenstein Third Generation Foundation Fellowship Award in Depression
Address: Dr. Anne L. Glowinski, Washington University School of Medicine Campus Box 8134 Department of Psychiatry, 40 N. Kingshighway, Suite 1,Saint Louis, MO 63108
Phone: 314 286 2217 Fax: 314 286 2213 Email: glowinsa@matlock.wustl.edu
The Relationship between Attention-Deficit/Hyperacitvity Disorder, Reading Disorder, and Communication Disorder Symptomatology
1School of Psychology, Curtin University of Technology, Perth Western Australia
Address: School of Psychology, Curtin University of Technology, GPO Box U1987, Perth Western Australia, Australia 6845
Phone: +61 8 9266 2944 Fax: +61 8 9266 2464 Email: e.hagemann@curtin.edu.au
Investigating Age Differences in the Genetic and Environmental Structure of the TPQ in Later Adulthood3
1Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309
2Center for Dev. & Health Genetics, Pennsylvania State University, University Park, PA 16802
3Supported by NIH Grant AG-17949
Address: Institute for Behavioral Genetics Campus Box 447 University of Colorado, Boulder CO 80309-0447
Phone: 303 735 2428 Fax: 303 492 8063 Email: noa.heiman@colorado.edu
Factor analyses of phenotypic correlations of animal behaviors assessed in multiple test events are often not informative2
1Department of Psychology, Oberlin College, Oberlin, OH 44074
2Supported by NIMH Grant MH-53480
Address: Department of Psychology, Severance Laboratory, Oberlin College, Oberlin, OH 44074
Phone: 440 775 7695 Fax: 440 775 8356 Email: fhenders@oberlin.edu
A Twin Study of the Genetics of Fear Conditioning
1Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, VA
2Roche AB, Stockholm, Sweden
3Department of Psychology, Uppsala University, Uppsala, Sweden
Address: Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, P.O. Box 980126, Richmond, VA 23298-0126
Phone: 804 828 8592 Fax: 804 828 1471 Email: jhettema@hsc.vcu.edu
Common Genetic and Environmental Vulnerability for Alcohol and Tobacco Use in a Volunteer Sample of Older Female Twins3
1University of Colorado Health Sciences Center, Denver, CO 80262
2Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309
3Supported by NIDA grants DA 09842, DA 11015, DA 12845, DA 00357
Address: Box C-268-35. Dept. of Psychiatry. University of Colorado Health Sciences Center, Denver, CO 80262
Phone: 303 315 0798 Fax: 303 315 0394 Email: Christian.Hopfer@uchsc.edu