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Analysis of ten candidate genes in autism by association and linkage

Journal article
Authors Anne Philippe
Michel Guilloud-Bataille
Maria Martinez
Christopher Gillberg
Maria Råstam
Eili Sponheim
Mary Coleman
Michele Zappella
Harald Aschauer
Christiane Penet
Josué Feingold
Alexis Brice
Marion Leboyer
Published in American Journal of Medical Genetics
Volume 114
Issue 2
Pages 125-128
ISSN 0148-7299
Publication year 2002
Published at Institute for the Health of Women and Children, Dept of Child and Adolescent Psychiatry
Pages 125-128
Language en
Keywords Alleles, Autistic Disorder, Genetics, Chromosome Mapping, DNA, Genetics, Family Health, Female, Genetic Predisposition to Disease, Genetics, Genotype, Humans, Linkage Disequilibrium, Male, Microsatellite Repeats, Monoamine Oxidase, Genetics, Nuclear Family, Receptors, Dopamine, Genetics, Tyrosine 3-Monooxygenase, Genetics
Subject categories Psychiatry, Medical and Health Sciences


We studied the possible involvement of ten candidate genes in autism: proenkephalin, prodynorphin, and proprotein convertase subtilisin/kexin type 2 (opioid metabolism); tyrosine hydroxylase, dopamine receptors D2 and D5, monoamine oxidases A and B (monoaminergic system); brain-derived neurotrophic factor, and neural cell adhesion molecule (involved in neurodevelopment). Thirty-eight families with two affected siblings and one family with two affected half-siblings, recruited by the Paris Autism Research International Sibpair Study (PARIS), were tested using the transmission disequilibrium test and two-point affected sib-pair linkage analysis. We found no evidence for association or linkage with intragenic or linked markers. Our family sample has good power for detecting a linkage disequilibrium of 0.80. Thus, these genes are unlikely to play a major role in the families studied, but further studies in a much larger sample would be needed to highlight weaker genetic effects.

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