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Association of ADHD, tics, and anxiety with dopamine transporter ( DAT1 ) genotype in autism spectrum disorder
Author(s) -
Gadow Kenneth D.,
Roohi Jasmin,
DeVincent Carla J.,
Hatchwell Eli
Publication year - 2008
Publication title -
journal of child psychology and psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.652
H-Index - 211
eISSN - 1469-7610
pISSN - 0021-9630
DOI - 10.1111/j.1469-7610.2008.01952.x
Subject(s) - psychology , autism spectrum disorder , tics , impulsivity , dopamine transporter , anxiety , attention deficit hyperactivity disorder , autism , psychiatry , genotype , clinical psychology , tic disorder , social anxiety , variable number tandem repeat , dopamine , genetics , dopaminergic , neuroscience , gene , biology
Background: Autism spectrum disorder (ASD) is associated with high rates of psychiatric disturbance to include attention‐deficit/hyperactivity disorder (ADHD), tic disorder, and anxiety disorders. The aim of the present study was to examine the association between a variable number tandem repeat (VNTR) functional polymorphism located in the 3’‐untranslated region of the dopamine transporter gene ( DAT1 ) and the severity of these symptoms as well as the association between the DAT1 Dde I polymorphism and severity of tics. Methods: Parents ( n = 62) and teachers ( n = 57) completed a DSM‐IV‐referenced rating scale for 67 children with ASD. Results: According to parent ratings, children with the 10‐10 repeat allele (versus a combined group of all other genotypes) exhibited less severe symptoms of hyperactivity and impulsivity as well as less severe language deficits. Teacher ratings indicated that social anxiety and tic symptoms were more severe for children with the 10‐10 genotype versus all others. Exploratory analyses provided preliminary support for the notion that heterozygosity (9–10 repeat genotype) may be a risk/protective factor. There were no associations of tic severity with the DAT1 Dde I polymorphism. Conclusion: Collectively, these results suggest that the extraordinary variability in ASD clinical phenotypes may be explained in part by the same genes that are implicated in a host of other psychiatric disorders in non‐ASD populations. Nevertheless, replication with independent samples is necessary to confirm this preliminary finding.