Conflict of interest statement: No conflicts declared.
Association of ADHD, tics, and anxiety with dopamine transporter (DAT1) genotype in autism spectrum disorder
Article first published online: 21 NOV 2008
© 2008 The Authors. Journal compilation © 2008 Association for Child and Adolescent Mental Health
Journal of Child Psychology and Psychiatry
Volume 49, Issue 12, pages 1331–1338, December 2008
How to Cite
Gadow, K. D., Roohi, J., DeVincent, C. J. and Hatchwell, E. (2008), Association of ADHD, tics, and anxiety with dopamine transporter (DAT1) genotype in autism spectrum disorder. Journal of Child Psychology and Psychiatry, 49: 1331–1338. doi: 10.1111/j.1469-7610.2008.01952.x
- Issue published online: 21 NOV 2008
- Article first published online: 21 NOV 2008
- Manuscript accepted 7 May 2008
- Asperger’s syndrome;
- autism spectrum disorder;
- attention-deficit/hyperactivity disorder;
- social anxiety;
- dopamine transporter gene;
- Tourette syndrome
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 DdeI 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 DdeI 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.