Genome-wide association scan of attention deficit hyperactivity disorder

✍ Scribed by Benjamin M. Neale; Jessica Lasky-Su; Richard Anney; Barbara Franke; Kaixin Zhou; Julian B. Maller; Alejandro Arias Vasquez; Philip Asherson; Wai Chen; Tobias Banaschewski; Jan Buitelaar; Richard Ebstein; Michael Gill; Ana Miranda; Robert D. Oades; Herbert Roeyers; Aribert Rothenberger; Joseph Sergeant; Hans Christoph Steinhausen; Edmund Sonuga-Barke; Fernando Mulas; Eric Taylor; Nan Laird; Christoph Lange; Mark Daly; Stephen V. Faraone

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 134 KB
• Volume: 147B
• Category: Article
• ISSN: 1552-4841
• DOI: 10.1002/ajmg.b.30866

✦ Synopsis

Abstract

Results of behavioral genetic and molecular genetic studies have converged to suggest that genes substantially contribute to the development of attention deficit/hyperactivity disorder (ADHD), a common disorder with an onset in childhood. Yet, despite numerous linkage and candidate gene studies, strongly consistent and replicable association has eluded detection. To search for ADHD susceptibility genes, we genotyped approximately 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2,803 individuals comprising 909 complete trios using ADHD diagnosis as phenotype. We present the initial TDT findings as well as considerations for cleaning family‐based TDT data. None of the SNP association tests achieved genome‐wide significance, indicating that larger samples may be required to identify risk loci for ADHD. We additionally identify a systemic bias in family‐based association, and suggest that variable missing genotype rates may be the source of this bias. © 2008 Wiley‐Liss, Inc.