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Genome‐wide association scan of attention deficit hyperactivity disorder
Author(s) -
Neale Benjamin M.,
LaskySu Jessica,
Anney Richard,
Franke Barbara,
Zhou Kaixin,
Maller Julian B.,
Vasquez Alejandro Arias,
Asherson Philip,
Chen Wai,
Banaschewski Tobias,
Buitelaar Jan,
Ebstein Richard,
Gill Michael,
Miranda Ana,
Oades Robert D.,
Roeyers Herbert,
Rothenberger Aribert,
Sergeant Joseph,
Steinhausen Hans Christoph,
SonugaBarke Edmund,
Mulas Fernando,
Taylor Eric,
Laird Nan,
Lange Christoph,
Daly Mark,
Faraone Stephen V.
Publication year - 2008
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30866
Subject(s) - genetic association , single nucleotide polymorphism , attention deficit hyperactivity disorder , candidate gene , genome wide association study , genetics , snp , association test , biology , genetic linkage , linkage (software) , gene , genotype , psychology , psychiatry
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.