TY - JOUR
T1 - Genome-wide association scan of attention deficit hyperactivity disorder
AU - Neale, Benjamin M.
AU - Lasky-Su, Jessica
AU - Anney, Richard
AU - Franke, Barbara
AU - Zhou, Kaixin
AU - Maller, Julian B.
AU - Vasquez, Alejandro Arias
AU - Asherson, Philip
AU - Chen, Wai
AU - Banaschewski, Tobias
AU - Buitelaar, Jan
AU - Ebstein, Richard
AU - Gill, Michael
AU - Miranda, Ana
AU - Oades, Robert D.
AU - Roeyers, Herbert
AU - Rothenberger, Aribert
AU - Sergeant, Joseph
AU - Steinhausen, Hans Christoph
AU - Sonuga-Barke, Edmund
AU - Mulas, Fernando
AU - Taylor, Eric
AU - Laird, Nan
AU - Lange, Christoph
AU - Daly, Mark
AU - Faraone, Stephen V.
PY - 2008/12/5
Y1 - 2008/12/5
N2 - 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.
AB - 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.
KW - ADHD
KW - Genetic association information network
KW - Genome-wide association
KW - SNP chip
UR - https://www.scopus.com/pages/publications/57349166006
U2 - 10.1002/ajmg.b.30866
DO - 10.1002/ajmg.b.30866
M3 - Article
C2 - 18980221
SN - 1552-4841
VL - 147
SP - 1337
EP - 1344
JO - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
JF - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
IS - 8
ER -