Please cite this article as follows: Neale BM, Lasky-Su J, Anney R, Franke B, Zhou K, Maller JB, Vasquez AA, Asherson P, Chen W, Banaschewski T, Buitelaar J, Ebstein R, Gill M, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Steinhausen HC, Sonuga-Barke E, Mulas F, Taylor E, Laird N, Lange C, Daly M, Faraone SV. 2008. Genome-Wide Association Scan of Attention Deficit Hyperactivity Disorder. Am J Med Genet Part B 147B:1337–1344.
Genome-wide association scan of attention deficit hyperactivity disorder†
Article first published online: 3 NOV 2008
Copyright © 2008 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Special Issue: Special Issue on the Genetics of ADHD Dedicated to the Memory of Richard Todd
Volume 147B, Issue 8, pages 1337–1344, 5 December 2008
How to Cite
Neale, B. M., Lasky-Su, J., Anney, R., Franke, B., Zhou, K., Maller, J. B., Vasquez, A. A., Asherson, P., Chen, W., Banaschewski, T., Buitelaar, J., Ebstein, R., Gill, M., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Sergeant, J., Steinhausen, H. C., Sonuga-Barke, E., Mulas, F., Taylor, E., Laird, N., Lange, C., Daly, M. and Faraone, S. V. (2008), Genome-wide association scan of attention deficit hyperactivity disorder. Am. J. Med. Genet., 147B: 1337–1344. doi: 10.1002/ajmg.b.30866
- Issue published online: 18 NOV 2008
- Article first published online: 3 NOV 2008
- Manuscript Accepted: 27 AUG 2008
- Manuscript Received: 5 MAY 2008
- NIH. Grant Number: R01MH62873
- genome-wide association;
- SNP chip;
- genetic association information network
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.