Neale, B. M., Su, J., Anney, R. J. L., Franke, B., Zhou, K., Maller, J. B., Vasquez, A. A., Asherson, P., Chen, W., Banaschewski, T., Buitelaar, J. K., Ebstein, R. P., Gill, M., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Sergeant, J. A., Steinhausen, H-C., Sonuga-Barke, E. J. S., Mulas, F., Taylor, E. A., Laird, N., Lange, C., Daly, M. & Faraone, S. V.

Genome-wide Association Scan of Attention Deficit Hyperactivity Disorder.
American Journal of Medical Genetics Part B, 147B, 1337-1344.
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Introduction: Results of behavioral genetic & molecular genetic studies have converged to suggest that genes substantially contribute to the development of ADHD, a common disorder that onsets in childhood. --- Yet, despite numerous linkage & candidate gene studies, strongly consistent & replicable association has eluded detection.

Methods: To search for ADHD susceptibility genes, we genotyped c, 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2803 Ss 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.

1 - None of the SNP association tests achieved genome-wide significance, indicating that larger samples may be required to identify risk loci for ADHD.

2 - We additionally identify a systemic bias in family-based association, & suggest that variable missing genotype rates may be the source-of this bias.

Discussion: As the current study is part of the GAIN initiative, all data are available online at

Access to the dataset requires gaining approval from the Data Access Committee, but the results disclosed here will be made available on the dbGap server for browsing. Additionally the top results from the TDT analysis described here are available upon request.