identify genetic variants that could predispose children to an earlier age of onset of disease symptoms. Additive, dominant and recessive genetic models were tested. A total of 16 SNPs reached P values for association <10−5 including 14 unique findings (Table 4). There is no overlap with the results from the other GWAS. Although potentially due to chance it is remarkable to see that this list contains a number of genes that are involved in the response of the body to environmental exposures and/or are regulated by the environment, like the inflammation related ADAMTS2, the stress regulator MAP3K7 or the vitamin A-responsive NAV2 gene.Table 4Findings from genome-wide analysis of ADHD age of onset by Lasky-Su et al. (2008a), including genes in or near which the association finding is presentSNPGenetic modelDirection of effect P valueChromosome, base pairsPositionGene functiona Additional remarksrs1517484AdditiveEarlier onset5.42E-07chr2:225945904Within 28 kb of KIAA1486Gene of unknown function, expressed in brain and other tissuesrs9845475DominantLater onset3.95E-06chr3:32817105Within 20 kb upstream of TRIM71Gene of unknown function, expressed in brain and other tissues. Potentially plays an important role in development. Finding lies within linkage region for schizophrenia from meta-analysis (Lewis et al. 2003)rs3892715DominantEarlier onset6.46E-06chr3:196239299Within 31 kb upstream of C3orf21Gene of unknown function, codes for membrane protein
