The published GWAS for ADHD 116 and AN 117 are small, but larger samples are in progress (e.g., by the Wellcome Trust Case-Control Consortium for AN). Given low power, no conclusions about common variation can be made. In ADHD, increased SV burden has been reported (OR=2.1), 118,119 an effect higher in ADHD cases with MR (OR=5.7). 118 Pathway analysis in ADHD found association signals enriched in the same GO categories also overrepresented for large SV. 120 The weak signals in ADHD GWAS are not randomly distributed but index the same pathophysiological pathways as rare SV. Thus, it appears that the reason no common variants have yet confidently been implicated in ADHD by GWAS is lack of power, not lack of variants to be found.
