In summary, we found evidence that (1) three regions in EAs harbor variants predisposing to AD comorbid with DD: exon 3 in TTC12 (the region for which evidence for association is the strongest and most consistent), the two adjacent 3′ regions of DRD2 and ANKK1 (i.e., between exon 7 of DRD2 and exon 8 of ANKK1), and risk or protective variants close to exon 12 to intron 13 of NCAM1; (2) For AD without DD comorbidity, NCAM1 intron 14 to 18 and the junction of ANKK1 and DRD2 were associated globally; no individual haplotype was significantly associated. We showed in our previous study that overall, risk for AD, irrespective of comorbidity of DD, was attributable in part to variants in four regions: exon 3 of TTC12, exon 12 of NCAM1, and exons 2 and 5 of ANKK1, but not the junction of DRD2 and ANKK1.
