We conclude that exon 3 of TTC12, and the region close to exon 12 of NCAM1, both regulate risk for AD+DD. Variants at the two 3′ ends of ANKK1 and DRD2 also regulate risk for AD, with effects depending on comorbidity with DD. The complexity of these relationships, many of which were replicated in our independent samples, may explain prior inconsistent results. Further replication in other samples and functional analysis of this allelic variation are warranted.
