NCAM1, and exons 2 and 5 of ANKK1. LD contrasts between cases and controls supported historical selection at TTC12 exon 3 and ANKK1 exon 2, and corroborated the identified risk variants from the association analysis. Further, the risk variants in TTC12 suggested a fundamental neurobiological basis for SD that involves dopaminergic neurotransmission, since the armadillo repeat domain encoded by TTC12 interacts with dopamine through the Wnt signal transduction pathway and may have effects on dopamine neuronal development in the ventral midbrain (Castelo-Branco and Arenas, 2006; Castelo-Branco et al., 2006). In the present article, we examined the effects of DD comorbidity on the observed association, with the goal of evaluating its specificity. To that end, we undertook analyses comparing AD with or without DD comorbidity (AD+DD vs AD-only) using the same 43 SNP markers in the NTAD gene cluster. By doing so, we hoped to learn whether AD or DD was the primary driver of the observed association.
