Findings from this study support the hypothesis that heterogeneity of the SD disorders studied and their high rates of comorbidity are reflected in genetic association findings. The contrast among the findings for the four phenotypes – AD+DD, AD-only, AD irrespective of DD comorbidity (AD-all), and ND irrespective of AD or DD (ND-all) from the current and prior studies, provides important insight not evident when the previous studies are considered individually, as summarized in Table 7 and Figure 1(B). In a previous article (Gelernter et al., 2006), we reported very strong evidence of association of ND (ND-all) to a single haplotype spanning TTC12 and ANKK1. In another recent article (Yang et al., 2007), we reported that risk for AD (AD-all) is attributable in part to variants in four regions within the NTAD gene cluster: exon 3 of TTC12, exon 12/intron13 of 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
