al. 2006, 2007). We have since found similar evidence for association of AD to markers in the same haplotype block in a completely independent sample; in this case, the associated region centers on two TTC12 SNPs (Yang et al. 2007). The COGA group has reported consistent results for ANKK1 (they did not study TTC12) (Dick et al. 2007a). These studies provide an alternate explanation for the weak DRD2 association reports that have surfaced regularly over the years—they may be explained by linkage disequilibrium with adjacent loci wherein map the actual risk alleles. Also, although investigators were led to this genomic region by a candidate gene hypothesis, our interpretation of all of the available data is that it was not the candidate gene that was driving the association. We have speculated, though, that the genes actually associated with phenotype may be functionally related to DRD2.
