for association at this locus in multiple samples and two major populations, AAs and EAs, appears strong, but is apparently accounted for by variation elsewhere in the ADH cluster, that is, it most likely reflects linkage disequilibrium with other variants. Conditional analyses to determine whether there was evidence for multiple independent AD risk loci showed that the peak ADH1B SNP in EAs (rs1229984), but not the peak ADH1B SNP in AAs (rs2066702), remained highly significant after adjustment for peak SNPs in either LOC100507053 or PDLIM5. In AAs, ADH1C remained significant after adjusting for any of the other loci tested in this region, suggesting that there exists a functional AD risk variant in ADH1C in this population. Future studies using gene resequencing are needed to validate this hypothesis.
