Gelernter et al., 2014c) and the analysis by Wang et al. (2013), the authors tested for association with a quantitative DSM-IV AD criterion count phenotype. They controlled for cocaine, opioid, and nicotine dependence criteria in the sample and meta-analyzed the results with those from the SAGE sample (Bierut et al., 2010) and ultimately with their discovery and replication samples. In AAs, they identified several GWS findings at the ADH locus on chromosome 4, with the strongest finding in ADH1B (rs2066702, P=1.50 × 10−23). In EAs, the strongest finding was also in ADH1B (rs1229984, P=1.52 × 10−22). Both ADH1B SNPs are missense polymorphisms and both associations replicated in an independent sample. Thus, as in other AD GWAS (Frank et al., 2012, Park et al., 2013), the ADH gene cluster appears to have the greatest effect on AD risk.
