The present loci identified via GWAS for MaxDrinks overlap partially with loci identified in our previous GWAS for AD, but independent loci were also observed in each study. These findings suggest that shared genetic influences on MaxDrinks and AD phenotypes are attributable in large part to alcohol metabolism genes. These results are consistent with prior genetic epidemiologic findings from a twin study of alcohol consumption phenotypes, where a high degree of genetic overlap between the heaviness of consumption and AD symptoms was observed (Grant et al., 2009). In our Yale-UPenn sample, significant correlation of Maxdrinks and AD symptoms were also observed in both EAs and AAs (Sartor et al., 2014). Numerous genes that were reported genome wide significant in GWAS for AD (Gelernter et al., 2014), including PDL1M5 in EAs, METAP in AAs, MTIF2 and CCDC88A in both EAs and AAs, were not associated with MaxDrinks in the current study. Similarly, several of the genes associated with MaxDrinks in this study have not been reported previously to be associated with AD, suggesting specific genetic loci contribution to Maxdrinks.
