Individuals with low LR, and consequently, higher SRE scores are at increased likelihood of drinking heavily and developing problems AD (Schuckit et al., 1997a). The present study found that a preponderance of this correlation is attributable to genetic factors, as indexed by strong correlations in latent heritable factors influencing SRE and AD phenotypes. However, these high correlations should be interpreted within the context of our ascertainment strategy, which oversampled for individuals with family history of AD. It should also be distinguished from more recent SNP-based genetic correlations that examine the extent of similarity between genomewide effect sizes for two traits. In contrast to the high rg from the pedigree data, our study also added a novel exploration of the extent to which polygenic liability to SRE relates to AD. Overall, PRS mostly explained modest proportions of variance in AD phenotypes. Nearly 2.5% and 1.4% of the variance in AD diagnosis and criterion count, respectively, were explained by polygenic liability to SRE-T in the SAGE-EA data. Predictions were less significant in other target cohorts, potentially due to the similar ascertainment for
