Building upon twin and family studies documenting the moderate heritability of alcohol use and use disorders (30–50%) (9,10), large-scale genome-wide association studies (GWASs) have begun to reliably characterize the polygenic architecture of alcohol involvement (11,12). Polygenic risk scores (PRS) that effectively capture this polygenic liability can be combined with neuroimaging data to investigate whether individual differences in neural phenotypes may be partially attributable to common underlying genomic vulnerability and/or arise following substance exposure, use, and/or problematic use. However, given the ubiquity of lifetime alcohol use, efforts to disentangle such predispositional effects from neurotoxic consequences of chronic exposure have been limited.
