which polygenic risk increases risk for AUD. While polygenic risk scores for AUD have yet to reach the point of clinical utility (i.e., family history of AUD remains a stronger predictor than any PRS), larger and more diverse GWAS of AUD currently underway hold promise for the future. Well-characterized, longitudinal, and diverse samples are needed to ‘translate’ results emerging from GWAS, particularly with respect to brain function, which might serve as a pathway for genetic vulnerability for AUD to be expressed. While additional research is needed in this area, this study is a first step in understanding one potential neural mechanism linking genetic variants emerging from GWAS to neural development and may help to identify specific points in adolescence or young adulthood when neurocognitive prevention and intervention efforts may be most effective.
