Neuroimaging studies of normative or at-risk populations have proven particularly useful in determining potential biological targets for prevention of AUD. The majority of available studies have sought to map individual differences in the functioning of a corticostriatal circuit supporting reward processing and motivation onto behavioral or psychometric indices of AUD risk. This work has collectively demonstrated that reward-related activity of the ventral striatum (VS), which serves as a neural hub through which information processing is coordinated within the corticostriatal circuit, is positively correlated with risk-related behaviors including delay discounting12 and self-reported impulsivity.13, 14 Other studies have demonstrated a direct positive association between reward-related VS activity and harmful drinking patterns.15, 16 In contrast to this relative VS hyper-activity associated with risk and disorder, an extensive parallel literature has highlighted the contribution of relative VS hypo-activity to drug-seeking behaviors, possibly as a means to compensate for blunted positive incentive processing.17 Thus, both hyper- and hypo-activity of the VS in response to reward-related stimuli may confer relative risk for AUD.
