Two robust findings in AUD research are: (1) deficient self-regulation is an underlying phenotype of AUD and related disorders (Petersen et al., 2018); and (2) high-risk offspring of individuals with AUD manifest low target P3 and FT—two important neural endophenotypes associated with heightened risk for AUD-development. Self-regulation is related to the constructs of effortful control and executive functioning that are in turn related to the functioning of the prefrontal cortex (PFC) and anterior cingulate cortex (ACC). The functioning of PFC and ACC representing behavioral regulation in inhibition tasks is reflected in P3 and FT activity. Accordingly, it has been hypothesized that high-risk offspring may present a neurodevelopmental lag in the growth of PFC and ACC, which may result in their hypoactivation during inhibition tasks (e.g., the Visual Oddball Task). This hypoactivation of PFC and ACC may then manifest as low P3 and FT. In a recent study, low target-related P3 and FT in early adolescence were shown to prospectively predict drinking in late adolescence, independent of one another. The study also showed that among alcohol-naïve individuals, low P3 and FT
