Importantly, most extant research on AUD adopts a risk perspective with a focus on aspects that contribute to the liability to develop AUD and neural and behavioral deficits associated with it. Accordingly, ample work has focused on endophenotypes such as low P3 and low FT as indices of genetic risk for developing AUD and related disorders. However, little work has examined factors that can improve this disadvantage, promote normative development, and buffer against this liability. Previous research has shown: (a) that adolescence is when important brain development is underway and concomitantly when alcohol initiation and escalation also occur; (b) that secure attachment is particularly related to development of the frontal cortex, which is responsible for decision making, judgment, reasoning, and inhibitory processing (Dozier et al., 2009); and (c) that parenting factors during adolescence are among the most important variables in gene–environment interaction (GxE) effects on resilience and risk for AUD and related disorders. Yet, it is unknown whether among high-risk offspring greater closeness with one’s parents, during adolescence, is associated with better neurocognitive functioning (indexed by P3 amplitude and FT)
