Premorbid behavioral, cognitive, and psychobiological risk factors have been observed in children and youth with a family history of alcoholism that are predictive of early initiation of drinking behavior or subsequent AUD (Crum et al. 2008; Hill et al. 2008; Iacono et al. 2008; Johnson and Leff 1999; Kramer et al. 2008; Kuo et al. 2008; Porjesz and Rangaswamy 2007). Notably, individuals at heightened risk for AUD commonly display deficits in response inhibition, cognitive control, and emotional regulation (i.e. aggressiveness/ irritability/mood lability), and often suffer from comorbid conditions (e.g. anxiety disorder, ADHD, conduct disorder, major depression, and antisocial personality disorder) that share features of behavioral and affective dysregulation. Also, offspring of alcoholics have been reported to have diverse neuropsychological deficits, and tend to exhibit electrophysiological abnormalities. Emerging literature suggests that these neurophysiological differences may be related to inherited variation in brain structures that are part of the neurocircuitry responsible for these differences. Although multiple pathways to alcohol use and abuse during adolescence and young adulthood have been identified, the mechanisms of heightened risk have not been fully elucidated. The purpose of this review is to elaborate on the neural underpinnings of risk for AUD.
