The current model provides some indication of the neuroanatomical circuits that may underlie the core features of risk for AUD. Others have proposed similar brain regions associated with AUD, including the cerebellothalamocortical system (Sullivan 2003; Sullivan et al. 2003), extended amygdala (Koob and Le Moal 2008), and mesocorticolimbic dopamine system (Comings and Blum 2000; Blum et al. 2000; Bowirrat and Oscar-Berman, 2005; Makris et al. 2008). However, these conceptualizations have been largely based on the effects of chronic alcohol exposure on brain systems. The present review has focused on identifying the neural circuitry that may provides clues concerning how familial genetic loading for alcohol dependence is translated into higher risk for succeeding generations to become alcohol dependent as well. In doing so, we have described findings obtained in those with familial loading for AUD who have had minimal alcohol exposure at the time of examination. Consequently, the findings described do imply that abnormalities of the cerebellothalamocortical, extended limbic network, and HPA system may precede the initiation of alcohol use and are therefore particularly important in the etiology of AUD.
