In summary, recent studies continue to show that corticolimbic systems, such as the PFC, mesolimbic reward system and hippocampus, are undergoing significant developmental transitions during adolescence that make them primary targets for alcohol-induced structural and functional changes [5,7,26,38]. The adolescent's decreased response to the negative aspects of alcohol consumption (motor impairment, sedation, anxiety, and social depression) coupled with increased or altered response to the positive and rewarding effects of alcohol may promote excessive intake. Repeated exposure to excessive intake and the adolescent's enhanced susceptibility to alcohol-induced damage - whether through toxicity, teratogenicity, or other effects on plasticity - further dysregulates behavioral control of consumption. Thus, the adolescent's unique response to alcohol combined with increased susceptibility to alcohol-induced neurodegeneration interact to facilitate excessive alcohol consumption, the hallmark of an AUD. However, the mechanisms behind the adolescent's unique response to and consequences of alcohol use/abuse are not well understood. Additional research is desperately needed to understand the responses and consequences of alcohol exposure on the dynamic and developing adolescent brain. Because AUDs commonly begin in adolescence and AUDs affect over 8% of
