Although mechanisms of alcoholism remain to be elucidated, the molecular hypothesis postulates that that alcohol dependence and toxicity result from neuroadaptations to chronic alcohol consumption based on alterations in gene expression. Molecular and cellular adaptations in the nucleus accumbens, ventral tegmental area, amygdala and prefrontal cortex (PFC) [1], [2] have been implicated in the behavioral changes such as craving and relapse induced by chronic alcohol consumption. Chronic alcohol abuse also causes deficits in perceptual-motor skills, visual-spatial functions, abstraction and problem solving [3], [4]. These impairments may be related to alcohol-induced damage to the PFC and hippocampus [5], [6]. White matter and cell loss in the PFC, loss of hippocampal volume and shrinkage of hippocampal neurons are characteristic of these maladaptations [7]–[11].
