Unraveling the molecular mechanisms of alcohol dependence

Alcohol dependence (AD) is a common, chronic, relapsing disorder. Compelling epidemiological evidence indicates that >50% of the risk for becoming alcoholic stems from genetic susceptibility and genetic studies have identified several risk genes. Alcohol intake alters gene expression patterns, thereby producing long-lasting cellular and molecular adaptations that might explain the development and maintenance of AD. The heterogeneous nature of AD indicates a complex etiology involving mechanisms related to motivational behavior, reward and learning, adaptations in signaling pathways owing to interactions between alcohol and target molecules, and chromatin remodeling. Emerging methodologies present opportunities to determine how alcohol might disrupt the synergistic actions of molecular systems and to assess gene-environment interactions for elucidating the behavioral and physiological dysfunctions underlying AD.