Alcohol use disorders (AUD) are extremely prevalent, with an estimated 18 million Americans meeting diagnostic criteria for an AUD (2007 Survey on Alcohol and Drug Use). However, only a small subset of the wider population that regularly consumes alcohol will ever meet clinical criteria for alcohol abuse or alcoholism. AUD susceptibility is strongly influenced by genetic factors, accounting for as much as 40–60% of the risk for developing an AUD [1], [2]. While population and family-based association studies have discovered a number of genetic markers linked to AUD susceptibility [3], [4], [5], the highly complex and multifactorial nature of the disorder suggests that, independently, each of these associations accounts for only a small portion of the overall genetic variance. Moreover, the molecular mechanisms underlying the neuroplasticity accounting for AUD likely involves networks comprised of many more genes than currently identified as affecting behavioral responses to ethanol in animal models or genetically associated with AUD in humans.
