Understanding how individual differences in genetic risk factors influences the risk for AD across individuals requires interpreting gene effects across different systems because no single gene determines the overall risk for AD. While a complete review of the pharmacology and neurobiology of AD is beyond the scope of this paper, the moderate success of addiction pharmacotherapies highlights the importance of the opioid, GABA, serotonin, dopamine, and corticotropin-releasing factor systems in the liability to alcoholism. We refer readers to recent a review by Vengeliene et al. (2008), which describes the pharmacodynamic and pharmacokinetics of AD, a review by Heilig et al. (2011), which highlights brain systems that have been targeted by pharmacological agents in the treatment of alcoholism and a review by Koob and Volkow (2010) that describes different systems that facilitate preoccupation with addictive substances. Based on research in these areas, a key component to understanding alcohol’s effect on the brain can be found in variation both within and across biological mechanisms that regulate ethanol concentration and intercellular communication among neurons. Studies have demonstrated that the liver enzymes, alcohol dehydrogenase
