The role of innate, immune-related genes in alcohol dependency is supported by genetic association studies in humans (Pastor et al., 2000, 2005; Edenberg et al., 2008; Saiz et al., 2009), gene expression microarray studies in postmortem brains of alcoholics (Liu et al., 2006b; Ökvist et al., 2007), and transcriptome meta-analysis in rat brains (Mulligan et al., 2006). Furthermore, recent behavioral studies in mutant mice indicated that deletion of genes involved in aspects of the neuroimmune response to alcohol (B2m, Ctss, Il1rn, Cd14, and Il6) could reduce ethanol consumption in mice (Blednov et al., 2012). Based on these and additional related findings, a hypothesis is developing in part of the alcohol research community that the neurobiology of addiction is due to altered brain signaling driven by immune signaling.
