Given the role of neuroimmune activation in drug reward, dependence [1*–3], depression-negative affect [64], and neurodegeneration [65] and the involvement of all of these pathologies in alcohol abuse, the possibility of an overactive immune system promoting alcohol consumption is a hypothesis that we can now consider. Interestingly, abstinence from alcohol and other drugs of abuse is regulated by a common gene network that includes the transcription factor NF-κB [66], which may also regulate development of dependence to alcohol [42]. Thus, common gene networks containing neuroimmune genes may be a hallmark of adaptive molecular mechanisms of drug dependence and abstinence. Although the translocation and amplification of neuroimmune signaling complicates our understanding of alcohol’s direct effect on innate immunity, the role of alcoholism as a chronic inflammatory disease opens a new chapter in alcohol research. Treatment strategies that target innate immune responses in the peripheral and central nervous systems may uncover revolutionary therapies for this neurodegenerative disease and address the pivotal role of neuroimmune signaling in the neurobiology of alcoholism.
