Alcohol dependent individuals are chronically exposed to large quantities of ethanol. This leads to multiple organ damage, including the liver (Osna, Donohue, & Kharbanda, 2017), brain (Zahr & Pfefferbaum, 2017) and immune system (Szabo & Saha, 2015). Gene expression studies of post mortem human brain tissue can shed light on how the brain is damaged by and adapts to chronic ethanol exposure (Farris, Arasappan, Hunicke-Smith, Harris, & Mayfield, 2015; Flatscher-Bader et al., 2006; Hermann et al., 2017; Mayfield, Ferguson, & Harris, 2013; McClintick et al., 2013). Changes to the brain include direct effects of ethanol and also insults caused by circulating cytokines that can cross the blood-brain barrier (Crews & Vetreno, 2016). These studies identified effects on NFκB, TLRs, IL1β and TNFα and thereby point toward neuroimmune signaling as an important effect of chronic ethanol exposure and potential contributor to AD (Crews & Vetreno, 2016; Mayfield et al., 2013; Pascual, Pla, Miñarro, & Guerri, 2014). Ethanol has been shown to potentiate and prolong the effects of proinflammatory cytokines and microglial activation (Qin et al., 2008). This suggests that immune cells
