Expression levels of proinflammatory genes, microglial markers, and Aβ1–42 in the post-mortem basal forebrain negatively correlated with expression of ChAT as well as age of drinking onset, suggesting that heavy alcohol use initiated at an early age (i.e., adolescence) may contribute to AD-associated neuropathology later in life. The gene discussed is CHAT; the disease is Alzheimer disease.