Loss of BFCNs occurs in both AUD and AD [8, 9], and is accompanied by induction of proinflammatory neuroimmune signaling molecules, including Toll-like receptor 4 (TLR4), receptor for advanced glycation end-products (RAGE), and the endogenous TLR4/RAGE ligand high-mobility group box 1 (HMGB1) [10–12]. This evidence concerns the gene HMGB1 and Alzheimer disease.