Among the many findings implicating inflammation in AD mechanisms: the presence of pro-inflammatory cytokines, chemokines, acute-phase reactants, and other mediators of inflammation in AD brains [6, 7]; the mutual antagonism between NFκB (nuclear factor κ-light-chain enhancer of activated B cells) and the sirtuin SirT1 [8] is altered in favor of inflammation, with reduced SirT1, in the brains of patients with AD [9]; genomic studies implicate multiple inflammation-associated genes in AD [10]; and phagocytosis of amyloid-β peptide is reduced by inflammation in patients with AD [11]. This evidence concerns the gene NFKB1 and Alzheimer disease.