New research suggests that pathological accumulation of Aβ is a key factor that drives neuroinflammatory responses in Alzheimer's disease; these Aβ aggregates bind to cell-surface receptors on microglia, inducing an inflammatory activation that results in the secretion of proinflammatory cytokines [19], including TNF-α, interleukin 1β, and IFN-γ. This evidence concerns the gene IFNG and Alzheimer disease.