IL1B and Alzheimer disease: In the early stages of AD pathogenesis, Aβ deposition–induced inflammatory responses activate microglia and astrocytes, which secrete pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), transforming growth factor-α, and chemokines and 5-lipoxygenase (5-LO), and thus disrupting the blood–brain barrier and exacerbating neuronal damage in the hippocampus, eventually worsening the presentation of early-stage AD [18,65,68,69,70].