IL1B and Alzheimer disease: This is manifested as overactivation of glial cells, which turn into a pro‐inflammatory phenotype, and then produce numerous neuroinflammatory factors, including tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6, interferon and nitric oxide (NO), which promote the development of AD pathology and induce progressive degeneration and death of neurons.2