IL1B and Alzheimer disease: Activated microglia are able to secrete vast amounts of proinflammatory cytokines, such as tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β, which generate neuroinflammation and cause neuronal apoptosis or death, eventually resulting in the behavioral and psychological symptoms of AD.4, 5 Therefore, based on the neuropathological features of the AD etiology, the inhibition of microglial activation and the protection of neurons from neuroinflammation may be an alternative strategy that could be used for the treatment of AD.