Microglia have complex roles that are detrimental and beneficial to AD pathogenesis: M1 phenotypes are characterized by the production of inducible nitric oxide synthase (iNOS) and inflammatory cytokines (such as IL-1β) and damage healthy cells, such as neurons, leading to Aβ accumulation; M2 phenotypes express mannose receptor (CD206) and arginase 1 (Arg1) and downregulate neuroinflammation and remove Aβ plaques. Here, IL1B is linked to Alzheimer disease.