In early stages of AD, microglia activation becomes protective and delays the disease progression by effective clearance of pathological lesions [55–57], while in the later stages, microglia lose their protective function and release pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) [4,5,58–60]. This evidence concerns the gene IL1B and Alzheimer disease.