Under abnormal conditions, microglia are activated, and although they do initially have a defensive role, if abnormal stimuli persist, chronic neuroinflammation occurs, and the release of cytokines (TNF-α, IL-1β, etc.) leads to a proinflammatory response, and the persistence of these cytokines continues to induce the production of APP in the AD brain, which itself has a disrupted Aβ homeostasis and produces more APP. This evidence concerns the gene APP and Alzheimer disease.