In AD patients and AD mouse models, microglia clusters around plaques and vascular amyloid, moving toward newly formed plaques within 24 h of their formation as well as toward existing plaques [136,137], displaying an activated phenotype capable of producing cytokines and chemokines such as IL-1, IL-6, TNF-α, TGF-β1, TGF-β2, MIP-1α, and MCP-1, enriching the brain’s neuroinflammatory profile [138]. This evidence concerns the gene IL1B and Alzheimer disease.