In AD, senile plaque deposition can activate M1 microglia, reduce the phagocytosis and clearance of senile plaque deposits, and release neurotoxic substances, such as TNF-α, IL-1β, IL-6, chemokines, and reactive oxygen and nitrogen species, leading to an increased neuroinflammatory response and neurodegeneration [35, 36]. Here, IL6 is linked to Alzheimer disease.