Throughout AD progression, the long-term exposure to damage-associated molecular patterns (DAMPs) causes a noteworthy oxidative stress, endoplasmic reticulum (ER) stress, and the generation of NOD-like receptor protein 3 (NLRP3) in the activated microglia, thereby stimulating the insertion of nuclear factor kappa B (NF-κB) into nucleus, and up-regulating inflammatory genes such as IL-18 and IL-1β to reestablish neural homeostasis [68]. Here, IL1B is linked to Alzheimer disease.