Intriguingly, the administration and modulation of IL-33 were found to alleviate the neuropathology of AD in mice by reducing the soluble βA levels and plaque accumulation through the recruitment of βA phagocytic activity and the proinflammatory responses involving of IL-1β, IL-6, and NLR family pyrin domain containing 3 (NLRP3) through the polarisation of macrophages/microglia [16]. Here, NLRP3 is linked to Alzheimer disease.