In a mouse model of Alzheimer’s disease, IL-33 could reduce levels of β-amyloid (Aβ) in the brain, repair synaptic damage, and ameliorate the disease by promoting the recruitment and phagocytosis of microglia cells, as well as the secretion of anti-inflammatory factors by microglia cells and macrophages [216]. This evidence concerns the gene IL33 and early-onset autosomal dominant Alzheimer disease.