IL1B and Alzheimer disease: However, the perpetual accumulation of Aβ in AD and the associated toxicity induced by oligomeric Aβ species skews the activation of these cells into a proinflammatory phenotype that enhances synaptic loss via microglia-mediated phagocytosis [16] and exacerbates neurodegeneration through the release of neurotoxic proinflammatory mediators, including IL-1β, IL-6 and TNFα [19, 27, 28, 30], that contribute to the development of the chronic neuroinflammation observed in AD.