The continual accumulation of Aβ in AD pathogenesis induces significant increases in [Ca2+]i in astrocytes and in microglia [10, 11], resulting in the secretion of proinflammatory cytokines, including IL-1β and TNFα, from these cells [21], as confirmed here for microglia using the model BV2 line (Fig. 3), in a feed-forward mechanism that skews their activation state to a proinflammatory phenotype that exacerbates neuronal death [104, 105]. Here, IL1B is linked to Alzheimer disease.