IL1B and Alzheimer disease: Animal models and in vitro studies indicate that astrocytes respond to immune- and AD-associated triggers, such as TNF-α, IFN-γ, IL-1β, bacterial lipopolysaccharide and Aβ by releasing cytokines and modifying the expression and activity of APP processing enzymes, which in turn exacerbate neuroinflammatory and neuropathological changes in the AD brain [19, 20, 27–30].