Overexpression of mutant forms of amyloid β-protein precursor (APP) in the brains of transgenic mice produced amyloid plaques surrounded by activated microglia and reactive astrocytes and upregulated IL-1β, IL-6, and TNF-α, which resembled the alterations found in patients with AD (Morgan et al., 2005; Jin et al., 2008). Here, IL1B is linked to Alzheimer disease.