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 interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-α, which resembled the alterations found in patients with AD [9]. This evidence concerns the gene APP and Alzheimer disease.