In different preclinical models of AD, we have already shown the Aβ(1–42)-induced increase in expression level of both inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, which are two enzymes responsible for NO and prostaglandins production, respectively, as well as of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α [38,79,80]. This evidence concerns the gene IL6 and Alzheimer disease.