Specifically in Alzheimer’s disease, it has been shown that in addition to plaques and neurofibrillary tangles, chronic neuroinflammation is the third main pathological feature of Alzheimer’s disease, and is generated by the activation of microglia cells and the release of cytokines [87] such as TNF-α, a proinflammatory cytokine, which is elevated in patients with Alzheimer’s disease [88,89] as well as IL-6, IL-12, and IL-18, IFN-γ, chemokine (MCP-1), and other neurotoxic agents [90,91]. This evidence concerns the gene TNF and early-onset autosomal dominant Alzheimer disease.