Deposition of Aβ was shown to trigger the activation of both astrocytes and microglia leading to the production of pro-inflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, among other inflammatory mediators (Wyss-Coray, 2006), thus generating neuroinflammation and contributing to AD progression and severity (Heneka et al., 2015). This evidence concerns the gene TNF and Alzheimer disease.