Several investigations have demonstrated that LPS is responsible for activating microglia and astrocytes and has the potential to enhance the expression level of pro-inflammatory cytokines, which in turn induce interleukin IL-1β, tumor necrosis factor (TNF-α), and nitric oxide (NO), specifically through the activation of nuclear factor-κB (NF-κB) signaling [14], further, leading to oxidative stress and synaptic failure [13], which are defining characteristics of AD [5,15]. This evidence concerns the gene TNF and Alzheimer disease.