Experimental findings demonstrated that in AD pathogenesis, the 4.2-kD amyloid β peptide (Aβ)-dependent microglial activation leads to neuronal injury through a complex cascade by involving the secretion of various pro-inflammatory molecules such as tumor necrosis factor-α (TNF-α), interleukin (IL) IL-6, IL-1β, reactive oxygen species (ROS), and reactive nitrogen species (NOS) (Agostinho et al., 2010). This evidence concerns the gene TNF and Alzheimer disease.