Animal models of AD with cerebral Aβ accumulation show an increased expression of pro-inflammatory chemokines and cytokines, such as TNF-α, IFN-γ, IL-1b, and IL-6 [14,15,16], and there is evidence showing that the anti-inflammatory profile of microglia has an important role in reducing Aβ accumulation in AD [17]. This evidence concerns the gene TNF and Alzheimer disease.