Chronic neuroinflammation is well accepted as the most relevant pathological features of AD, regulating other pathological hallmarks of AD, such as the accumulation of amyloid-β (Aβ) and hyperphosphorylation of Tau, both of which are involved in the neuronal dysfunction in AD (Carlyle et al., 2014; Chen, 2015). This evidence concerns the gene MAPT and Alzheimer disease.