Increasing evidence suggests that AD pathogenesis is not only limited to the production of misfolded or aggregated Aβ and Tau-hyperphosphorylation but also depends on the innate immune response through activation of microglia/astrocytes leading to the activation of inflammatory pathways that induce neuronal apoptosis in response to the excessive Aβ production (Heneka et al., 2015; Calsolaro and Edison, 2016; Ardura-Fabregat et al., 2017). This evidence concerns the gene MAPT and Alzheimer disease.