Although the role of AD-associated pathologies in AD onset as a causal agent is uncertain, it remains evident that the accumulations of Aβ and tau contribute to the progression of neurodegeneration and synaptic dysfunction, which give rise to cognitive deficits and clinical symptoms in AD (Ballatore et al., 2007; Crews and Masliah, 2010). This evidence concerns the gene MAPT and Alzheimer disease.