Following this paradigm, the most commonly used animal models of AD are designed to recapitulate the lesions of AD [5], namely amyloid-β (Aβ) plaques and neurofibrillary tangles through transgenic induction of mutations related to amyloid and tau production (amyloid precursor protein (APP), presenilin-1 (PS1) and PS2, or tau mutations [6,1,7]). This evidence concerns the gene MAPT and Alzheimer disease.