Although the etiology of AD is still rather vague, multiple neuropathological hallmarks of AD have been characterized, including insoluble, extracellular aggregates of amyloid-β peptides (Aβ), named amyloid plaques, and intracellular accumulations of hyperphosphorylated microtubule-associated protein tau, named neurofibrillary tangles (NFTs), as well as neuronal loss [1–4]. This evidence concerns the gene MAPT and Alzheimer disease.