Alzheimer’s disease (AD) is a neurodegenerative disease characterized by two major histological hallmarks: (1) the neurofibrillary tangles (NFTs) corresponding to intracellular aggregates of abnormally hyperphosphorylated Tau protein (pTau) and, (2) senile plaques that are mainly composed of extracellular aggregates of β amyloid peptide (Aβ) derived from the sequential cleavage of its precursor, the amyloid precursor protein (APP), by β-secretase and γ-secretase enzymes [1,2]. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.