While the exact pathogenic contribution of these two AD hallmarks and their constituents, such as aggregation-prone amyloid β (Aβ) peptide species and hyperphosphorylated tau protein, remain unclear, a growing body of evidence suggests that their development may be paralleled or even preceded by alterations or dysfunctions in the endolysosomal and the autophagic systems [4]. This evidence concerns the gene MAPT and Alzheimer disease.