Alteration of these cellular pathways results in the accumulation of specific pathogenic proteins, for instance, extracellular amyloid beta (Aβ) plaques and intraneuronal tau-containing neurofibrillary tangles (NFTs) in AD or misfolded α-synuclein (α-syn) in PD, which are ultimately responsible for the clinical and pathological diversity of disease phenotypes [9]. This evidence concerns the gene MAPT and Alzheimer disease.