The tau hypothesis of Alzheimer’s disease assumes that the hyperphosphorylation of tau is the predominant mechanism [112], whereas according to the amyloid hypothesis of Alzheimer’s disease, accumulation of the amyloid plaque as a result of imbalance between production and clearance of Aβ peptide is the primary cause of the disease with development of neurofibrillary tangles, neuronal dysfunction, and degeneration as the secondary processes [113]. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.