MAPT and Alzheimer disease: The sequence of their development in OXYS rats is consistent with the modern understanding of the pathogenesis of the most common, i.e., sporadic (>90% of cases) form of AD: Dysfunction of mitochondria, tau protein hyperphosphorylation, an aberration of long-term post-tetanic potentiation, synaptic insufficiency, destructive changes in neurons, behavioral disorders, a decrease in cognitive functions at the early stages, aggravation of these functions during an increase in the amyloid-protein precursor level, enhanced accumulation of Aβ, and formation of Aβ plaques in the brain [12,13,14,15].