The sequence of these diseases is as follows: dysfunction of mitochondria, hyperphosphorylation of tau protein, disruption of long-term post-tetanic potentiation, synaptic insufficiency, destructive changes in neurons, behavioral disorders and a decrease in cognitive functions in the early stages and their progression against the background of an increase in the level of APP, and increased accumulation of Aβ and the formation of amyloid plaques in the brain, corresponding to modern ideas about the pathogenesis of the sporadic form of this disease in humans [19]. This evidence concerns the gene MAPT and Atypical behavior.