Here we demonstrated that significant cerebrovascular disturbances were observed in the hippocampus of OXYS rats at the age of 18 months, when the cognitive impairments and neurodegenerative processes in the brain were well pronounced and accompanied by significant accumulation of toxic forms of Аβ, formation of amyloid plaques, hyperphosphorylation of the tau protein, mitochondrial dysfunction, and a deficit of synapses [7–9]. The gene discussed is PPIB; the disease is amyloidosis.