Vascular Component of Neuroinflammation in Experimental Alzheimer’s Disease in Mice

New RAGE- and CD147-mediated mechanisms of damage to the hippocampus of mice due to the accumulation of amyloid β (Aβ), the development of local inflammation, metabolic disorders and damage to the blood–brain barrier in two experimental models of Alzheimer’s disease were studied in vivo. The new effects of Aβ in the hippocampal tissue in chronic Alzheimer’s type neurodegeneration, which characterize neuroplasticity disorders, were studied, as were angiogenesis, the structural and functional integrity of the blood–brain barrier, and the development of local neuroinflammation in conjunction with the features of the expression of RAGE and CD147 proteins. Early neurodegenerative changes in the hippocampus associated with the accumulation of Aβ are associated with the intensification of neoangiogenesis and the formation of aberrant intercellular contacts in the endothelial layer of cerebral microvessels in individual hippocampal subregions and the development of local neuroinflammation. As neurodegeneration progresses, neoangiogenesis in the hippocampus is suppressed.