Abstract

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.

中文翻译：

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实验性阿尔茨海默氏病小鼠神经炎症的血管成分

摘要

在两个阿尔茨海默氏病实验模型中，由于淀粉样β（Aβ）的积累，局部炎症的发展，代谢紊乱和血脑屏障的破坏，RAGE和CD147介导的小鼠海马损伤的新机制是在体内进行了研究。研究了Aβ在慢性阿尔茨海默氏型神经变性中海马组织中的新作用，这种作用表征了神经可塑性疾病，还研究了血管生成，血脑屏障的结构和功能完整性以及局部神经炎症的发展及其特征。 RAGE和CD147蛋白的表达 与Aβ积累相关的海马早期神经退行性变化与新血管生成的加剧以及单个海马亚区域的脑微血管内皮层中异常细胞间接触的形成以及局部神经炎症的发展有关。随着神经变性的发展，海马中的新血管生成被抑制。