Department of Pathophysiology, Medical University of Lublin, 20-059 Lublin, Poland.
Int J Mol Sci. 2023 Jun 27;24(13):10739. doi: 10.3390/ijms241310739.
The aim of this review is to present evidence of the impact of ischemic changes in the blood-brain barrier on the maturation of post-ischemic brain neurodegeneration with features of Alzheimer's disease. Understanding the processes involved in the permeability of the post-ischemic blood-brain barrier during recirculation will provide clinically relevant knowledge regarding the neuropathological changes that ultimately lead to dementia of the Alzheimer's disease type. In this review, we try to distinguish between primary and secondary neuropathological processes during and after ischemia. Therefore, we can observe two hit stages that contribute to Alzheimer's disease development. The onset of ischemic brain pathology includes primary ischemic neuronal damage and death followed by the ischemic injury of the blood-brain barrier with serum leakage of amyloid into the brain tissue, leading to increased ischemic neuronal susceptibility to amyloid neurotoxicity, culminating in the formation of amyloid plaques and ending in full-blown dementia of the Alzheimer's disease type.
本文旨在阐述血脑屏障缺血改变对具有阿尔茨海默病特征的缺血后脑神经退行性变成熟的影响的证据。了解再灌注期间缺血后血脑屏障通透性的相关过程，将为最终导致阿尔茨海默病类型痴呆的神经病理变化提供具有临床相关性的知识。在本文中，我们试图在缺血期间和之后区分原发性和继发性病理过程。因此，我们可以观察到两个导致阿尔茨海默病发展的打击阶段。缺血性脑病理的发病包括原发性缺血性神经元损伤和死亡，随后是血脑屏障的缺血性损伤，导致淀粉样蛋白漏入脑组织，增加了缺血性神经元对淀粉样蛋白神经毒性的易感性，最终形成淀粉样斑块，并导致完全型阿尔茨海默病类型的痴呆。
