Pluta Ryszard, Januszewski Sławomir, Czuczwar Stanisław J
Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, Poland.
Department of Pathophysiology, Medical University of Lublin, Jaczewskiego 8b Str., 20-090 Lublin, Poland.
Int J Mol Sci. 2021 Dec 28;23(1):306. doi: 10.3390/ijms23010306.
In this review, we summarize, inter alia, the protein and gene changes associated with Alzheimer's disease and their role in post-ischemic hippocampal neurodegeneration. In the hippocampus, studies have revealed dysregulation of the genes for the amyloid protein precursor metabolism and tau protein that is identical in nature to Alzheimer's disease. Data indicate that amyloid and tau protein, derived from brain tissue and blood due to increased permeability of the blood-brain barrier after ischemia, play a key role in post-ischemic neurodegeneration of the hippocampus, with concomitant development of full-blown dementia. Thus, the knowledge of new neurodegenerative mechanisms that cause neurodegeneration of the hippocampus after ischemia, resembling Alzheimer's disease proteinopathy, will provide the most important therapeutic development goals to date.
在本综述中，我们特别总结了与阿尔茨海默病相关的蛋白质和基因变化及其在缺血后海马神经退行性变中的作用。在海马体中，研究揭示了淀粉样蛋白前体代谢基因和tau蛋白的失调，其本质与阿尔茨海默病相同。数据表明，由于缺血后血脑屏障通透性增加，源自脑组织和血液的淀粉样蛋白和tau蛋白在海马体缺血后神经退行性变中起关键作用，并伴有全面痴呆的发展。因此，了解导致缺血后海马体神经退行性变的新神经退行性机制，类似于阿尔茨海默病蛋白病，将提供迄今为止最重要的治疗发展目标。
