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阿尔茨海默病中毛细血管功能障碍的发展

Development of capillary dysfunction in Alzheimer's disease.

作者信息

Vorobev S, Yanishevskiy S, Efimtsev S, Sokolov A, Dyachuk V

机构信息

Laboratory of Neurogenesis and Neurodevelopmental Disorders, World-Class Research Center for Personalized Medicine, Almazov Center, Saint-Petersburg, Russia.

出版信息

Front Aging Neurosci. 2024 Aug 29;16:1458455. doi: 10.3389/fnagi.2024.1458455. eCollection 2024.

DOI:10.3389/fnagi.2024.1458455
PMID:39267722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11391207/
Abstract

Alzheimer's disease (AD) is currently considered the major cause of cognitive impairment in older adults. This explains the close attention to the issue of AD research. The pathomorphological basis of the disease is a neurodegenerative process, the early stages of which are formed in the hippocampus and the morphofunctionally deep parts of the temporal lobes of the brain closely related to it. Several hypotheses have been advanced concerning the causes of neurodegeneration: the amyloid hypothesis, the calcium homeostasis impairment hypothesis, the inflammatory hypothesis, and the prion hypothesis. However, these hypotheses cannot explain the early stages of the pathogenesis of neurodegenerative diseases, in particular Alzheimer's disease. This health problem requires further comprehensive study of available data, as well as additional investigations to determine the nature of such a process. In this review, the data on microcirculatory disorders in the capillaries of the hippocampus and mediobasal structures of the temporal lobes of the brain, which may be an initiating factor that triggers neurodegenerative events, are analyzed.

摘要

阿尔茨海默病(AD)目前被认为是老年人认知障碍的主要原因。这解释了对AD研究问题的密切关注。该疾病的病理形态学基础是一个神经退行性过程,其早期阶段在海马体以及与其密切相关的大脑颞叶形态功能深层部位形成。关于神经退行性变的原因已经提出了几种假说:淀粉样蛋白假说、钙稳态受损假说、炎症假说和朊病毒假说。然而,这些假说无法解释神经退行性疾病,特别是阿尔茨海默病发病机制的早期阶段。这个健康问题需要对现有数据进行进一步的全面研究,以及进行额外的调查以确定这种过程的性质。在这篇综述中,分析了有关海马体和大脑颞叶中基底结构毛细血管微循环障碍的数据,这些障碍可能是引发神经退行性事件的起始因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38ac/11391207/3f293ca7d639/fnagi-16-1458455-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38ac/11391207/80087c51061c/fnagi-16-1458455-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38ac/11391207/3f293ca7d639/fnagi-16-1458455-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38ac/11391207/80087c51061c/fnagi-16-1458455-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38ac/11391207/3f293ca7d639/fnagi-16-1458455-g002.jpg

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本文引用的文献

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Oxidative stress in Alzheimer's disease: current knowledge of signaling pathways and therapeutics.阿尔茨海默病中的氧化应激:信号通路和治疗学的当前知识。
Mol Biol Rep. 2024 Jan 2;51(1):48. doi: 10.1007/s11033-023-09021-z.
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Capillary function progressively deteriorates in prodromal Alzheimer's disease: A longitudinal MRI perfusion study.前驱期阿尔茨海默病中毛细血管功能逐渐恶化:一项纵向MRI灌注研究。
Aging Brain. 2022 Feb 19;2:100035. doi: 10.1016/j.nbas.2022.100035. eCollection 2022.
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Capillary dysfunction correlates with cortical amyloid load in early Alzheimer's disease.
毛细血管功能障碍与早期阿尔茨海默病的皮质淀粉样蛋白负荷相关。
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Alzheimer's disease - Where do we go from here?阿尔茨海默病——我们将何去何从?
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5
Loss of perivascular aquaporin-4 localization impairs glymphatic exchange and promotes amyloid β plaque formation in mice.血管周围水通道蛋白-4定位的丧失会损害小鼠的类淋巴系统交换并促进淀粉样β斑块的形成。
Alzheimers Res Ther. 2022 Apr 26;14(1):59. doi: 10.1186/s13195-022-00999-5.
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PKCε Activation Restores Loss of PKCε, Manganese Superoxide Dismutase, Vascular Endothelial Growth Factor, and Microvessels in Aged and Alzheimer's Disease Hippocampus.蛋白激酶Cε(PKCε)激活可恢复衰老及阿尔茨海默病海马体中PKCε、锰超氧化物歧化酶、血管内皮生长因子和微血管的缺失。
Front Aging Neurosci. 2022 Mar 1;14:836634. doi: 10.3389/fnagi.2022.836634. eCollection 2022.
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