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动脉粥样硬化与阿尔茨海默病交叉点上的免疫反应

Immune Response at the Crossroads of Atherosclerosis and Alzheimer's Disease.

作者信息

Stahr Natalie, Galkina Elena V

机构信息

Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA, United States.

出版信息

Front Cardiovasc Med. 2022 Jul 6;9:870144. doi: 10.3389/fcvm.2022.870144. eCollection 2022.

DOI:10.3389/fcvm.2022.870144
PMID:35872901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9298512/
Abstract

Alzheimer's disease (AD) and cardiovascular disease (CVD) are pathologies that are characterized by common signatures of vascular dysfunction and chronic inflammation that are accelerated with aging. Importantly, epidemiological studies report an independent interaction between AD and CVD and data suggest that chronic inflammation in CVD may accelerate AD development. Atherosclerosis affects most large to medium sized arteries including those supplying the cerebral circulation. Vascular dysfunction caused by atherosclerosis results in blood brain barrier breakdown, inflammation, an impaired clearance of amyloid-beta (Aβ), and finally ends with neurovascular dysfunction. Numerous data indicate that innate and adaptive immune responses shape atherogenesis and increasing evidence suggests an implication of the immune response in AD progression. Currently, mechanisms by which these two diseases are interconnected with each other are not well-defined. In this review, we discuss the recent advances in our understanding of the intertwined role of the immune response in atherosclerosis and AD and the implications of these findings for human health.

摘要

阿尔茨海默病(AD)和心血管疾病(CVD)是具有血管功能障碍和慢性炎症共同特征的病理状态,且这些特征会随着年龄增长而加速。重要的是,流行病学研究报告了AD与CVD之间存在独立的相互作用,数据表明CVD中的慢性炎症可能会加速AD的发展。动脉粥样硬化影响大多数大中型动脉,包括那些为脑循环供血的动脉。动脉粥样硬化引起的血管功能障碍会导致血脑屏障破坏、炎症、β淀粉样蛋白(Aβ)清除受损,最终导致神经血管功能障碍。大量数据表明,先天性和适应性免疫反应塑造了动脉粥样硬化的发生发展,越来越多的证据表明免疫反应在AD进展中也有影响。目前,这两种疾病相互关联的机制尚不清楚。在这篇综述中,我们讨论了我们对免疫反应在动脉粥样硬化和AD中相互交织作用的最新理解进展,以及这些发现对人类健康的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/036a/9298512/b0f463d74535/fcvm-09-870144-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/036a/9298512/95bfebd0bd03/fcvm-09-870144-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/036a/9298512/b0f463d74535/fcvm-09-870144-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/036a/9298512/95bfebd0bd03/fcvm-09-870144-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/036a/9298512/b0f463d74535/fcvm-09-870144-g0002.jpg

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CD4+ effector T cells accelerate Alzheimer's disease in mice.CD4+效应 T 细胞加速了小鼠的阿尔茨海默病进程。
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IL-17 triggers the onset of cognitive and synaptic deficits in early stages of Alzheimer's disease.
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Improvements in Exercise for Alzheimer's Disease: Highlighting FGF21-Induced Cerebrovascular Protection.阿尔茨海默病运动疗法的进展:聚焦成纤维细胞生长因子21诱导的脑血管保护作用
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