Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.

IF 2.9 Q2 NEUROSCIENCES
Neuroscience Insights Pub Date : 2025-03-20 eCollection Date: 2025-01-01 DOI:10.1177/26331055251323292
Gabrielle Cognacq, Jonathan E Attwood, Gabriele C DeLuca
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引用次数: 0

Abstract

Traumatic brain injury (TBI) is a modifiable risk factor for Alzheimer's disease (AD). TBI and AD share several histopathological hallmarks: namely, beta-amyloid aggregation, tau hyperphosphorylation, and plasma protein infiltration. The relative contributions of these proteinopathies and their interplay in the pathogenesis of both conditions remains unclear although important differences are emerging. This review synthesises emerging evidence for the critical role of the neurovascular unit in mediating protein accumulation and neurotoxicity in both TBI and AD. We propose a shared pathogenic cascade centred on a neurovascular unit, in which increased blood-brain barrier permeability induces a series of noxious mechanisms leading to neuronal loss, synaptic dysfunction and ultimately cognitive dysfunction in both conditions. We explore the application of this hypothesis to outstanding research questions and potential treatments for TBI and AD, as well as other neurodegenerative and neuroinflammatory conditions. Limitations of this hypothesis, including the challenges of establishing a causal relationship between neurovascular damage and proteinopathies, are also discussed.

创伤性脑损伤和阿尔茨海默病:一个共同的神经血管假说。
创伤性脑损伤(TBI)是阿尔茨海默病(AD)的一个可改变的危险因素。TBI和AD有几个共同的组织病理学特征:即β -淀粉样蛋白聚集、tau蛋白过度磷酸化和血浆蛋白浸润。这些蛋白病变的相对作用及其在这两种疾病的发病机制中的相互作用仍不清楚,尽管重要的差异正在出现。这篇综述综合了神经血管单位在TBI和AD中介导蛋白质积累和神经毒性的关键作用的新证据。我们提出了以神经血管单元为中心的共同致病级联,其中血脑屏障通透性增加诱导了一系列有害机制,导致两种情况下的神经元丧失、突触功能障碍和最终的认知功能障碍。我们将探索这一假设在TBI和AD以及其他神经退行性和神经炎症疾病的突出研究问题和潜在治疗中的应用。这一假设的局限性,包括在神经血管损伤和蛋白质病变之间建立因果关系的挑战,也进行了讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neuroscience Insights
Neuroscience Insights Neuroscience-Neuroscience (all)
CiteScore
6.10
自引率
0.00%
发文量
24
审稿时长
9 weeks
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