阿尔茨海默病模型中运动诱导的神经炎症调节。

Áine M Kelly
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引用次数: 0

摘要

阿尔茨海默病(AD)是一种以毒性β-β淀粉样蛋白(aβ)斑块积聚为特征的渐进性神经退行性疾病,是全球痴呆症的主要原因之一。作为AD标志的认知障碍可能是由aβ蛋白的存在引发和维持的大脑炎症引起的,最终导致神经元功能障碍和丧失。由于AD具有重要的炎症成分,因此推测抗炎策略可能对AD具有预防或治疗作用。其中一种策略是定期进行体育活动,流行病学研究表明,这种策略可以预防包括AD在内的各种形式的痴呆。运动在外周器官中诱导抗炎环境,并增加大脑中抗炎分子的表达。在这里,我们回顾了主要来自AD动物模型的证据,支持运动可以通过调节神经炎症来减少或减缓与AD相关的细胞和认知障碍的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exercise-Induced Modulation of Neuroinflammation in Models of Alzheimer's Disease.

 Alzheimer's disease (AD), a progressive, neurodegenerative condition characterised by accumulation of toxic βeta-amyloid (Aβ) plaques, is one of the leading causes of dementia globally. The cognitive impairment that is a hallmark of AD may be caused by inflammation in the brain triggered and maintained by the presence of Aβ protein, ultimately leading to neuronal dysfunction and loss. Since there is a significant inflammatory component to AD, it is postulated that anti-inflammatory strategies may be of prophylactic or therapeutic benefit in AD. One such strategy is that of regular physical activity, which has been shown in epidemiological studies to be protective against various forms of dementia including AD. Exercise induces an anti-inflammatory environment in peripheral organs and also increases expression of anti-inflammatory molecules within the brain. Here we review the evidence, mainly from animal models of AD, supporting the hypothesis that exercise can reduce or slow the cellular and cognitive impairments associated with AD by modulating neuroinflammation.

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