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The proteostatic effects of traffic-derived air pollution on Alzheimer's disease risk.
Open Biology ( IF 5.8 ) Pub Date : 2020-08-19 , DOI: 10.1098/rsob.200146
Elise A Kikis 1
Affiliation  

Alzheimer's disease (AD) is an age-related neurodegenerative disease and the leading cause of dementia in the elderly. Recent decades have been marked by considerable advances in our understanding of genetic and environmental risk factors and also of the AD mechanism(s) of action. Nonetheless, there is still no cure and the myriad ways AD affects the brain is overwhelmingly complex. Such complexity is manifest in part by the fact that genetic background interacts with the environment, including traffic-derived particulate air pollution, to greatly exacerbate AD risk. Determining the mechanisms by which particulate air pollution acts as an AD risk factor has the potential to reveal yet unknown aspects of AD pathology. This review carefully peels back the layers of complexity to discern whether a unifying disease model, one with proteostasis imbalance at its core, holds up to scrutiny in light of the recent literature. While the data are compelling, it is now time for carefully designed studies to definitively determine whether particulate air pollution acts with ageing, genetic background and other sources of proteotoxic stress to disrupt the delicate proteostasis balance.



中文翻译:

交通源性空气污染对阿尔茨海默病风险的蛋白质抑制作用。

阿尔茨海默病 (AD) 是一种与年龄相关的神经退行性疾病,也是老年人痴呆的主要原因。近几十年来,我们对遗传和环境风险因素以及 AD 作用机制的理解取得了重大进展。尽管如此,仍然没有治愈方法,并且 AD 影响大脑的无数方式极其复杂。这种复杂性部分体现在遗传背景与环境相互作用的事实,包括交通衍生的颗粒空气污染,从而大大加剧 AD 风险。确定颗粒物空气污染作为 AD 风险因素的机制有可能揭示 AD 病理学尚不为人知的方面。这篇评论仔细地剥离了复杂的层次,以辨别一个统一的疾病模型,根据最近的文献,以蛋白质平衡失衡为核心的一种经得起审查。虽然数据令人信服,但现在是时候进行精心设计的研究,以明确确定颗粒空气污染是否与衰老、遗传背景和其他蛋白毒性压力来源有关,从而破坏微妙的蛋白稳态平衡。

更新日期:2020-08-19
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