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探讨体力活动、β-淀粉样蛋白和 tau 之间的关系:叙述性综述。

Exploring the relationship between physical activity, beta-amyloid and tau: A narrative review.

机构信息

School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia; Australian Alzheimer's Research Foundation, Sarich Neuroscience Research Institute, Nedlands, Western Australia, Australia; Ageing, Cognition and Exercise Research Group, School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia.

School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia; Ageing, Cognition and Exercise Research Group, School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia.

出版信息

Ageing Res Rev. 2019 Mar;50:9-18. doi: 10.1016/j.arr.2019.01.003. Epub 2019 Jan 4.

Abstract

Several prospective cohort studies have reported an association between higher levels of physical activity and decreased risk of cognitive decline and dementia, years later. To support physical activity as a preventative measure against dementia, including Alzheimer's disease (AD; the most common form of dementia), evidence regarding the underlying mechanisms is vital. Here, we review previous work examining the role of physical activity in modulating levels of AD pathological hallmarks, beta-amyloid (Aβ) and tau (in the brain, cerebrospinal fluid and blood). Robust evidence from transgenic animal studies suggests that physical activity (voluntary wheel running) and exercise (forced wheel running) are implicated in lowering levels of brain Aβ and tau. Nevertheless, evidence from human studies, utilising measurements from positron emission tomography and cerebrospinal fluid biomarkers, is less consistent. Rigorous randomised controlled trials utilising long exercise interventions are vital to further understand the relationship between physical activity and Alzheimer's disease.

摘要

几项前瞻性队列研究报告称,较高水平的身体活动与日后认知能力下降和痴呆的风险降低有关。为了支持身体活动作为预防痴呆症(包括阿尔茨海默病,即最常见的痴呆症)的措施,关于潜在机制的证据至关重要。在这里,我们回顾了之前检查身体活动在调节阿尔茨海默病病理标志物(β-淀粉样蛋白(Aβ)和tau)水平中的作用的研究。来自转基因动物研究的有力证据表明,身体活动(自愿轮跑)和运动(强制轮跑)与降低大脑 Aβ和 tau 水平有关。然而,利用正电子发射断层扫描和脑脊液生物标志物进行的人体研究证据不太一致。利用长期运动干预进行严格的随机对照试验对于进一步了解身体活动与阿尔茨海默病之间的关系至关重要。

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