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Is it possible to maintain a plaque-free healthy brain by treadmill?

作者信息

Pahan Swarupa, Pahan Kalipada

机构信息

Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA (Pahan S, Pahan K).

Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA (Pahan K).

出版信息

Neural Regen Res. 2025 Dec 1;20(12):3525-3526. doi: 10.4103/NRR.NRR-D-24-00936. Epub 2024 Nov 13.

DOI:10.4103/NRR.NRR-D-24-00936
PMID:39589729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11974655/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee2/11974655/e7c42663faa5/NRR-20-3525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee2/11974655/e7c42663faa5/NRR-20-3525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee2/11974655/e7c42663faa5/NRR-20-3525-g001.jpg

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Is it possible to maintain a plaque-free healthy brain by treadmill?通过跑步机锻炼有可能维持大脑无斑块且保持健康吗?
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2
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Exercise-induced asthma in children: a comparative study of free and treadmill running.儿童运动诱发性哮喘:自由跑步与跑步机跑步的比较研究
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Treadmill exercise enhances synaptic plasticity, but does not alter β-amyloid deposition in hippocampi of aged APP/PS1 transgenic mice.跑步机运动可增强突触可塑性,但不会改变老年APP/PS1转基因小鼠海马体中的β-淀粉样蛋白沉积。
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本文引用的文献

1
Identification of Cinnamein, a Component of Balsam of Tolu/Peru, as a New Ligand of PPARα for Plaque Reduction and Memory Protection in a Mouse Model of Alzheimer's Disease.鉴定秘鲁香脂中的成分肉桂酸甲酯作为过氧化物酶体增殖物激活受体α(PPARα)的新型配体,用于在阿尔茨海默病小鼠模型中减少斑块和保护记忆。
J Alzheimers Dis Rep. 2024 May 24;8(1):903-922. doi: 10.3233/ADR-230179. eCollection 2024.
2
Tau fibrils induce glial inflammation and neuropathology via TLR2 in Alzheimer's disease-related mouse models.tau 纤维通过 TLR2 在阿尔茨海默病相关的小鼠模型中诱导神经胶质炎症和神经病理学。
J Clin Invest. 2023 Sep 15;133(18):e161987. doi: 10.1172/JCI161987.
3
Treadmill workout activates PPARα in the hippocampus to upregulate ADAM10, decrease plaques and improve cognitive functions in 5XFAD mouse model of Alzheimer's disease.
跑步机锻炼激活海马体中的 PPARα,上调 ADAM10,减少斑块并改善阿尔茨海默病 5XFAD 小鼠模型的认知功能。
Brain Behav Immun. 2023 Mar;109:204-218. doi: 10.1016/j.bbi.2023.01.009. Epub 2023 Jan 19.
4
Treadmill exercise reduces α-synuclein spreading via PPARα. treadmill 运动通过 PPARα 减少 α-突触核蛋白的扩散。
Cell Rep. 2022 Jul 12;40(2):111058. doi: 10.1016/j.celrep.2022.111058.
5
Selective Secretase Targeting for Alzheimer's Disease Therapy.选择性分泌酶靶向治疗阿尔茨海默病。
J Alzheimers Dis. 2021;81(1):1-17. doi: 10.3233/JAD-201027.
6
Treadmill Exercise Decreases Aβ Deposition and Counteracts Cognitive Decline in APP/PS1 Mice, Possibly Hippocampal Microglia Modifications.跑步机运动可减少APP/PS1小鼠的Aβ沉积并对抗认知衰退,可能与海马小胶质细胞的改变有关。
Front Aging Neurosci. 2019 Apr 5;11:78. doi: 10.3389/fnagi.2019.00078. eCollection 2019.
7
Selective disruption of TLR2-MyD88 interaction inhibits inflammation and attenuates Alzheimer's pathology.选择性破坏 TLR2-MyD88 相互作用可抑制炎症反应并减轻阿尔茨海默病病理。
J Clin Invest. 2018 Oct 1;128(10):4297-4312. doi: 10.1172/JCI96209. Epub 2018 Jul 10.
8
Activation of peroxisome proliferator-activated receptor α stimulates ADAM10-mediated proteolysis of APP.过氧化物酶体增殖物激活受体α的激活刺激了ADAM10介导的淀粉样前体蛋白的蛋白水解。
Proc Natl Acad Sci U S A. 2015 Jul 7;112(27):8445-50. doi: 10.1073/pnas.1504890112. Epub 2015 Jun 15.
9
ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function.ADAM10 错义突变通过损害前导肽伴侣功能促进 β-淀粉样蛋白的积累。
Neuron. 2013 Oct 16;80(2):385-401. doi: 10.1016/j.neuron.2013.08.035. Epub 2013 Sep 19.
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Blocking ADAM10 synaptic trafficking generates a model of sporadic Alzheimer's disease.阻断 ADAM10 突触转运可建立散发性阿尔茨海默病模型。
Brain. 2010 Nov;133(11):3323-35. doi: 10.1093/brain/awq217. Epub 2010 Aug 30.