Treadmill exercise produces neuroprotective effects in a murine model of Parkinson’s disease by regulating the TLR2/MyD88/NF-κB signaling pathway

Koo, Jung-Hoon; Jang, Yong-Chul; Hwang, Dong-Ju; Um, Hyun-Seob; Lee, Namhee; Jung, Jae Hwan; Cho, Joon-Yong

doi:10.1016/j.neuroscience.2017.05.016

Cited by 55 publications

(32 citation statements)

References 37 publications

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“…Jang et al [22] suggested that exercise protects against the neuronal degeneration in PD by attenuating neuroinflammation. Koo et al [23] also analyzed the neuroprotective effect of exercise in PD and indicated the mediating role of the TLR2/MyD88/NF-κB signaling pathway in the protective influence. As a frequent neurodegenerative disease in the elderly, AD has also been reported to be improved by physical exercise [24,25].…”

Section: Discussionmentioning

confidence: 99%

Physical Exercise Ameliorates the Cognitive Function and Attenuates the Neuroinflammation of Alzheimer’s Disease via miR-129–5p

Chen

Liu

et al. 2020

Dement Geriatr Cogn Disord

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Introduction: Physical exercise has a significant neuroprotective role in Alzheimer's disease (AD), but the underlying mechanisms remain elusive. Objective: This study aimed to explore the molecular mechanisms of physical exercise by analyzing the role of microRNA-129-5p (miR-129-5p) in AD mice and patients. Methods: AD mice and patients were treated with 4-week and 3-month physical exercise, respectively. The expression of miR-129-5p was measured using quantitative realtime PCR. The Morris water-maze test was used for cognition evaluation, and enzyme-linked immunosorbent assay was used for inflammation analysis. Results: In both AD mice and patients, the expression of miR-129-5p was elevated by physical exercise. By in vivo regulation of miR-129-5p, we found that the improved cognitive function and reduced inflammatory responses were reversed by the knockdown of miR-129-5p. In patients with AD, the serum expression of miR-129-5p was further found to be correlated with the serum levels of cognitive function markers and proinflammatory cytokines. Conclusion: All data indicated that the expression of miR-129-5p in AD mice and patients is significantly upregulated by physical exercise. The knockdown of miR-129-5p can abrogate the neuroprotective effect of exercise on cognition and neuroinflammation in AD mice. This study provides a novel insight into the molecular mechanisms underlying the neuroprotective effect of physical exercise in AD, and miR-129-5p may provide a novel therapeutic target for AD treatment.

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Section: Discussionmentioning

confidence: 99%

Physical Exercise Ameliorates the Cognitive Function and Attenuates the Neuroinflammation of Alzheimer’s Disease via miR-129–5p

Chen

Liu

et al. 2020

Dement Geriatr Cogn Disord

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“…The moderate treadmill exercise and one-time exhaustion exercise, in addition to effectively reducing the risk of PD [1], can also enhance motor deficits in PD patients [54], improve cognitive impairment, and depression [50], which is consistent with the role of light physical activity. Besides, animal experiments demonstrated that moderate to vigorous physical exercise could enhance mitochondrial function [69] and reduce oxidative stress [70,71] in the brain of PD mice. More importantly, exercise can reduce the accumulation of the pathogenic protein α-Syn and prevent neuronal apoptosis [71].…”

Section: Therapy Regimen By Comparing the Effects Of Differentmentioning

confidence: 99%

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

Fan

Jabeen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Aim. This study was aimed at investigating the effects and molecular mechanisms of physical activity intervention on Parkinson’s disease (PD) and providing theoretical guidance for the prevention and treatment of PD. Methods. Four electronic databases up to December 2019 were searched (PubMed, Springer, Elsevier, and Wiley database), 176 articles were selected. Literature data were analyzed by the logic analysis method. Results. (1) Risk factors of PD include dairy products, pesticides, traumatic brain injury, and obesity. Protective factors include alcohol, tobacco, coffee, black tea, and physical activity. (2) Physical activity can reduce the risk and improve symptoms of PD and the beneficial forms of physical activity, including running, dancing, traditional Chinese martial arts, yoga, and weight training. (3) Different forms of physical activity alleviate the symptoms of PD through different mechanisms, including reducing the accumulation of α-syn protein, inflammation, and oxidative stress, while enhancing BDNF activity, nerve regeneration, and mitochondrial function. Conclusion. Physical activity has a positive impact on the prevention and treatment of PD. Illustrating the molecular mechanism of physical activity-induced protective effect on PD is an urgent need for improving the efficacy of PD therapy regimens in the future.

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“…In this context, candesartan cilexetil, a drug used for treatment of hypertension also known to suppress the expression of TLR2, reversed the pro-inflammatory microglia phenotype activated by α-synuclein exposure (Daniele et al, 2015 ). Interestingly, TLR2 and its downstream signaling were shown to play a key role in the neuroprotective effects achieved through exercise approaches in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD (Jang et al, 2017 ; Koo et al, 2017 ).…”

Section: Tlr2mentioning

confidence: 99%

Role of Microglia TLRs in Neurodegeneration

Fiebich

Cra

et al. 2018

Front. Cell. Neurosci.

228

152

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Toll-like receptors (TLRs) are a group of receptors widely distributed in the organism. In the central nervous system, they are expressed in neurons, astrocytes and microglia. Although their involvement in immunity is notorious, different articles have demonstrated their roles in physiological and pathological conditions, including neurodegeneration. There is increasing evidence of an involvement of TLRs, especially TLR2, 4 and 9 in neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). In this sense, their expression in microglia might modulate the activity of these cells, which in turn, lead to protective or deleterious effects over neurons and other cells. Therefore, TLRs might mediate the link between inflammation and neurodegenerative diseases. However, further studies have to be performed to elucidate the role of the other TLRs in these diseases and to further prove and confirm the pathophysiological role of all TLRs in neurodegeneration. In this article, we revise and summarize the current knowledge regarding the role of TLRs in neurodegeneration with the focus on the possible functions of these receptors in microglia.

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Treadmill exercise produces neuroprotective effects in a murine model of Parkinson’s disease by regulating the TLR2/MyD88/NF-κB signaling pathway

Cited by 55 publications

References 37 publications

Physical Exercise Ameliorates the Cognitive Function and Attenuates the Neuroinflammation of Alzheimer’s Disease via miR-129–5p

Physical Exercise Ameliorates the Cognitive Function and Attenuates the Neuroinflammation of Alzheimer’s Disease via miR-129–5p

What and How Can Physical Activity Prevention Function on Parkinson’s Disease?

Role of Microglia TLRs in Neurodegeneration

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