ArticleCNS neuroscience & therapeutics2025
Aerobic Exercise Training Exerts Neuroprotective Effects in Alzheimer's Disease Mice by Regulating Endoplasmic Reticulum Stress-Autophagy Pathway-Mediated Pyroptosis.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Exercise-Mediated Modulation of the NLRP3 Inflammasome in Aging and Neurodegenerative Diseases: Mechanisms, Microglial Crosstalk, and Translational Perspectives.Molecular neurobiology · 2026Review
- Molecular mechanisms underlying exercise-enhanced autophagy in improving neuroplasticity in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Exercise-induced modulation of astrocyte in Alzheimer's disease: mechanisms and therapeutic implications.Frontiers in physiology · 2026Review
- Aerobic Exercise Training Exerts Neuroprotective Effects in Alzheimer's Disease Mice by Regulating Endoplasmic Reticulum Stress-Autophagy Pathway-Mediated Pyroptosis.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
objectiveThis study probed into the neuroprotective effects of aerobic exercise training (AET) on Alzheimer's disease (AD) mice and further explored the molecular mechanisms through which AET regulates the endoplasmic reticulum stress (ERS)-autophagy pathway to mediate pyroptosis.
methodsAPP/PS1 mice (AD model) underwent 8 weeks of treadmill-based AET. In addition to the exercise regimen, mice were treated with intraperitoneal injections of an NLRP3 inflammasome activator, an autophagy inhibitor, an ERS inducer, and a PERK activator for assessing cognitive function and neuronal damage in the hippocampal CA1 region through cognitive assessments, histological analyses, and biochemical assays. BrdU/EdU labeling combined with NeuN and doublecortin immunostaining was used to evaluate AET-stimulated neuronal proliferation and differentiation in the hippocampus.
resultsAET improved cognitive function in AD mice. Following AET, neuronal damage in the hippocampal CA1 region was reduced, the number of Nissl bodies increased, and Aβ
conclusionAET reduces NLRP3 inflammasome-mediated pyroptosis and neuronal damage in the hippocampal CA1 region of AD mice by regulating the ERS-autophagy pathway through the inhibition of the PERK-eIF2α pathway, thereby improving cognitive function in AD mice.
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Registered trials
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