Exercise-induced alleviation of memory impairment in aged mice with neuroinflammation is linked with modulation of mitochondrial homeostasis in the hippocampus

作者：Peng Li, Chong Hyun Han, Yuanyuan Qin, Zhi Jiang, Shan-Yao Pan, Bo Liao, Nan Wang, Xin-Han Cao, Gang Zhao, Jiaqi Zhou, Zheng‐Hong Qin, Yiqing Lu, Yaping Huai, Li Luo · 发表于：The Journals of Gerontology Series A · 年份：2025 · DOI：10.1093/gerona/glaf233 · 被引用次数：2 · 研究领域：Neuroinflammation and Neurodegeneration Mechanisms、Tryptophan and brain disorders、Neurogenesis and neuroplasticity mechanisms

BACKGROUND: Neuroinflammation is a critical aspect of aging and neurodegenerative disorders, increasingly recognized for its significant role in the progression of cognitive impairments. Mitochondrial homeostasis is closely linked to cognitive function in the aging brain. However, it remains unclear whether exercise can safeguard cognitive function by enhancing mitochondrial homeostasis in the aged hippocampus affected by neuroinflammation. METHODS: In this study, we established mouse models exhibiting memory impairment and neuroinflammation in the aged hippocampus to investigate whether exercise can reverse lipopolysaccharides (LPS)-induced cognitive dysfunction in aged mice, reduce neuroinflammation, and simultaneously improve mitochondrial homeostasis in the hippocampus. Eighteen-month-old male ICR mice underwent 8 weeks of moderate-intensity aerobic exercise. RESULTS: The exercise regimen enhanced memory function in LPS-injected aged mice, which was accompanied by reductions in inflammation, oxidative stress, and apoptosis in the aged hippocampus. Importantly, exercise improved mitochondrial homeostasis in the hippocampus of LPS-injected aged mice. CONCLUSION: our results provide the first evidence that exercise can protect cognitive function in the context of neuroinflammation in the aged hippocampus, suggesting that this effect may be associated with the improvement of mitochondrial homeostasis.