Jiang Hanlin, Zhao Tingrui, He Chunxiao, Liu Bin, Ai Wanlin, Chen Yuxin, Moriyama Hideki
Department of Rehabilitation Science, Graduate School of Health Sciences, Kobe University, Kobe, Japan.
Life and Medical Sciences Area, Health Sciences Discipline, Kobe University, Tomogaoka 7-10-2, Suma-ku, Kobe, Hyogo, 654-0142, Japan.
Geroscience. 2025 May 28. doi: 10.1007/s11357-025-01717-3.
The global increase in aging populations has heightened the urgency to develop effective interventions for age-related cognitive decline. Skeletal muscle has recently emerged as a potential modulator of brain health, particularly in the context of aging. This study investigates the effects of electrical muscle stimulation (EMS) on cognitive function and neuropathology in Senescence-Accelerated Mouse (SAMP8), a model of aging-associated cognitive decline. SAMP8 mice were divided into 3 groups: healthy controls (SAMR1), untreated SAMP8, and EMS-treated SAMP8. EMS was applied daily for 30 days, and behavioral, histological, and molecular markers were analyzed. Results demonstrated that EMS significantly improved muscle strength and endurance while reducing amyloid-β accumulation and phosphorylated tau (p-Tau) levels in the hippocampus. Furthermore, EMS decreased neuroinflammation and partially restored synaptic plasticity. However, EMS had limited effects on cortical pathology and cognitive function, suggesting that localized brain changes may not fully translate to behavioral improvements. These findings indicate that EMS exerts neuroprotective effects through skeletal muscle activation, providing a potential non-pharmacological intervention for age-related neurodegeneration. Future studies should explore the underlying mechanisms and translational applicability to human dementia treatment.
全球人口老龄化的加剧使得开发针对与年龄相关的认知衰退的有效干预措施变得更加紧迫。骨骼肌最近已成为大脑健康的潜在调节因子，尤其是在衰老的背景下。本研究调查了电肌肉刺激（EMS）对衰老加速小鼠（SAMP8）认知功能和神经病理学的影响，SAMP8是一种与衰老相关的认知衰退模型。将SAMP8小鼠分为3组：健康对照组（SAMR1）、未治疗的SAMP8组和接受EMS治疗的SAMP8组。每天进行30天的EMS治疗，并分析行为、组织学和分子标志物。结果表明，EMS显著提高了肌肉力量和耐力，同时减少了海马体中β-淀粉样蛋白的积累和磷酸化tau（p-Tau）水平。此外，EMS减轻了神经炎症并部分恢复了突触可塑性。然而，EMS对皮质病理学和认知功能的影响有限，这表明局部大脑变化可能无法完全转化为行为改善。这些发现表明，EMS通过骨骼肌激活发挥神经保护作用，为与年龄相关的神经退行性变提供了一种潜在的非药物干预措施。未来的研究应探索其潜在机制以及对人类痴呆症治疗的转化适用性。
