Effect of low-intensity motor balance and coordination exercise on cognitive functions, hippocampal Aβ deposition, neuronal loss, neuroinflammation, and oxidative stress in a mouse model of Alzheimer's disease
Effect of low-intensity motor balance and coordination exercise on cognitive functions, hippocampal Aβ deposition, neuronal loss, neuroinflammation, and oxidative stress in a mouse model of Alzheimer's disease
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DOI：
10.1016/j.expneurol.2020.113590
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发表时间：
2021-01-06
影响因子：
5.3
通讯作者：
Kikuchi, Kiyoshi
中科院分区：
文献类型：
--
作者：
Nakanishi, Kazuki;Sakakima, Harutoshi;Kikuchi, Kiyoshi
众所周知，体育锻炼可以降低阿尔茨海默病（AD）和与年龄相关的认知能力下降的风险。然而，其机制仍不完全清楚。本研究旨在探讨衰老和旋转棒运动（Ex）对加速老化小鼠8（SAMP8）海马认知功能和AD发病机制的影响。认知功能在9个月大时明显下降。淀粉样β（A β）沉积，神经元损失，神经胶质细胞激活诱导的神经炎症随着年龄的增长而增加。mtarod Ex预防了与A β沉积、神经炎症、神经元损失、诱导型一氧化氮合酶（NOS）活性和神经元NOS活性的抑制相对应的认知功能的下降。此外，旋转棒Ex抑制促炎性M1表型小胶质细胞和A1表型星形胶质细胞。我们的研究结果表明，低强度的运动平衡和协调运动可以预防AD进展早期与年龄相关的认知功能下降，这可能是通过抑制海马A β沉积、神经元丢失、氧化应激和神经炎症，包括减少M1和A1表型小胶质细胞和星形胶质细胞。
It is well known that physical exercise reduces the risk of Alzheimer's disease (AD) and age-related cognitive decline. However, its mechanisms are still not fully understood. This study aimed to investigate the effect of aging and rotarod exercise (Ex) on cognitive function and AD pathogenesis in the hippocampus using senescence-accelerated mice prone 8 (SAMP8). Cognitive functions clearly declined at 9-months of age. Amyloid-beta (A beta) deposition, neuronal loss, and glia activation-induced neuroinflammation increased with aging. The mtarod Ex prevented the decline of cognitive functions corresponding to the suppression of A beta deposition, neuroinflammation, neuronal loss, inducible nitric oxide synthase (NOS) activities, and neuronal NOS activities. In addition, the rotarod Ex suppressed proinflammatory M1 phenotype microglia and A1 phenotype astrocytes. Our findings suggest that low-intensity motor balance and coordination exercise prevented age-related cognitive decline in the early stage of AD progression, possibly through the suppression of hippocampal A beta deposition, neuronal loss, oxidative stress, and neuroinflammation, including reduced M1 and A1 phenotypes microglia and astrocytes.