Journal
FRONTIERS IN AGING NEUROSCIENCE
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnagi.2019.00078
Keywords
Alzheimer's disease; treadmill exercise; cognitive function; amyloid-beta; microglia; neuroinflammation; oxidative stress
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Funding
- China Postdoctoral Science Foundation [2017M612244]
- Fundamental Research Funds of Shandong University [2016GN001]
- Shandong Provincial Social Science Foundation [17DTYJ01, 16CTYJ01]
- National Natural Science Foundation of China [31571225, 31600965]
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Recent studies have suggested that exercise may be beneficial for delaying or attenuating Alzheimer's disease (AD). However, the underlying mechanisms were not clear. Microglia-mediated neuroinflammation is suggested to play an important role in the pathology of AD. The present study investigated the beneficial effects of treadmill exercise on amyloid-beta (A beta) deposition and cognitive function in amyloid precursor protein (APP)/PS1 mice in the early stage of AD progression and microglia-mediated neuroinflammation was mainly analyzed. The results demonstrated that 12 weeks of treadmill exercise preserved hippocampal cognitive function in APP/PSI mice and substantially suppressed A beta accumulation in the hippocampus. Treadmill exercise significantly inhibited neuroinflammation, which was characterized by a remarkably reduced expression of pro-inflammatory factors and increased expression of anti-inflammatory mediators in the hippocampus, resulting from a shift in activated microglia from the M1 to M2 phenotype. Treadmill exercise also attenuated oxidative stress presented by a marked reduction in methane dicarboxylic aldehyde (MDA) level and dramatically elevated SOD and Mn-SOD activities in the hippocampus. These findings suggest that treadmill exercise can effectively prevent the decrease in hippocampal-dependent cognitive function and A beta deposits in early AD progression possibly via modulating microglia-mediated neuroinflammation and oxidative stress.
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