| First Author | Zhang X | Year | 2019 |
| Journal | Front Aging Neurosci | Volume | 11 |
| Pages | 78 | PubMed ID | 31024293 |
| Mgi Jnum | J:276039 | Mgi Id | MGI:6313767 |
| Doi | 10.3389/fnagi.2019.00078 | Citation | Zhang X, et al. (2019) Treadmill Exercise Decreases Abeta Deposition and Counteracts Cognitive Decline in APP/PS1 Mice, Possibly via Hippocampal Microglia Modifications. Front Aging Neurosci 11:78 |
| abstractText | 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 (Abeta) 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/PS1 mice and substantially suppressed Abeta 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 Abeta deposits in early AD progression possibly via modulating microglia-mediated neuroinflammation and oxidative stress. |
