期刊
NEUROSCIENCE LETTERS
卷 610, 期 -, 页码 207-212出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2015.11.010
关键词
Alzheimer's disease; Cytokines; Chemokines; Immunohistochemistry; Microglia
资金
- program for the Strategic Research Foundation at Private Universities from the Ministry of Education Culture, Sports, Science, and Technology of Japan (MEXT)
- MEXT KAKENHI Grant [26460921]
- Grants-in-Aid for Scientific Research [26460921] Funding Source: KAKEN
Physical exercise has been identified as a preventive measure for Alzheimer's disease (AD), one of the neuropathological hallmarks of which, neurofibrillary tangles, consist of hyperphosphorylated insoluble tau. Previous studies demonstrated that long-term treadmill exercise reduced tau hyperphosphorylation and insolubility; however, whether short-term treadmill exercise (STE) alters tau modifications currently remains unknown. In the present study, we attempted to characterize the effects of STE on tau solubility and determine its relationship with neuroinflammation using tauopathy model mice (Tg601), which express wild-type human tau. The results obtained showed that 3 weeks of non-shock treadmill exercise in Tg601 and non-transgenic female mice markedly increased insoluble tau. An analysis of phosphorylation patterns indicated that changes in tau solubility were related to an increase in phosphorylation at the tau C-terminal end. The results of immunohistochemical analyses revealed that STE increased the number of lba-1-positive microglial cells in the hippocampus. Elevations in the levels of the lipid peroxidation markers, 4-hydroxy-trans-2-noneal and malondialdehyde, indicated the presence of oxidative stress. Moreover, higher levels of cytokines, IL-1 beta and IL-18, and chemokines, CXCL-1 and CXCL-12, supported neuroinflammation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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