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Repression of tau hyperphosphorylation by chronic endurance exercise in aged transgenic mouse model of tauopathies
- Repression of tau hyperphosphorylation by chronic endurance exercise in aged transgenic mouse model of tauopathies
- Leem Y.-H.; Lim H.-J.; Shim S.-B.; Cho J.-Y.; Kim B.-S.; Han P.-L.
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- Journal of Neuroscience Research
- vol. 87, no. 11, pp. 2561 - 2570
- SCI; SCIE; SCOPUS
- The present study was undertaken to investigate whether chronic endurance exercise affects tau phosphorylation levels in the brain with Alzheimer's disease (AD)-like pathology. To address this, the transgenic (Tg) mouse model of tauopathies, Tg-NSE/htau23, which expresses human tau23 in the brain, was chosen. Animals were subjected to chronic exercise for 3 months from 16 months of age. The exercised Tg mouse groups were treadmill run at speeds of 12 m/min (intermediate exercise group) or 19 m/min (high exercise group) for 1 hr/day, 5 days/week, during the 3-month period. Chronic endurance exercise in Tg mice increased the expression of Cu/Zn-superoxide dismutase (SOD) and catalase, and also their enzymatic activities in the brain. In parallel, chronic exercise in Tg mice up-regulated the expression of phospho-PKCα, phospho-AKT, and phospho-PI3K, and down-regulated the expressions of phospho-PKA, phosphor-p38, phospho-JNK, and phospho-ERK. Moreover, chronic exercise up-regulated both cytosolic and nuclear levels of b-catenin, and the expression of T-cell factor-4 (Tcf-4) and cyclin D1 in the brain. As a consequence of such changes, the levels of phospho-tau in the brain of Tg mice were markedly decreased after exercise. Immunohistochemical analysis showed an exercised-induced decrease of the phosphotau levels in the CA3 subregion of the hippocampus. These results suggest that chronic endurance exercise may provide a therapeutic potential to alleviate the tau pathology. © 2009 Wiley-Liss, Inc.
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