• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.418-428
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• 2020

The aim of this study was to investigate the effect of resistance exercise(RE) on beta-amyloid(Aβ) metabolism, neuronal cell death, and cognitive function in the transgenic mice model of Alzheimer's disease(AD). Fourteen transgenic(tg) mice and fourteen non-transgenic(non-tg) mice were divided into four groups: (1)non-tg-control(NTC, n=7) (2)non-tg-RE(NTRE, n=7) (3)tg-control(TC, n=7), and (4)tg-RE(TRE, n=7). The groups with RE were performed to progressive RE on ladder equipment for 8 weeks. The groups with RE were performed to progressive RE on ladder equipment for 8 weeks. After then, the cognitive function was measured by using the water maze test, and Aβ metabolism-related proteins, neuronal cell death, and SIRT1/PGC-1α pathway were also measured. Here, we found escape latency and time were significantly increased in the TC compared to the NTC group, but it was significantly reduced in the TRE group, indicating RE may ameliorate cognitive dysfunction. Next, we found an increased in Aβ protein of TC compared to NTC, but it was significantly reduced in the TRE group following RE. In neuronal cell death, Bcl-2 was also significantly decreased and Bax was significantly increased in the TC compared to the NTC group, but RE can increase Bcl-2 and reduce Bax, which may elevate the ratio of Bcl-2/Bax. We further found a decrease in the level of ADAM10 and RARβ protein was significantly increased whereas increased in ROCK1 and BACE1 expression level was significantly reduced following RE in the TRE compared to the TC group. In addition, the level of SIRT1/PGC-1α proteins was decreased in the TC group compared to NTC group, but, these markers were significantly increased in the TRE group following RE. Therefore, our finding indicated that RE may ameliorate cognitive deficits by reducing Aβ protein and neuronal cell death via regulating SIRT1/PGC-1α, amyloidogenic pathway, and non-amyloidogenic pathway, which may play a role in an effective strategy for AD.