Treadmill exercise decreases amyloid-beta burden possibly via activation of SIRT-1 signaling in a mouse model of Alzheimer's disease
- Authors
- Koo, Jung-Hoon; Kang, Eun-Bum; Oh, Yoo-Sung; Yang, Dae-Seung; Cho, Joon-Yong
- Issue Date
- Feb-2017
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Alzheimer' s disease; Amyloid-beta; Treadmill exercise; Sirtuin-1; Non-amyloidogenic pathway
- Citation
- EXPERIMENTAL NEUROLOGY, v.288, pp.142 - 152
- Journal Title
- EXPERIMENTAL NEUROLOGY
- Volume
- 288
- Start Page
- 142
- End Page
- 152
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6437
- DOI
- 10.1016/j.expneurol.2016.11.014
- ISSN
- 0014-4886
- Abstract
- Accumulation of amyloid-beta (A beta) correlates significantly with progressive cognitive deficits, a main symptom of Alzheimer's disease (AD). Although treadmill exercise reduces A beta levels, the molecular mechanisms underlying the effects are not fully understood. We hypothesize that treadmill exercise decreases All production and alleviates cognitive deficits by activating the non-amyloidogenic pathway via SIRT-1 signaling. Treadmill exercise improved cognitive deficits and alleviated neurotoxicity. Most importantly, treadmill exercise increased SIRT-1 level, which subsequently resulted in increased ADAM-10 level by down-regulation of ROCK-1 and upregulation of RAR beta, ultimately facilitating the non-amyloidogenic pathway. Treadmill exercise-induced activation in SIRT-1 level also elevated PGC-1 alpha level and reduced BACE-1 and C-99 level, resulting in inhibition of the amyloidogenic pathway. Treadmill exercise may thus inhibit Ala production via upregulation of SIRT-1, which biases amyloid precursor protein processing toward the non-amyloidogenic pathway. This study provides novel and valuable insight into the molecular mechanisms possibly by which treadmill exercise reduces A beta production. (C) 2016 Elsevier Inc. All rights reserved.
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