Treadmill exercise decreases amyloid-beta burden possibly via activation of SIRT-1 signaling in a mouse model of Alzheimer's disease
DC Field | Value | Language |
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dc.contributor.author | Koo, Jung-Hoon | - |
dc.contributor.author | Kang, Eun-Bum | - |
dc.contributor.author | Oh, Yoo-Sung | - |
dc.contributor.author | Yang, Dae-Seung | - |
dc.contributor.author | Cho, Joon-Yong | - |
dc.date.available | 2020-02-27T19:44:04Z | - |
dc.date.created | 2020-02-07 | - |
dc.date.issued | 2017-02 | - |
dc.identifier.issn | 0014-4886 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6437 | - |
dc.description.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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.relation.isPartOf | EXPERIMENTAL NEUROLOGY | - |
dc.subject | PRECURSOR PROTEIN | - |
dc.subject | CALORIE RESTRICTION | - |
dc.subject | VOLUNTARY EXERCISE | - |
dc.subject | ALPHA-SECRETASE | - |
dc.subject | TRANSGENIC MICE | - |
dc.subject | A-BETA | - |
dc.subject | PATHOGENIC PHENOTYPES | - |
dc.subject | FORCED EXERCISE | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | UP-REGULATION | - |
dc.title | Treadmill exercise decreases amyloid-beta burden possibly via activation of SIRT-1 signaling in a mouse model of Alzheimer's disease | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000392461100014 | - |
dc.identifier.doi | 10.1016/j.expneurol.2016.11.014 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL NEUROLOGY, v.288, pp.142 - 152 | - |
dc.identifier.scopusid | 2-s2.0-84997787317 | - |
dc.citation.endPage | 152 | - |
dc.citation.startPage | 142 | - |
dc.citation.title | EXPERIMENTAL NEUROLOGY | - |
dc.citation.volume | 288 | - |
dc.contributor.affiliatedAuthor | Yang, Dae-Seung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | Amyloid-beta | - |
dc.subject.keywordAuthor | Treadmill exercise | - |
dc.subject.keywordAuthor | Sirtuin-1 | - |
dc.subject.keywordAuthor | Non-amyloidogenic pathway | - |
dc.subject.keywordPlus | PRECURSOR PROTEIN | - |
dc.subject.keywordPlus | CALORIE RESTRICTION | - |
dc.subject.keywordPlus | VOLUNTARY EXERCISE | - |
dc.subject.keywordPlus | ALPHA-SECRETASE | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordPlus | A-BETA | - |
dc.subject.keywordPlus | PATHOGENIC PHENOTYPES | - |
dc.subject.keywordPlus | FORCED EXERCISE | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | UP-REGULATION | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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