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NRF2/ARE pathway negatively regulates BACE1 expression and ameliorates cognitive deficits in mouse Alzheimer's models

DC FieldValueLanguage
dc.contributor.author배수한-
dc.date.accessioned2019-09-20T07:34:09Z-
dc.date.available2019-09-20T07:34:09Z-
dc.date.issued2019-
dc.identifier.issn0027-8424-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/170953-
dc.description.abstractBACE1 is the rate-limiting enzyme for amyloid-β peptides (Aβ) generation, a key event in the pathogenesis of Alzheimer's disease (AD). By an unknown mechanism, levels of BACE1 and a BACE1 mRNA-stabilizing antisense RNA (BACE1-AS) are elevated in the brains of AD patients, implicating that dysregulation of BACE1 expression plays an important role in AD pathogenesis. We found that nuclear factor erythroid-derived 2-related factor 2 (NRF2/NFE2L2) represses the expression of BACE1 and BACE1-AS through binding to antioxidant response elements (AREs) in their promoters of mouse and human. NRF2-mediated inhibition of BACE1 and BACE1-AS expression is independent of redox regulation. NRF2 activation decreases production of BACE1 and BACE1-AS transcripts and Aβ production and ameliorates cognitive deficits in animal models of AD. Depletion of NRF2 increases BACE1 and BACE1-AS expression and Aβ production and worsens cognitive deficits. Our findings suggest that activation of NRF2 can prevent a key early pathogenic process in AD.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherNational Academy of Sciences-
dc.relation.isPartOfProceedings of the National Academy of Sciences of the United States of America-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleNRF2/ARE pathway negatively regulates BACE1 expression and ameliorates cognitive deficits in mouse Alzheimer's models-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorGahee Bahn-
dc.contributor.googleauthorJong-Sung Park-
dc.contributor.googleauthorUi Jeong Yun-
dc.contributor.googleauthorYoon Jee Lee-
dc.contributor.googleauthorYuri Choi-
dc.contributor.googleauthorJin Su Park-
dc.contributor.googleauthorSeung Hyun Baek-
dc.contributor.googleauthorBo Youn Choi-
dc.contributor.googleauthorYoon Suk Cho-
dc.contributor.googleauthorHark Kyun Kim-
dc.contributor.googleauthorJihoon Han-
dc.contributor.googleauthorJae Hoon Sul-
dc.contributor.googleauthorSang-Ha Baik-
dc.contributor.googleauthorJinhwan Lim-
dc.contributor.googleauthorNobunao Wakabayashi-
dc.contributor.googleauthorSoo Han Bae-
dc.contributor.googleauthorJeung-Whan Han-
dc.contributor.googleauthorThiruma V. Arumugam-
dc.contributor.googleauthorMark P. Mattson-
dc.contributor.googleauthorDong-Gyu Jo-
dc.identifier.doi10.1073/pnas.1819541116-
dc.contributor.localIdA01798-
dc.relation.journalcodeJ02550-
dc.identifier.eissn1091-6490-
dc.identifier.pmid31164420-
dc.identifier.urlhttps://www.pnas.org/content/116/25/12516.long-
dc.subject.keyword3xTg-AD mice-
dc.subject.keyword5xFAD mice-
dc.subject.keywordAlzheimer’s disease-
dc.subject.keywordBACE1-
dc.subject.keywordNRF2-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.affiliatedAuthor배수한-
dc.citation.volume116-
dc.citation.number25-
dc.citation.startPage12516-
dc.citation.endPage12523-
dc.identifier.bibliographicCitationProceedings of the National Academy of Sciences of the United States of America, Vol.116(25) : 12516-12523, 2019-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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