Nec-1 alleviates cognitive impairment with reduction of A and tau abnormalities in APP/PS1 mice
DC Field | Value | Language |
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dc.contributor.author | Yang, Seung-Hoon | - |
dc.contributor.author | Lee, Dongkeun Kenneth | - |
dc.contributor.author | Shin, Jisu | - |
dc.contributor.author | Lee, Sejin | - |
dc.contributor.author | Baek, Seungyeop | - |
dc.contributor.author | Kim, Jiyoon | - |
dc.contributor.author | Jung, Hoyong | - |
dc.contributor.author | Hah, Jung-Mi | - |
dc.contributor.author | Kim, YoungSoo | - |
dc.date.accessioned | 2021-06-22T14:43:09Z | - |
dc.date.available | 2021-06-22T14:43:09Z | - |
dc.date.created | 2021-01-21 | - |
dc.date.issued | 2017-01 | - |
dc.identifier.issn | 1757-4676 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/10587 | - |
dc.description.abstract | Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive symptoms of learning and memory deficits. Such cognitive impairments are attributed to brain atrophy resulting from progressive neuronal and synaptic loss; therefore, alleviation of neural cell death is as an important target of treatment as other classical hallmarks of AD, such as aggregation of amyloid- (A) and hyperphosphorylation of tau. Here, we found that an anti-necroptotic molecule necrostatin-1 (Nec-1) directly targets A and tau proteins, alleviates brain cell death and ameliorates cognitive impairment in AD models. In the cortex and hippocampus of APP/PS1 double-transgenic mice, Nec-1 treatment reduced the levels of A oligomers, plaques and hyperphosphorylated tau without affecting production of A, while it altered the levels of apoptotic marker proteins. Our results showing multiple beneficial modes of action of Nec-1 against AD provide evidence that Nec-1 may serve an important role in the development of preventive approach for AD. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.title | Nec-1 alleviates cognitive impairment with reduction of A and tau abnormalities in APP/PS1 mice | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Hah, Jung-Mi | - |
dc.identifier.doi | 10.15252/emmm.201606566 | - |
dc.identifier.scopusid | 2-s2.0-85006065082 | - |
dc.identifier.wosid | 000392431800006 | - |
dc.identifier.bibliographicCitation | EMBO MOLECULAR MEDICINE, v.9, no.1, pp.61 - 77 | - |
dc.relation.isPartOf | EMBO MOLECULAR MEDICINE | - |
dc.citation.title | EMBO MOLECULAR MEDICINE | - |
dc.citation.volume | 9 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 61 | - |
dc.citation.endPage | 77 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | BETA-AMYLOID PEPTIDE | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | A-BETA | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | HYPOTHETICAL MODEL | - |
dc.subject.keywordPlus | DIFFUSE PLAQUES | - |
dc.subject.keywordPlus | BRAIN ATROPHY | - |
dc.subject.keywordPlus | CROSS-LINKING | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | A aggregation | - |
dc.subject.keywordAuthor | cognitive deficit | - |
dc.subject.keywordAuthor | necrostatin-1 | - |
dc.subject.keywordAuthor | tau hyperphosphorylation | - |
dc.identifier.url | https://www.embopress.org/doi/full/10.15252/emmm.201606566 | - |
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