Full metadata record
DC Field | Value | Language |
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dc.citation.number | 23 | - |
dc.citation.startPage | 13136 | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 22 | - |
dc.contributor.author | Koh, Han Seok | - |
dc.contributor.author | Lee, SangJoon | - |
dc.contributor.author | Lee, Hyo Jin | - |
dc.contributor.author | Min, Jae-Woong | - |
dc.contributor.author | Iwatsubo, Takeshi | - |
dc.contributor.author | Teunissen, Charlotte E. | - |
dc.contributor.author | Cho, Hyun-Jeong | - |
dc.contributor.author | Ryu, Jin-Hyeob | - |
dc.date.accessioned | 2023-12-21T14:48:15Z | - |
dc.date.available | 2023-12-21T14:48:15Z | - |
dc.date.created | 2022-01-12 | - |
dc.date.issued | 2021-12 | - |
dc.description.abstract | Alzheimer's disease (AD) is a form of dementia characterized by progressive memory decline and cognitive dysfunction. With only one FDA-approved therapy, effective treatment strategies for AD are urgently needed. In this study, we found that microRNA-485-3p (miR-485-3p) was overexpressed in the brain tissues, cerebrospinal fluid, and plasma of patients with AD, and its antisense oligonucleotide (ASO) reduced A beta plaque accumulation, tau pathology development, neuroinflammation, and cognitive decline in a transgenic mouse model of AD. Mechanistically, miR-485-3p ASO enhanced A beta clearance via CD36-mediated phagocytosis of A beta in vitro and in vivo. Furthermore, miR-485-3p ASO administration reduced apoptosis, thereby effectively decreasing truncated tau levels. Moreover, miR-485-3p ASO treatment reduced secretion of proinflammatory cytokines, including IL-1 beta and TNF-alpha, and eventually relieved cognitive impairment. Collectively, our findings suggest that miR-485-3p is a useful biomarker of the inflammatory pathophysiology of AD and that miR-485-3p ASO represents a potential therapeutic candidate for managing AD pathology and cognitive decline. | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.22, no.23, pp.13136 | - |
dc.identifier.doi | 10.3390/ijms222313136 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.scopusid | 2-s2.0-85120617658 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/56567 | - |
dc.identifier.url | https://www.mdpi.com/1422-0067/22/23/13136 | - |
dc.identifier.wosid | 000735655600001 | - |
dc.language | 영어 | - |
dc.publisher | MDPI | - |
dc.title | Targeting MicroRNA-485-3p Blocks Alzheimer's Disease Progression | - |
dc.type | Article | - |
dc.description.isOpenAccess | TRUE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology; Chemistry, Multidisciplinary | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology; Chemistry | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | beta-amyloid | - |
dc.subject.keywordAuthor | tau | - |
dc.subject.keywordAuthor | IL-1 beta | - |
dc.subject.keywordAuthor | TNF-alpha | - |
dc.subject.keywordAuthor | neuroinflammation | - |
dc.subject.keywordAuthor | cognitive function | - |
dc.subject.keywordAuthor | microRNA | - |
dc.subject.keywordAuthor | miR-485-3p | - |
dc.subject.keywordAuthor | antisense oligonucleotide | - |
dc.subject.keywordPlus | AMYLOID-BETA | - |
dc.subject.keywordPlus | A-BETA | - |
dc.subject.keywordPlus | INFLAMMASOME ACTIVATION | - |
dc.subject.keywordPlus | PHAGOCYTOSIS | - |
dc.subject.keywordPlus | MODEL | - |
dc.subject.keywordPlus | CONTRIBUTES | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PATHOLOGY | - |
dc.subject.keywordPlus | PLAQUES | - |
dc.subject.keywordPlus | TRIALS | - |
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