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DC Field | Value | Language |
---|---|---|
dc.citation.endPage | 595 | - |
dc.citation.startPage | 575 | - |
dc.citation.title | FREE RADICAL BIOLOGY AND MEDICINE | - |
dc.citation.volume | 160 | - |
dc.contributor.author | Lee, Hyun-ju | - |
dc.contributor.author | Woo, Hanwoong | - |
dc.contributor.author | Lee, Ha-Eun | - |
dc.contributor.author | Jeon, Hyongjun | - |
dc.contributor.author | Ryu, Ka-Young | - |
dc.contributor.author | Nam, Jin han | - |
dc.contributor.author | Jeon, Seong Gak | - |
dc.contributor.author | Park, HyunHee | - |
dc.contributor.author | Lee, Ji-Soo | - |
dc.contributor.author | Han, Kyung-Min | - |
dc.contributor.author | Lee, Sang Min | - |
dc.contributor.author | Kim, Jeongyeon | - |
dc.contributor.author | Kang, Ri Jin | - |
dc.contributor.author | Lee, Young-Ho | - |
dc.contributor.author | Kim, Jae-Ick | - |
dc.contributor.author | Hoe, Hyang-Sook | - |
dc.date.accessioned | 2023-12-21T16:45:35Z | - |
dc.date.available | 2023-12-21T16:45:35Z | - |
dc.date.created | 2020-09-14 | - |
dc.date.issued | 2020-11 | - |
dc.description.abstract | Regulating amyloid beta (A beta) pathology and neuroinflammatory responses holds promise for the treatment of Alzheimer's disease (AD) and other neurodegenerative and/or neuroinflammation-related diseases. In this study, the effects of KVN93, an inhibitor of dual-specificity tyrosine phosphorylation-regulated kinase-1A (DYRK1A), on cognitive function and A beta plaque levels and the underlying mechanism of action were evaluated in 5x FAD mice (a mouse model of AD). KVN93 treatment significantly improved long-term memory by enhancing dendritic synaptic function. In addition, KVN93 significantly reduced A beta plaque levels in 5x FAD mice by regulating levels of the A beta degradation enzymes neprilysin (NEP) and insulin-degrading enzyme (IDE). Moreover, A beta induced microglial and astrocyte activation were significantly suppressed in the KVN-treated 5xFAD mice. KVN93 altered neuroinflammation induced by LPS in microglial cells but not primary astrocytes by regulating TLR4/AKT/STAT3 signaling, and in wild-type mice injected with LPS, KVN93 treatment reduced microglial and astrocyte activation. Overall, these results suggest that the novel DYRK1A inhibitor KVN93 is a potential therapeutic drug for regulating cognitive/synaptic function, A beta plaque load, and neuroinflammatory responses in the brain. | - |
dc.identifier.bibliographicCitation | FREE RADICAL BIOLOGY AND MEDICINE, v.160, pp.575 - 595 | - |
dc.identifier.doi | 10.1016/j.freeradbiomed.2020.08.030 | - |
dc.identifier.issn | 0891-5849 | - |
dc.identifier.scopusid | 2-s2.0-85090591370 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/48333 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0891584920312375?via%3Dihub | - |
dc.identifier.wosid | 000595212600002 | - |
dc.language | 영어 | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.title | The novel DYRK1A inhibitor KVN93 regulates cognitive function, amyloid-beta pathology, and neuroinflammation | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology; Endocrinology & Metabolism | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology; Endocrinology & Metabolism | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | DYRK1A | - |
dc.subject.keywordAuthor | Long-term memory | - |
dc.subject.keywordAuthor | Amyloid beta | - |
dc.subject.keywordAuthor | IDE | - |
dc.subject.keywordAuthor | NEP | - |
dc.subject.keywordAuthor | Neuroinflammation | - |
dc.subject.keywordAuthor | Microglia | - |
dc.subject.keywordPlus | LONG-TERM POTENTIATION | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | DOWN-SYNDROME | - |
dc.subject.keywordPlus | PRECURSOR PROTEIN | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | BRAIN | - |
dc.subject.keywordPlus | MICROGLIA | - |
dc.subject.keywordPlus | TAU | - |
dc.subject.keywordPlus | LIPOPOLYSACCHARIDE | - |
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