File Download

There are no files associated with this item.

  • Find it @ UNIST can give you direct access to the published full text of this article. (UNISTARs only)
Related Researcher


Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
Read More

Views & Downloads

Detailed Information

Cited time in webofscience Cited time in scopus
Metadata Downloads

Full metadata record

DC Field Value Language
dc.citation.endPage 595 -
dc.citation.startPage 575 -
dc.citation.volume 160 - Lee, Hyun-ju - Woo, Hanwoong - Lee, Ha-Eun - Jeon, Hyongjun - Ryu, Ka-Young - Nam, Jin han - Jeon, Seong Gak - Park, HyunHee - Lee, Ji-Soo - Han, Kyung-Min - Lee, Sang Min - Kim, Jeongyeon - Kang, Ri Jin - Lee, Young-Ho - Kim, Jae-Ick - Hoe, Hyang-Sook - 2023-12-21T16:45:35Z - 2023-12-21T16:45:35Z - 2020-09-14 - 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 -
dc.identifier.url -
dc.identifier.wosid 000595212600002 -
dc.language 영어 -
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 -


Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.