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College of Natural Sciences(자연과학대학)Dept. of Chemistry(화학과)CH-Journal Papers(저널논문)

A Glycosylated Prodrug to Attenuate Neuroinflammation and Improve Cognitive Deficits in Alzheimer's Disease Transgenic Mice

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dc.contributor.authorKim, Mingeunko
dc.contributor.authorPark, Min Heeko
dc.contributor.authorNam, Geewooko
dc.contributor.authorLee, Misunko
dc.contributor.authorKang, Juhyeko
dc.contributor.authorSong, Im-Sookko
dc.contributor.authorChoi, Min-Kooko
dc.contributor.authorJin, Hee Kyungko
dc.contributor.authorBae, Jae-Sungko
dc.contributor.authorLim, Mi Heeko
dc.date.accessioned2021-02-09T02:10:06Z-
dc.date.available2021-02-09T02:10:06Z-
dc.date.created2021-01-13-
dc.date.issued2021-01-
dc.identifier.citationMOLECULAR PHARMACEUTICS, v.18, no.1, pp.101 - 112-
dc.identifier.issn1543-8384-
dc.identifier.urihttp://hdl.handle.net/10203/280669-
dc.description.abstractWe report a prodrug, Glu-DAPPD, to overcome the shortcomings of an anti-neuroinflammatory molecule, N,N'-diacetyl-p-phenylenediamine (DAPPD), in biological applicability for potential therapeutic applications. We suspect that Glu-DAPPD can release DAPPD through endogenous enzymatic bioconversion. Consequently, Glu-DAPPD exhibits in vivo efficacies in alleviating neuroinflammation, reducing amyloid-beta aggregate accumulation, and improving cognitive function in Alzheimer's disease transgenic mice. Our studies demonstrate that the prodrug approach is suitable and effective toward developing drug candidates against neurodegeneration.-
dc.languageEnglish-
dc.publisherAMER CHEMICAL SOC-
dc.titleA Glycosylated Prodrug to Attenuate Neuroinflammation and Improve Cognitive Deficits in Alzheimer's Disease Transgenic Mice-
dc.typeArticle-
dc.identifier.wosid000606803900008-
dc.identifier.scopusid2-s2.0-85097750576-
dc.type.rimsART-
dc.citation.volume18-
dc.citation.issue1-
dc.citation.beginningpage101-
dc.citation.endingpage112-
dc.citation.publicationnameMOLECULAR PHARMACEUTICS-
dc.identifier.doi10.1021/acs.molpharmaceut.0c00677-
dc.contributor.localauthorLim, Mi Hee-
dc.contributor.nonIdAuthorPark, Min Hee-
dc.contributor.nonIdAuthorNam, Geewoo-
dc.contributor.nonIdAuthorLee, Misun-
dc.contributor.nonIdAuthorKang, Juhye-
dc.contributor.nonIdAuthorSong, Im-Sook-
dc.contributor.nonIdAuthorChoi, Min-Koo-
dc.contributor.nonIdAuthorJin, Hee Kyung-
dc.contributor.nonIdAuthorBae, Jae-Sung-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorprodrug-
dc.subject.keywordAuthoranti-neuroinflammation-
dc.subject.keywordAuthormicroglial function-
dc.subject.keywordAuthoramyloid-beta-
dc.subject.keywordPlusARYLAMINE N-ACETYLTRANSFERASES-
dc.subject.keywordPlusMESENCHYMAL STEM-CELLS-
dc.subject.keywordPlusMICROGLIAL DYSFUNCTION-
dc.subject.keywordPlusBETA-GLUCOSIDASES-
dc.subject.keywordPlusSPECIFICITY-
dc.subject.keywordPlusTARGET-
dc.subject.keywordPlusMETABOLISM-
dc.subject.keywordPlusCLEARANCE-
dc.subject.keywordPlusMECHANISM-
dc.subject.keywordPlusPROTEIN-
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