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

Author(s)
Kim, MingeunPark, Min HeeNam, GeewooLee, MisunKang, JuhyeSong, Im-SookChoi, Min-KooJin, Hee KyungBae, Jae-SungLim, Mi Hee
Issued Date
2021-01
DOI
10.1021/acs.molpharmaceut.0c00677
URI
https://scholarworks.unist.ac.kr/handle/201301/56607
Fulltext
https://pubs.acs.org/doi/10.1021/acs.molpharmaceut.0c00677
Citation
MOLECULAR PHARMACEUTICS, v.18, no.1, pp.101 - 112
Abstract
We 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.
Publisher
AMER CHEMICAL SOC
ISSN
1543-8384
Keyword (Author)
Alzheimer&aposs diseaseprodruganti-neuroinflammationmicroglial functionamyloid-beta
Keyword
ARYLAMINE N-ACETYLTRANSFERASESMESENCHYMAL STEM-CELLSMICROGLIAL DYSFUNCTIONBETA-GLUCOSIDASESSPECIFICITYTARGETMETABOLISMCLEARANCEMECHANISMPROTEIN

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