Effect of cx-DHED on Abnormal Glucose Transporter Expression Induced by AD Pathologies in the 5xFAD Mouse Model
DC Field | Value | Language |
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dc.contributor.author | Kim, Jinho | - |
dc.contributor.author | Kang, ShinWoo | - |
dc.contributor.author | Chang, Keun-A | - |
dc.date.accessioned | 2022-10-28T03:40:09Z | - |
dc.date.available | 2022-10-28T03:40:09Z | - |
dc.date.created | 2022-10-28 | - |
dc.date.issued | 2022-09 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85886 | - |
dc.description.abstract | Alzheimer's disease (AD) is a form of dementia associated with abnormal glucose metabolism resulting from amyloid-beta (A beta) plaques and intracellular neurofibrillary tau protein tangles. In a previous study, we confirmed that carboxy-dehydroevodiamine center dot HCl (cx-DHED), a derivative of DHED, was effective at improving cognitive impairment and reducing phosphorylated tau levels and synaptic loss in an AD mouse model. However, the specific mechanism of action of cx-DHED is unclear. In this study, we investigated how the cx-DHED attenuates AD pathologies in the 5xFAD mouse model, focusing particularly on abnormal glucose metabolism. We analyzed behavioral changes and AD pathologies in mice after intraperitoneal injection of cx-DHED for 2 months. As expected, cx-DHED reversed memory impairment and reduced A beta plaques and astrocyte overexpression in the brains of 5xFAD mice. Interestingly, cx-DHED reversed the abnormal expression of glucose transporters in the brains of 5xFAD mice. In addition, otherwise low O-GlcNac levels increased, and the overactivity of phosphorylated GSK-3 beta decreased in the brains of cx-DHED-treated 5xFAD mice. Finally, the reduction in synaptic proteins was found to also improve by treatment with cx-DHED. Therefore, we specifically demonstrated the protective effects of cx-DHED against AD pathologies and suggest that cx-DHED may be a potential therapeutic drug for AD. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.title | Effect of cx-DHED on Abnormal Glucose Transporter Expression Induced by AD Pathologies in the 5xFAD Mouse Model | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000856395600001 | - |
dc.identifier.doi | 10.3390/ijms231810602 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, no.18 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.scopusid | 2-s2.0-85138341861 | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 23 | - |
dc.citation.number | 18 | - |
dc.contributor.affiliatedAuthor | Kim, Jinho | - |
dc.contributor.affiliatedAuthor | Kang, ShinWoo | - |
dc.contributor.affiliatedAuthor | Chang, Keun-A | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | cx-DHED | - |
dc.subject.keywordAuthor | Alzheimer&apos | - |
dc.subject.keywordAuthor | s disease | - |
dc.subject.keywordAuthor | glucose transport | - |
dc.subject.keywordAuthor | GSK-3 beta | - |
dc.subject.keywordAuthor | O-GlcNac | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | O-GLCNACYLATION | - |
dc.subject.keywordPlus | TAU PATHOLOGY | - |
dc.subject.keywordPlus | METABOLISM | - |
dc.subject.keywordPlus | DEHYDROEVODIAMINE | - |
dc.subject.keywordPlus | GLCNAC | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | GLUT1 | - |
dc.subject.keywordPlus | EVODIAMINE | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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