Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 고성호 | - |
dc.date.accessioned | 2019-12-04T04:48:21Z | - |
dc.date.available | 2019-12-04T04:48:21Z | - |
dc.date.issued | 2018-01 | - |
dc.identifier.citation | EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY, v. 14, no. 1, page. 83-90 | en_US |
dc.identifier.issn | 1742-5255 | - |
dc.identifier.issn | 1744-7607 | - |
dc.identifier.uri | https://www.tandfonline.com/doi/full/10.1080/17425255.2018.1417387 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/117156 | - |
dc.description.abstract | Introduction: Levodopa (L-DOPA) is the most commonly used drug for Parkinson's disease (PD), but its long-term use is associated with various complications, including L-DOPA-induced dyskinesia (LID). Many studies have suggested that L-DOPA neurotoxicity and LID are associated with glycogen synthase kinase-3 (GSK-3) activation.Areas covered: LID is caused by striatal dopamine (DA) denervation in PD and pulsatile L-DOPA treatment. These factors lead to dysregulated DA transmission, abnormal intracellular signaling and transcription factors in striatal neurons, and altered gene expression and plasticity at corticostriatal synapses. The mechanisms of L-DOPA toxicity involve oxidative stress, L-DOPA oxidation to quinone, mitochondrial dysfunction, and a-synuclein. GSK-3 has been suggested to play key roles in all the mechanisms associated of L-DOPA toxicity and LID in PD.Expert opinion: GSK-3 plays critical roles in L-DOPA-induced neurotoxicity, and the development of specific methods to inhibit GSK-3 function may help prevent L-DOPA neurotoxicity and LID in PD. However, balanced GSK-3 inhibition and less beta-catenin degradation is essential for preventing LID, because too much GSK-3 inhibition increases beta-catenin levels, which is related to cancers. | en_US |
dc.description.sponsorship | This work was supported by the Basic Science Research Program of the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning (2015R1A2A2A04004865), by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI17C2160), by the Korea Drug Development Fund (KDDF) funded by the Ministry of Science and ICT, Ministry of Trade, Industry & Energy, and Ministry of Health & Welfare (KDDF-201609-02, Republic of Korea), and by and the Medical Research Center (2017R1A5A2015395). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | TAYLOR & FRANCIS LTD | en_US |
dc.subject | Parkinson's disease | en_US |
dc.subject | glycogen synthase kinase-3 (GSK-3) | en_US |
dc.subject | l-3 | en_US |
dc.subject | 4-dihydroxyphenylalanine (L-DOPA) | en_US |
dc.subject | neurotoxicity | en_US |
dc.title | Understanding the role of glycogen synthase kinase-3 in L-DOPA-induced dyskinesia in Parkinson's disease | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 14 | - |
dc.identifier.doi | 10.1080/17425255.2018.1417387 | - |
dc.relation.page | 83-90 | - |
dc.relation.journal | EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY | - |
dc.contributor.googleauthor | Choi, Hojin | - |
dc.contributor.googleauthor | Koh, Seong-Ho | - |
dc.relation.code | 2018006102 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | ksh213 | - |
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