Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김승현 | - |
dc.date.accessioned | 2018-02-28T05:17:18Z | - |
dc.date.available | 2018-02-28T05:17:18Z | - |
dc.date.issued | 2012-09 | - |
dc.identifier.citation | Journal of the Neurological Sciences, Sep 2012, 320(1-2), P.1-5 | en_US |
dc.identifier.issn | 0022-510X | - |
dc.identifier.uri | https://linkinghub.elsevier.com/retrieve/pii/S0022510X12002663 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/41176 | - |
dc.description.abstract | Background: Glycogen synthase kinase-3 beta (GSK-3 beta) activity plays a central role in motor neuron degeneration. We hypothesized that GSK-3 beta inhibitor would prolong the survival of motor neuron and suppress the disease progression in amyotrophic lateral sclerosis (ALS).Methods: A total of 40 transgenic mice harboring the human G93A mutated SOD1 gene and 14 wild type mice were used following confirmation of their genotype. The 40 transgenic mice were divided into 2 groups; ALS transgenic mice_control and ALS transgenic mice_GSK-3 beta inhibitor treatment. The clinical status, rotarod test and survival of the transgenic ALS mice and wild-type mice were evaluated. Additionally, motor neuron counting, GSK-3 beta activity and extrinsic apoptotic signals in spinal cord were also investigated.Results: The treatment with GSK-3 beta inhibitor showed excellent motor ability and delay of the symptom onset and survival in the ALS transgenic mice. However, after clinical symptoms developed, the neuroprotective effect of GSK-3 beta inhibitor was not significant. And the biochemical results revealed the weakly increased extrinsic apoptotic signals in the ALS transgenic mice by GSK-3 beta inhibitor treatment.Conclusion: The present study suggests that GSK-3 beta inhibitor would be a novel promising therapeutic strategy in ALS; however neuroprotective effect of GSK-3 beta inhibitor may be reduced via extrinsic apoptosis or non-neuronal patho-mechanism in late-stage of disease. | en_US |
dc.description.sponsorship | This study was supported by a grant of the Korea Healthcare technology R&D Project Ministry for Health, Welfare & Family Affairs, Republic of Korea (A091049). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Elsevier Science BV | en_US |
dc.subject | Glycogen synthase kinase-3 | en_US |
dc.subject | GSK-3 beta inhibitor | en_US |
dc.subject | Amyotrophic lateral sclerosis | en_US |
dc.subject | ALS | en_US |
dc.subject | Extrinsic apoptosis | en_US |
dc.title | The neuroprotective effect of the GSK-3 beta inhibitor and influence on the extrinsic apoptosis in the ALS transgenic mice | en_US |
dc.type | Article | en_US |
dc.relation.no | 1-2 | - |
dc.relation.volume | 320 | - |
dc.identifier.doi | 10.1016/j.jns.2012.05.038 | - |
dc.relation.page | 1-5 | - |
dc.relation.journal | JOURNAL OF THE NEUROLOGICAL SCIENCES | - |
dc.contributor.googleauthor | Ahn, Suk-Won | - |
dc.contributor.googleauthor | Kim, Jee-Eun | - |
dc.contributor.googleauthor | Park, Kyung Seok | - |
dc.contributor.googleauthor | Choi, Won-Jun | - |
dc.contributor.googleauthor | Hong, Yoon-Ho | - |
dc.contributor.googleauthor | Kim, Sung-Min | - |
dc.contributor.googleauthor | Kim, Seung Hyun | - |
dc.contributor.googleauthor | Lee, Kwang-Woo | - |
dc.contributor.googleauthor | Sung, Jung-Joon | - |
dc.contributor.googleauthor | 안석원 | - |
dc.contributor.googleauthor | 김지은 | - |
dc.contributor.googleauthor | 박경석 | - |
dc.contributor.googleauthor | 최원준 | - |
dc.contributor.googleauthor | 홍윤호 | - |
dc.contributor.googleauthor | 김성민 | - |
dc.contributor.googleauthor | 김승현 | - |
dc.contributor.googleauthor | 이광우 | - |
dc.contributor.googleauthor | 성정준 | - |
dc.relation.code | 2012206005 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | kimsh1 | - |
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