Development of new therapeutic avenues of multiple sclerosis with a focus on glial activation
Project/Area Number |
23700459
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | 公益財団法人東京都医学総合研究所 (2012) Tokyo Metropolitan Organization for Medical Research (2011) |
Principal Investigator |
KAKU Gyourei 公益財団法人東京都医学総合研究所, 運動・感覚システム研究分野, 主任研究員 (50443114)
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Project Period (FY) |
2011 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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Keywords | 多発性硬化症 / グリア / 自然免疫 / Angiotensin II / 抗炎症性物質 / angiotensin II / ASK1 / Dock8 / RASシステム / 視神経炎 / 抗酸化物質 / EAE / GEF |
Research Abstract |
Experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), was used in our study to develop new therapeutic avenues of multiple sclerosis. Firstly, we found that oral administration of spermidine, a natural component of our diet, reduced the severity of EAE, suggesting that spermidine might be suitable for the treatment of MS. Secondly, we revealed a novel pathway of RAS-NF.B-TLR4-ASK1 in neural and immune cells as a valid therapeutic target for autoimmune disorders in the central nervous system. Thirdly, we found that Dock8 deficiency or overexpression both reduced the severity of EAE, suggesting that modulation of Dock8 expression might be effective for the treatment of MS.
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Report
(3 results)
Research Products
(29 results)
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[Journal Article] Inhibition of ASK1-p38 pathway prevents neural cell death following optic nerve injury.2013
Author(s)
Katome, T., Namekata, K., Guo, X., Semba, K., Kittaka, D., Kawamura, K., Kimura, A., Harada, C., Ichijo, H., Mitamura, Y. and Harada, T.
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Journal Title
Cell Death Differ.
Volume: 20
Issue: 2
Pages: 270-280
DOI
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Peer Reviewed
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[Journal Article] Dock3 attenuates neural cell death due to NMDA neurotoxicity and oxidative stress in a mouse model of normal tension glaucoma
Author(s)
Namekata, K., Kimura, A., Kawamura, K., Guo, X., Harada, C., Tanaka, K. and Harada, T
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Journal Title
Cell Death and Differentiation
Volume: (in press)
Related Report
Peer Reviewed
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