2019 Fiscal Year Final Research Report
Development of neuroprotective strategies for treatment of neurodegenerative diseases
Project/Area Number |
17K07123
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
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Research Institution | Tokyo Metropolitan Institute of Medical Science |
Principal Investigator |
KIMURA Atsuko 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 (60569143)
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Project Period (FY) |
2017-02-23 – 2020-03-31
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Keywords | 神経変性疾患 / 緑内障 / グルタミン酸毒性 / グルタミン酸トランスポーター / 網膜神経節細胞 |
Outline of Final Research Achievements |
Glaucoma is a neurodegenerative disease of the eye and causes irreversible blindness, which is associated with retinal ganglion cell (RGC) death. Studies indicate multiple factors are involved in the pathogenesis of glaucoma. In this study, we explored potential therapeutic strategies for glaucoma. We generated a novel mouse line overexpressing a glutamate transporter, GLAST (GLAST Tg). RGC death was reduced in GLAST Tg mice compared with WT mice in the optic nerve injury model, an animal model of glaucoma, suggesting that overexpression of GLAST may be effective for treatment of glaucoma. On the other hand, when we examined αRGCs and ipRGCs, subtypes of RGCs, in two glaucoma mouse models, the survival rate of these cell types was very high compared with other RGC cell types. These data suggested understanding characteristics of these cell types might help developing new neuroprotective strategies for glaucoma.
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Free Research Field |
神経科学
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Academic Significance and Societal Importance of the Research Achievements |
超高齢化社会に突入した我が国では、緑内障の患者数が加齢と共に増大し続けることが予想されている。緑内障の治療法としては眼圧降下法が主流であるが、特に日本人に最も多い「正常眼圧緑内障」に対しては眼圧を下げる治療だけでは限界がある。そこで、神経保護に着目した今回の研究とその発見は緑内障の新たな治療法開発に大きく寄与することが期待される。
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