| Project/Area Number |
17591827
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
KASHIWAGI Kenji University of Yamanashi, University of Yamanashi Hospital, Assistant Professor, 医学部附属病院, 講師 (30194723)
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| Co-Investigator(Kenkyū-buntansha) |
KOGURE Satoshi University of Yamanashi, University of Yamanashi Hospital, Assistant Professor, 医学部附属病院, 講師 (40234736)
MABUCHI Tadashi University of Yamanashi, Department of Research Interdisciplinary Graduate School of Medicine and Engineering, Research Associate, 大学院医学工学総合研究部, 助手 (80150308)
MABUCHI Fumihiko University of Yamanashi, Department of Research Interdisciplinary Graduate' School of Medicine and Engineering, Research Associate, 大学院医学工学総合研究部, 助手 (20322125)
MAEDA Shu-ichiro University of Yamanashi, Department of Research Interdisciplinary Graduate School of Medicine and Engineering, Professor, 大学院医学工学総合研究部, 教授 (10117244)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Retinal ganglion cell / Glaucoma / Animal disease model / culture model / transgenic model / 培養実験 / 個体実験 / 遺伝子改変動物 / 網膜グリア細胞 / 動物実験モデル / 神経細胞培養 / グルタミン酸 / 一酸化窒素 |
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| Research Abstract |
Ocular disease targeting retinal ganglion cell (RGC) loss, such as glaucoma that is secondary cause of acquired blindness in the world, may cause severe and irreversible visual dysfunction. Many kinds of treatment including clinical applied for other diseases are subject to be candidated treatment for this insult. In this particular investigation., we aimed to investigate the effectiveness of either candidated or unknown factors for rescuing RGC loss using prompt and accurate evaluation system for pursuing new clinical treatment. In results, we success to establish new evaluation system for RGC damage, and we investigate several new potential neuron-protective drugs such as latanoprost and iganijipine. We also revealed new aspects regarding mechanism of damage of retinal neuron such as regulating kinase 1 that plays a important role in apoptosis of RGC and success to develop new approach for neuron-protection. We also investigated single nucleotide polymorphisms in glaucoma in genes of OPA-1, apolipoprotein E, and Methylenetetrahydrofolate reductase gene. Furthermore, at present, we are working on revising new in vivo and in vitro disease models, preparing several types of transgenic animals with new evaluation system for them, and developing new animal disease models using primate for investigating RGC disturbance for conducting good platform of translational research system. Those of them are expected to contribute investigation for new aspects of disturbance mechanism of RGC and development of new therapy.
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