| Project/Area Number |
11470362
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Gifu University |
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Principal Investigator |
SUGIYAMA Kazuhisa (2000-2001) Gifu University, School of Medicine, Associate Professor, 医学部, 助教授 (80179168)
北澤 克明 (1999) 岐阜大学, 医学部, 教授 (20009484)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASE Kazuhide Gifu University, School of Medicine, Assistant professor, 医学部・附属病院, 講師 (40234067)
TANIGUCHI Toru Gifu University, School of Medicine, Assistant professor, 医学部・附属病院, 講師 (30179840)
YAMAMOTO Tetsuya Gifu University, School of Medicine, Professor, 医学部, 教授 (50134581)
UCHIDA Hideya Gifu University, School of Medicine, Assistant professor, 医学部・附属病院, 講師 (70273133)
杉山 和久 岐阜大学, 医学部・附属病院, 講師 (80179168)
富田 剛司 東京大学, 医学部, 助教授 (30172191)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2001: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1999: ¥6,800,000 (Direct Cost: ¥6,800,000)
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| Keywords | glaucoma / optic neuropathy / neuroprotection / calcium-channel blocker / NMDA受容体阻害薬 / 二酸化炭素 |
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| Research Abstract |
We first established two experimental models of glaucomatous optic neuropathy: one by intracameral Indian ink injection followed by laser irradiation to the chamber angle and the other by direct optic nerve damage with a clip. Using the models, several kinds of drugs were investigated in terms of possible neuroprotective effect on glaucomatous.optic neuropathy. Noncompetitive NMDA receptor antagonists, T-588, tacrolimus and betaxolol successfully showed neuroprotective effects on the models, which were confirmed by retinal ganglion cell counts, histopathology and electroretinogram measurement. These results suggest the possibility of IOP-independent glaucoma therapy by pharmacological modification of the apoptotic process.
Another rat model for retinal ganglion cell apoptosis was created by thrombosis formation and reperfusion of the retinal arteries. Time-dependent apoptotic reaction was observed in the model, suggesting that the model might be used for investigation of glaucomatous optic neuropathy.
We investigated lOP-independent factors for development and progression of glaucomatous optic neuropathy in a clinical setting. A multivariate analysis demonstrated several lOP-independent factors such as optic disc hemorrhage, peripapillary atrophy and abnormal orbital hemodynamics were associated with progression of glaucomatous optic neuropathy. Calcium-channel blocker treatment was associated with favorable prognosis of optic neuropathy.
These results indicate the possibility of totally new treatment modalities for glaucoma other than currently used ocular hypotensive therapy.
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