| Project/Area Number |
17K16971
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 正常眼圧緑内障 / 神経保護 / Ripasudil / Edaravone / 網膜神経節細胞 / 軸索再生 / Dock3 |
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| Outline of Final Research Achievements |
Glaucoma, one of the leading causes of irreversible blindness, is characterized by progressive degeneration of optic nerves and retinal ganglion cells（RGCs）. In the mammalian retina, excitatory amino acid carrier 1（EAAC1）is expressed in neural cells, including RGCs, and the loss of EAAC1 leads to RGC degeneration without elevated intraocular pressure. We demonstrated that the topical administration of ripasudil reduces intraocular pressure and exerts neuroprotective effects on glaucomatous degeneration in EAAC1 knockout mice.
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| Academic Significance and Societal Importance of the Research Achievements |
緑内障は我が国における最大の失明原因だが、眼圧降下以外にエビデンスのある治療法は存在せず、新たな治療法が待たれる状況にある。特に日本人の場合は正常眼圧緑内障が全体の約７割を占めるが、眼圧降下が著効を示さないケースも多く、直接的な神経保護薬の開発などが期待される。
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