| Project/Area Number |
16K11308
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
HARADA Chikako 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, 研究員 (20435720)
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| Research Collaborator |
HARADA takayuki
NAMEKATA kazuhiko
KAKU gyorei
KIMURA atsuko
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 緑内障 / 神経保護 / 軸索再生 / 遺伝子発現 / 視神経外傷 / 既存薬 / 神経栄養因子 |
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| Outline of Final Research Achievements |
We demonstrated the neuroprotective effects of existing drugs, such as Rho/ROCK inhibitor eye drops, edaravone used for cerebral infarction, and N-acetylcysteine used as expectorant, and published these findings. In addition, we found that loss of neuritin, one of the trophic factors, increases neural cell death after optic nerve injury. We also found that loss of TrkB, one of the major neurotrophin receptors, induces normal tension glaucoma-like retinal degeneration after 6 months of age.
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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であり、眼圧降下以外の手法による神経保護療法の開発が期待されている。そこで本研究では複数の緑内障モデル動物を用いて、安全性が確立した既存薬による細胞保護療法の可能性を示した。また特定の遺伝子発現の変化が神経細胞の耐性に与える影響を検討して、将来の薬物開発や新たな疾患モデルの開発に道をつけた。
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