| Project/Area Number |
16K11318
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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 | Chiba University |
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Principal Investigator |
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| Research Collaborator |
Guzel Bikbova
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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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 神経保護 / 視神経再生 / 視神経挫滅モデル / 点眼 / 神経保護合剤 / 合剤 / 再生 / 再生医学 |
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| Outline of Final Research Achievements |
The purpose of this study is to determine the effectiveness of combined topical neurotrophic factors in neuroprotection and regeneration in the optic nerve crush model. The neurotrophic factors studied were TUDCA, citicoline, NT-4, TUDCA+citicoline (doublet-1), TUDCA+NT-4(doublet-2), and citicoline+TUDCA+NT-4(triplet). After two weeks, the number of RGCs and neurofilaments were counted. In all groups except for NT-4, the number of RGCs and neurofilaments were significantly increased. In the triplet group, the numbers were significantly higher than that in all of the single treatment group. In the triplet group, regenerating axons were significantly longer than the control. In conclusion, the combination of the tree neurotrophic factors was the most effective way to protect RGCs and regenerate axons after the optic nerve crush.
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| Academic Significance and Societal Importance of the Research Achievements |
緑内障の神経保護剤として期待されたメマンチンが臨床試験でfailして以来、どの網膜・視神経疾患にも有用な神経保護治療薬が登場してこない状態が続いているが、１つの理由としては、神経細胞死のメカニズムが複雑なため単剤による神経保護剤の治療では限界があることが挙げられる。本研究により、急性疾患のモデルである挫滅モデルで神経保護合剤点眼によって効果が得られる治療が開発される可能性が示された。点眼であれば慢性疾患であっても継続使用が可能であり、慢性の難治性疾患も含めた網膜・視神経疾患の管理において治療戦略の１つとして本研究の治療戦略が臨床応用されることが期待できる。
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