Optic neuropathy and related to the visual impairment, elucidation of the central nervous factor on retinal ganglion cell death

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K09722
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56060:Ophthalmology-related
• Research Institution: Hiroshima University
• Principal Investigator: Ko Ji-Ae 広島大学, 医系科学研究科(医), 准教授 (70314797)
• Co-Investigator(Kenkyū-buntansha): 木内 良明 広島大学, 医系科学研究科(医), 教授 (40214738)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 神経保護 / 神経眼科 / 共培養

Outline of Final Research Achievements

The purpose of this research is to develop effective therapeutic agents for neuroprotection against visual impairment. Research aimed at elucidating the interaction between retinal ganglion cells and the midbrain (superior colliculus) and their effects on glial cells, and as a results, established a co-culture method for ganglion cells, surrounding tissues, and cells. It's done. First, as a result of co-culturing retinal ganglion cells and midbrain tissue, we found that midbrain astrocyte-derived neurotrophic factor (MANF) was the signal, and published the results in a paper. Furthermore, three factors, NGF, IGFBP-5, and VEGF, were identified in their interactions with glial cells. We are currently analyzing how these factors affect the protection of retinal ganglion cells.

Free Research Field

細胞生理学

Academic Significance and Societal Importance of the Research Achievements

緑内障は網膜神経節細胞が障害され、視野が狭くなる病気である。その網膜神経節細胞の障害には高眼圧が大きな原因となり、その克服のためには第1選択として、眼圧の低下に効果がある既存の薬を点眼する治療法が優先になる。しかし、その点眼薬の適応も限界があり、いずれにしろ、網膜神経節細胞の変性を止めることができない。しかも、日本人に多い正常眼圧緑内障でも眼圧が正常にも拘らず、神経節細胞の変性が見られる。次第には失明に繋がる。本研究は、神経保護治療に着目し、その為に、一番生体内と変わらない環境で神経細胞に影響を及ぼす因子を突き止め、治療薬を開発することに学術、または社会的意義があると考えている。