2023 Fiscal Year Final Research Report
Analysis of molecular mechanism underling reactive astrocyte-induced multiple sclerosis
Project/Area Number |
19K07366
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 48040:Medical biochemistry-related
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Research Institution | Oita University (2022-2023) Nagoya University (2019, 2021) |
Principal Investigator |
Ito Norimichi 大分大学, 医学部, 客員研究員 (30726310)
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Project Period (FY) |
2021-01-01 – 2024-03-31
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Keywords | IFITM3 / astrocyte / 脱髄 |
Outline of Final Research Achievements |
Multiple sclerosis is chronic inflammatory disease of central nerve system characterized by demyelination. Molecular mechanism of etiology underling inflammation-induced demyelination is not well-known. Previous study found that IFITM3 is a key molecule in inflammation-induced neuronal impairment. However, It is unknown the involvement of IFITM3 in multiple sclerosis. The purpose of this study is to understand the role of IFITM3 in inflammation-induced demyelination. We found that expression level of IFITM3 increased in cuprizon-treated mice. Increased expression of IFITM3 occurred before demyelination and lasted during inflammation.
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Free Research Field |
神経化学
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Academic Significance and Societal Importance of the Research Achievements |
本研究によりIFITM3は脱髄に先立って惹起される脳内炎症反応により発現誘導されることが明らかとなった。今後IFITM3の発現変化をより詳細に解析することで、IFITM3の測定がMSの診断に役立つなど、臨床応用への発展が期待できる。
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