A novel model of multiple sclerosis and multiple system atrophy that are differentially manifested by the time of abnormal protein expression

About this project

Japan Grant Number
JP20K20470
Funding Program
Grants-in-Aid for Scientific Research
Funding organization
Japan Society for the Promotion of Science
Project/Area Number
20K20470
Research Category
Grant-in-Aid for Challenging Research (Pioneering)
Allocation Type
  • Multi-year Fund
  • Single-year Grants
Review Section / Research Field
  • Medium-sized Section 52:General internal medicine and related fields
Research Institution
  • International University of Health and Welfare
  • Kyushu University
Project Period (FY)
2019-06-28 〜 2023-03-31
Project Status
Completed
Budget Amount*help
26,000,000 Yen (Direct Cost: 20,000,000 Yen Indirect Cost: 6,000,000 Yen)

Research Abstract

私たちは中枢脱髄疾患の多発性硬化症(MS)患者が後に小脳/錐体外路等を侵す多系統萎縮症(MSA)を発症する例やMS病巣へのα-シヌクレイン(α-syn)蓄積から、両者共通のグリオパチーへのα-synの関与を考え、A53T変異α-synをTet-off系で任意の期間オリゴデンドログリアに発現できるマウスを樹立した。離乳直後から変異α-synを発現させると脳幹から頚髄の顕著な脱髄を示す進行型MS、成熟期以降に発現させると小脳型MSAを呈した。本研究では①変異α-syn発現時期によりMSとMSAを示す新規モデルを用いたグリオパチー機序の解明、②MSとMSAの髄液網羅的解析と分子病理学的解析による共通病態関連分子の同定、③グリア標的治療開発を行なう。

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