Novel Treatment of Traumatic Brain Injury by Combining Modulation of Trophic Factor Midkine Expression and Exercise Therapy

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K23291
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0909:Sports sciences, physical education, health sciences, and related fields
• Research Institution: Kagoshima University
• Principal Investigator: Takada Seiya 鹿児島大学, 医歯学総合研究科, 特任助教 (00878283)
• Project Period (FY): 2020-09-11 – 2022-03-31
• Keywords: ミッドカイン / 神経炎症 / 外傷性脳損傷

Outline of Final Research Achievements

This study examined whether anti-midkine aptamers, which suppress the expression of the neurotrophic factor midkine, reduce secondary damage after traumatic brain injury.
Deletion of the midkine gene and use of midkine inhibitors have been shown to reduce local inflammation. It has also been previously reported that deletion of the midkine gene reduces secondary injury after traumatic brain injury.
In the present study, anti-midkine aptamers were shown to significantly reduce the amount of brain injury after traumatic brain injury as much as in mice lacking the midkine gene.

Free Research Field

理学療法

Academic Significance and Societal Importance of the Research Achievements

外傷性脳損傷後の薬剤治療において、有効な方策を欠いているのが現状であるが、ミッドカインは新規の治療標的として大変魅力的である。ミッドカインは発生発達段階で一過性に発現が増加し、正常成体内ではほとんど発現しない。ミッドカイン遺伝子欠損マウスは明らかな発達遅延は観察されず、成体での異常行動も報告されていない。したがってミッドカインの発現抑制は副作用が小さいことが予想される。