Assessment the inflammatory processes after TBI
| Project/Area Number |
16K20388
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Emergency medicine
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
Hosomi Sanae 大阪大学, 医学系研究科, 招聘教員 (90644005)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 神経炎症 / ミクログリア / 頭部外傷 |
|---|
| Outline of Final Research Achievements |
Experimental and clinical evidence now suggest that TBI should not be viewed as a static acute disorder. Rather, TBI initiates chronic biochemical processes leading to prolonged neuroinflammation that may contribute to late neurologic dysfunction. Recent studies have only identified limited aspects of either acute or chronic inflammation in the brain post-TBI. In this experimental TBI mouse model study using 18F-DPA714 PET, we aimed to reveal the pathophysiology underlying how acute inflammation subsides, sustains and/or converts to chronic inflammation. We found that although inflammatory responses at the cortical injury site diminished after approximately 1 week, the ipsilateral thalamus still exhibited remote neuroinflammation and neurodegeneration for up to 14 weeks.
|
Report
(3 results)
Research Products
(3 results)
