Visual function and Pathogenesis of Experimental Optic Neuritis
| Project/Area Number |
25861654
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Ophthalmology
|
|---|
| Research Institution | Tokyo Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 神経眼科 / 視神経炎 / 視神経脊髄炎 / neurofascin / ago-glial junction / Neurofascin / 軸索障害 / 軸索変性 / 網膜 / 視力 / ミクログリア / 実験的自己免疫性視神経炎 |
|---|
| Outline of Final Research Achievements |
1.There is a possibility that functional axonal ｄｙsfunction precedes, pathological axonal damage in experimental optic neuritis. 2. Serum neurofascin may be a byproduct of axo-glial junction damage in patients with optic neuritis in neuromyelitis optica. 3. Anti-aquaporin-4 (AQP-4) antibody exists in the aqueous humor of AQP-4 positive optic neuritis patients. Therefore, there is a possibility that inner retinal layer thinning is a result of direct retinal damage.
|
Report
(4 results)
Research Products
(1 results)
