2016 Fiscal Year Final Research Report
Study of microglial transformation mechanism for ALS therapy
| Project/Area Number |
15K19006
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General medical chemistry
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Keywords | 脊髄損傷 / ミクログリア / ケラタン硫酸 / ALS / 脊髄変性疾患 / 形質転換 |
|---|
| Outline of Final Research Achievements |
We elucidated the mechanism of keratan sulfate involvement in ALS pathogenesis. Increased expression of chemokines (CCL 2, CCL 3, CCL 4, CC 5, CCL 7, CCL 12) was observed in the KSPG deficient mouse group. In addition, upregulation of ligand / receptor related to GAG binding was identified. Chemokines are basic proteins that exert their effects through G protein-coupled receptors. Then, chemokines cause migration such as white blood cells and are involved in the formation of inflammation. In summary, GAG binding due to the presence of KSPG was thought to be involved in the onset of spinal degeneration.
|
| Free Research Field |
脊椎外科
|
