| Project/Area Number |
15K15239
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Hygiene and public health
|
|---|
| Research Institution | Fukushima Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | パーキンソン病 / マンガン / ミクログリア |
|---|
| Outline of Final Research Achievements |
I examined the relationship between microglia activation by manganese that did not reach poisoning dose levels and ATP13A2 that functions as a manganese transporter and contributes to hereditary Parkinson's disease using established mouse microglia. Manganese concentration which did not affect cell death of microglia under exposure for 24 hours was up to 1μM, and at that concentration, production of various cytokines measured as an index of microglia activation and mRNA expression level of ATP13A2 showed no difference from control group. At 10μM, which affected cell death, there were significant increases in production of some cytokines and mRNA expression level of ATP13A2, suggesting that microglia activation is related to ATP13A2.
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究により、これまでまったく不明であったマンガンによるミクログリア活性化とATP13A2の役割について、何らかの関連性があることが推察された。このことは、マンガンによるパーキンソン病様症状発症メカニズムに、神経細胞のATP13A2だけでなくミクログリアのATP13A2も関与する可能性を示す重要な成果と思われた。
|
