| Project/Area Number |
22790841
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
|---|
| Research Field |
Neurology
|
|---|
| Research Institution | 防衛大学校 |
|---|
Principal Investigator |
AMO Taku 防衛大学校, 応用科学群, 助教 (40453922)
|
|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | パーキンソン病 / ミトコンドリア |
|---|
| Research Abstract |
In PINK1-deficient mouse embryonic fibroblasts(MEFs), mitochondrial membrane potential and cellular ATP levels were decreased compared with those in littermate wild-type MEFs. However, mitochondrial proton leak, which reduces membrane potential in the absence of ATP synthesis, was not altered by loss of PINK1.Instead, activity of the respiratory chain, which produces the membrane potential by oxidizing substrates using oxygen, declined.
|
