| Project/Area Number |
26870921
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurology
Pathological medical chemistry
|
|---|
| Research Institution | National Center for Geriatrics and Gerontology |
|---|
Principal Investigator |
SEKIYA Michiko 国立研究開発法人国立長寿医療研究センター, アルツハイマー病研究部, 研究員 (40367412)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | アルツハイマー病 / ミトコンドリア / ショウジョウバエ |
|---|
| Outline of Final Research Achievements |
Using a Drosophila model of Alzheimer’s disease (AD), I found that the reductions in mito-GFP signals in the synapses were not due to either morphological alterations, damages, or altered number of mitochondria. Rather, the results indicate that reduced mito-GFP signals in the synapses is due to reductions in the stability of mitochondrial proteins and/or the delivery of mitochondrial proteins to mitochondria in the cell body. I further demonstrate that that autophagy is upregulated in AD fly neurons, and forced induction of autophagy is sufficient to reduce mito-GFP signals in the synapses similar to that observed in the AD fly model. This study reveals a potential mechanism initiating mitochondrial abnormality in the synapses in the neurodegenerative conditions such as AD and sustained induction of autophagy is involved in this process.
|
