| Project/Area Number |
23591228
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurology
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKEDA Atsushi 東北大学, 大学院医学系研究科, 准教授 (70261534)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
NAGAI Yoshitaka 独立行政法人国立精神・神経医療研究センター, 神経研究所, 室長 (60335354)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | パーキンソン病 / 異常凝集タンパク / αシヌクレイン / プリオン仮説 / エキソソーム / 小胞輸送 / ダイナミン / エンドソーム / α-シヌクレイン / セルトラリン / 多系統萎縮症 / エンドサイトーシス / 神経細胞 / オリゴデンドログリア / 細胞間伝播 |
|---|
| Research Abstract |
The intracellular deposition of misfolded proteins is a common neuropathological hallmark of most neurodegenerative disorders. Increasing evidence suggests that these pathogenic proteins may spread to neighboring cells and induce the propagation of neurodegeneration. In this study, we showed that unlike prion protein, extracellular alpha-synuclein (aS), a major constituent of intraneuronal inclusions in Parkinson's disease, was mainly recovered in the supernatant fraction rather than in exosome-containing pellets from the neuronal culture medium and cerebrospinal fluid. In addition, we identified that the extracellular secretion of aS was secreted via Rab11-mediated recycling pathway (Hasegawa T, et al., PloS One 2011). Furthermore, we demonstrated that aSwas taken up by neuronal and oligodendroglial cells bu dynamic-dependent endocytosis (Konno M, et al., Mol Neurodegener 2012).
|
