| Project/Area Number |
22390175
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Yokohama City University (2012)
Nagoya University (2010-2011) |
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Principal Investigator |
TANAKA Fumiaki 横浜市立大学, 医学研究科, 教授 (30378012)
|
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| Co-Investigator(Kenkyū-buntansha) |
SOBUE Gen 名古屋大学, 医学系研究科, 教授 (20148315)
KATSUNO Masahisa 名古屋大学, 医学系研究科, 准教授 (50402566)
IIJIMA Masahiro 名古屋大学, 医学系研究科, 特任助教 (40437041)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2012: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2011: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2010: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
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| Keywords | ALS / 運動ニューロン / dynactin-1 / 線虫モデル / オートファジー / 孤発性ALS / dynactin1 / 神経変性 / マウスモデル |
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| Research Abstract |
In the present study, we generated a Caenorhabditis elegans model in which the expression of DNC-1, the homolog of dynactin 1, is specifically knocked down in motor neurons. This model exhibited severe motor defects together with axonal and neuronal degeneration. We also observed impaired movement and increased number of autophagosomes in the degenerated neurons. Furthermore, the combination of rapamycin, an activator of autophagy, and trichostatin which facilitates axonal transport dramatically ameliorated the motor phenotype and axonal degeneration of this model.
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