| Project/Area Number |
24700363
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | 独立行政法人国立精神・神経医療研究センター (2013)
Hirosaki University (2012) |
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Principal Investigator |
ODAGIRI Saori 独立行政法人国立精神・神経医療研究センター, 神経研究所疾病研究第四部, 流動研究員 (80374817)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 神経変性疾患 / p62 / αシヌクレイン / 該当なし |
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| Research Abstract |
p62 is highly involved with intracellular proteolysis, and it is a component of the ubiquitin-positive inclusions that are observed in various neurodegenerative disorders. In LBD such as dementia with LBs and Parkinson's disease, p62 is localised in LB; furthermore, several lines of evidence show that disrupted proteolysis occurs in this disorder. We used a mouse model of LBD that lacks p62. Immunohistochemical analyses showed that LB-like inclusions were observed in transgenic mice that overexpressed alpha-synuclein (Tg mice) with or without the p62 protein. However, a p62 deficiency enhanced alpha-synuclein pathology with regards to the number of inclusions and staining intensity compared with Tg mice that expressed p62. Furthermore we determined that NBR1 is significantly increased in Tg mice without p62.These findings suggest that p62 and NBR1 effect the pathogenesis of neurodegenerative diseases through the cooperative modulation of alpha-synuclein aggregation.
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