2013 Fiscal Year Final Research Report
The role of abnormal alpha-synuclein and its partners in synucleinopathy
| Project/Area Number |
23500425
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Hirosaki University |
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Principal Investigator |
TANJI kunikazu 弘前大学, 医学(系)研究科(研究院), 助教 (10271800)
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| Co-Investigator(Kenkyū-buntansha) |
WAKABAYASHI Koichi 弘前大学, 大学院・医学研究科, 教授 (50240768)
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| Project Period (FY) |
2011 – 2013
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| Keywords | タンパク質分解 / 異常蓄積 / 神経変性 |
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| Research Abstract |
Abnormal synuclein is deposited in the presynapses and cytoplasmic inclusions found in synucleinopathy such as Parkinsons disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy. Likewise, NUB1 is also accumulated in these specific regions together with abnormal synuclein. Although NUB1 can degrade synuclein expressed in cultured cells, it is not clear that NUB1 possesses this ability in vivo. We created transgenic mice expressing NUB1 and synuclein to investigate the role of NUB1 on abnormal synuclein deposition. Immunohistochemical and biochemical studies confirmed that NUB1 was expressed in the neurons. Unexpectedly, however, there were no alterations of abnormal synuclein deposition between mice expressing synuclein and synuclein/NUB1. These results suggest that NUB1 unlikely degrades synuclein in vivo.
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[Presentation] Accumulation of autophagic adaptor protein, p62/sequestosome 1, in the brains of Alzheimer's disease2013
Author(s)
Kunikazu Tanji, Tomoh Matsumiya, Atsushi Maruyama, Saori Odagiri, Fumiaki Mori, Ken Itoh, Akiyoshi Kakita, Hitoshi Takahashi and Koichi Wakabayashi
Organizer
15th International Congress of Immunology
Place of Presentation
Milan, Italy
Year and Date
20130822-27
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