| Project/Area Number |
20590335
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Hirosaki University |
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Principal Investigator |
TANJI Kunikazu Hirosaki University, 大学院・医学研究科, 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)
今泉 忠淳 弘前大学, 大学院・医学研究科, 助教 (90232602)
吉田 秀見 弘前大学, 大学院・医学研究科, 講師 (40201008)
松宮 朋穂 弘前大学, 大学院・医学研究科, 助教 (30344592)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 脳神経疾患 / 蛋白質 / プロテオーム / 封入体 |
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| Research Abstract |
α-Synuclein is a major component of Lewy bodies in Parkinson's disease (PD) and dementia with Lewy bodies (DLB), as well as of glial cytoplasmic inclusions in multiple system atrophy. NUB I also accumulates specifically in these α-synucleinopathy lesions. In this study, we established a method to detect abnormal α-synuclein found in patients with α-synucleinopathy. This system allowed us to identify abnormal α-synuclein is one of NUB 1-interacting proteins. Further examination revealed that abnormal α-synuclein with proteinase K (PK) resistance exists in presynapses and involved in early stage of patients with PD and DLB. Surprisingly, endogenous NUB1 was also accumulated together with PK-resistant α-synuclein in the presynapses in transgenic mice expressing human α-synuclein with an A53T mutation. These findings suggest that NUB 1 together with abnormal α-synuclein are involved in pathobiology of Lewy body disease.
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