2016 Fiscal Year Final Research Report
Involvement of NUB1 in the early phase of Lewy body disease
| Project/Area Number |
26430050
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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 |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 脳神経疾患 / レビー小体病 / シャペロン分子 |
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| Outline of Final Research Achievements |
Abnormal α-synuclein (Syn) is deposited in neuronal cytoplasmic inclusions and presynapses in Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Previously we have shown that NUB1 is accumulated in these specific regions together with abnormal Syn and that NUB1 is able to inhibit α-synuclein aggregation in cultured cells. We therefore created transgenic (Tg) mice expressing both NUB1 and abnormal Syn to investigate the role of NUB1 on degradation of abnormal Syn in vivo. Immunohistochemical and biochemical studies confirmed that NUB1 was over-expressed in neurons of mice expressing NUB1 (NUB1 Tg), and both NUB1 and abnormal Syn (double Tg). Normal and abnormal Syn levels were unchanged between abnormal Syn Tg mice (Lewy body disease model mice) and double Tg mice. Pathological observations were almost similar between them. Biochemical analysese showed that level of insoluble Syn were lower in double Tg mice compared with abnormal Syn Tg mice.
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| Free Research Field |
分子神経病理学
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