| Project/Area Number |
25830044
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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 | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
SEKIYAMA Kazunari 公益財団法人東京都医学総合研究所, 認知症・高次脳機能研究分野, 主任研究員 (40572764)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 神経変性疾患 / シヌクレイノパチー / アディポネクチン / α-シヌクレイン / トランスジェニックマウス / シヌクレイン / 神経変性 |
|---|
| Outline of Final Research Achievements |
The main objective of this study was to determine whether adiponectin (APN), a adipokine with anti-diabetic and anti-atherosclerosis properties, may protect against α-synucleinopathies, such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB). First, APN was protective in vitro; aggregation of α-synuclein (αS) in B103 neuroblastoma cells expressing αS, was significantly ameliorated by treatment with recombinant APN. Second, various neuropathological features in αS transgenic mice, including αS aggregation and movement disorder, were significantly ameliorated by nasal treatment of the mice with APN. Our results suggest that APN may act as anti-neuropathogenic in the pathogenesis of α-synucleinopathies and that APN signaling pathway might be a therapeutic target of α-synucleinopathies.
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