Effect of lysosomal enzymes on alpha-synuclein accumulation causing neurodegeneration
| Project/Area Number |
15K06764
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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 | Institute for Developmental Research, Aichi Human Service Center |
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Principal Investigator |
Suzuki Yasuyo 愛知県心身障害者コロニー発達障害研究所, 遺伝学部, 研究員 (60416188)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | α-synuclein / パーキンソン病 / リソソーム / カテプシン / β-グルコセレブロシダーゼ / リソソーム病 |
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| Outline of Final Research Achievements |
α-Synuclein is a 140-amino acid protein and abundant in presynaptic terminals of neurons. Intracellular aggregation of α-synuclein is a pathological feature of neurodegenerative diseases, such as Parkinson’s disease (PD). Lysosomal dysfunction and α-synuclein accumulation are considered as the major pathogenic features in PD. For instance, mutations in β-glucocerebrosidase (GBA) gene, responsible for Gaucher disease, are known as a risk factor for PD. Recent studies demonstrate that deficiency of lysosomal enzymes causes lysosomal dysfunction and α-synuclein accumulation; however, the molecular mechanism of α-synuclein accumulation remains unclear. In this study, we investigated the effects of reduced activity of lysosomal enzymes GBA and cathepsins B and D on α-synuclein accumulation. Our study suggested that dysfunctions of cathepsins B and D are more critical role in accumulation and insolubilization of α-synuclein than the GBA dysfunction.
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Report
(4 results)
Research Products
(14 results)
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[Journal Article] The effect of rapamycin, NVP-BEZ235, aspirin, and metformin on PI3K/AKT/mTOR signaling pathway of PIK3CA-related overgrowth spectrum (PROS).2017
Author(s)
Suzuki Y, Enokido Y, Yamada K, Inaba M, Kuwata K, Hanada N, Morishita T, Mizuno S, Wakamatsu N.
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Journal Title
Oncotarget
Volume: 8(28)
Issue: 28
Pages: 45470-45483
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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