Mechanism of action of Alzheimer's disease-related peptide p3-Alc on neurons
Project/Area Number |
18K07384
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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Research Institution | National Institute of Advanced Industrial Science and Technology (2020) Hokkaido University (2018-2019) |
Principal Investigator |
Hata Saori 国立研究開発法人産業技術総合研究所, 生命工学領域, 主任研究員 (40581012)
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Project Period (FY) |
2018-04-01 – 2021-03-31
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Project Status |
Completed (Fiscal Year 2020)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | アルツハイマー病 |
Outline of Final Research Achievements |
The rapid increase in the number of patients with Alzheimer's disease (AD), the most common form of dementia, has become a social problem, but no effective treatment has yet been established. In this study, we established a quantitative measurement system for the AD-related peptide p3-Alcβ and conducted quantitative analysis in AD patients. The analysis revealed that p3-Alcβ was decreased with the onset of AD. Analysis of the physiological function of p3-Alcβ in the brain revealed that p3-Alcβ has a protective effect against AD-causing factor Aβ-induced neurotoxicity, suggesting that p3-Alcβ may be useful as a novel therapeutic target for AD.
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Academic Significance and Societal Importance of the Research Achievements |
高齢化社会の加速に伴い、特に患者数が多いADへの対策が喫緊の課題となっている。これまでに多数開発されてきたAβをターゲットとしたAD治療薬候補としてとは異なメカニズムによって、本研究で着目した脳内内在性ペプチドであるp3-Alcβは抗AD作用を有することが明らかになった。ADは認知症を発症する20年以上前から脳内において病態変化が起こることから早期診断法の確立も重要なポイントなるが、p3-AlcβはAD発症に伴い減少するため、治療開始をモニターするマーカーとしての有用性も示唆され、AD対処法に診断・治療の両方から貢献しうる。
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Report
(4 results)
Research Products
(24 results)
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[Journal Article] Extracellular release of ILEI/FAM3C and amyloid-β is associated with the activation of distinct synapse subpopulations.2021
Author(s)
Nakano M, Mitsuishi Y, Liu L, Watanabe N, Hibino E, Hata S, Saito T, Saido C T, Murayama S, Kasuga K, Ikeuchi K, Suzuki T, Nishimura M
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Journal Title
Journal of Alzheimer’s disease
Volume: 80
Issue: 1
Pages: 159-174
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Induction of Amyloid-β42 Production by Fipronil and Other Pyrazole Insecticides2018
Author(s)
Cam M, Durieu E, Bodin M, Manousopoulou A, Koslowski S, Vasylieva N, Barnych B, Hammock BD, Bohl B, Koch P, Omori C, Yamamoto K, Hata S, Suzuki T, Karg F, Gizzi P, Haber VE, Bencetic Mihaljevic V, Tavcar B, Portelius E, Pannee J, Blennow K, Zetterberg H, Garbis SD, Auvray P, Gerber H, Fraering J, Fraering PC, Meijer L.
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Journal Title
Journal of Alzheimer's Disease
Volume: 62
Issue: 4
Pages: 1663-1681
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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