Simultaneous control of the production and degradation of Amyloid be-ta by Sphingosine kinase/sphingosine-1-phosphate signaling
Project/Area Number |
26430059
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Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | Okayama University (2015-2016) Juntendo University (2014) |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
TOMITA Taisuke 東京大学, 大学院 薬学系研究科, 教授 (30292957)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | アルツハイマー病 / S1P / SphK2 / 脂質代謝酵素 / アミロイドβ / スフィンゴシンキナーゼ / スフィンゴシン-1-リン酸 / アポリポプロテインE / スフィンゴシン-1-リン酸 / アストロサイト / Sphingosine kinase / Sphingosine-1-phosphate / APP / Amyloid-beta |
Outline of Final Research Achievements |
Alzheimer disease (AD)is a progressive neurodegenerative disease. The over-production and aggregation of Amyloid beta (Aβ) peptides in brains are considered to be the major pathogenic event for AD. We identified Sphingosine kinase 2 (SphK2) activity is upregulated in AD, and caused to increase the level of Aβ. These results strongly suggest SphK2 and its product sphingosine-1-phosphate are the therapeutic target for AD.
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Report
(4 results)
Research Products
(8 results)