Identification of Alzheimer's disease-relevant neuronal death inhibiting molecular basis and its application for drug development
| Project/Area Number |
25460343
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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 |
General pharmacology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUOKA MASAAKI 東京医科大学, 医学部, 教授 (70222297)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アルツハイマー病 / 神経細胞死 / ヒューマニン / 創薬化学 / 細胞内シグナル伝達 / CLSP / UNC5C / アミロイド前駆体タンパク質 / Apollon / 神経科学 |
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| Outline of Final Research Achievements |
In this research program, we have examined the neuronal cell death mechanism underlying Alzhemer’s disease (AD), identified of Humanin (HN), a secreted bioactive peptide factor against AD-relevant neurotoxicity, inducible signal molecules, and confirmed in vivo effect of calmodulin-like skin protein (CLSP) on scopolamine-induced amnesia.
The results were: (1) A598T-APP inhibited TGFbeta2/wild-type APP-induced neuronal death, (2) By differential display, we identified SH3BP5 and Apollon is mediator of HN-neuroprotective signals, and (3) recombinant CLSP, administered intracerebroventricularly or intraperitoneally, ameliorates scopolamine-induced dementia in mice.
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Report
(4 results)
Research Products
(10 results)
