A novel rescue factor for Alzheimer's disease
| Project/Area Number |
15H04689
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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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(Kenkyū-buntansha) |
羽生 春夫 東京医科大学, 医学部, 主任教授 (10228520)
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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 |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | CLSP / humanin / アルツハイマー病 / Humanin / 神経細胞死 / 神経細胞死抑制因子 / ヒューマニン / シグナル伝達 / 脳神経疾患 / 薬理学 / アルツハイマー病抑制因子 |
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| Outline of Final Research Achievements |
The mechanism underlying the Alzheimer’s disease (AD) pathogenesis and the detailed regulation of the rescue activity of calmodulin-like skin protein (CLSP)have been addressed. First, multiple CLSP-inhibitors have been identified and their ways of CLSP inhibition have been investigated in detail. The mechanism underlying the neuronal cell death by an uncoordinated-5C variant, an AD risk protein, has been elucidated. Second, it has been shown using CLSP transgenic mice that the overexpression of CLSP antagonizes the synaptic loss and memory impairment in AD model mice. Finally, the concentrations of CLSP in the human cerebrospinal fluids have been shown to be unaffected by the presence of AD.
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Report
(4 results)
Research Products
(11 results)
