Identification of neurotoxic Abeta oligomers and development of therapy against them
Project/Area Number |
15K09305
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Hirosaki University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
SHOJI Mikio 弘前大学, 大学院医学研究科, 教授 (60171021)
NAKAMURA Takumi 弘前大学, 医学部附属病院, 助教 (80744193)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | Abeta oligomer / Alzheimer's disease / tau / lipid rafts / vaccine / アルツハイマー病 / 神経毒性 / アミロイド / タウ / fyn / NMDA receptor / synapse / Abeta / oligomer / sinaptosome |
Outline of Final Research Achievements |
Abeta dimers were accumulated in synaptic lipid rafts with increased fyn, phosphorylated NMDA receptors and phosphorylated tau in Alzheimer’s disease (AD) model mice. Abeta dimers could be neurotoxic Abeta to induce fyn/NMDA cascade and phosphorylated tau. We generated a novel transgenic plant-based vaccine, a soybean storage protein containing Abeta4-10, named Abeta+. Abeta+ was administered orally to AD model mice. Spatial learning deterioration was prevented. Soluble Abeta oligomers were decreased. Abeta deposition and microgliosis was inhibited. Decrease of soluble Abeta oligomers by our vaccine could be a promising therapy for AD.
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Report
(4 results)
Research Products
(28 results)