| Project/Area Number |
26640031
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Doshisha University |
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Principal Investigator |
Saitoh Naoto 同志社大学, 生命医科学部, 准教授 (90334226)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 神経変性疾患 / 神経科学 |
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| Outline of Final Research Achievements |
I have focused on the mechanisms of the neurodegenerative disease. Especially, the relation between Ab toxicity and neuronal homeostatic plasticity is the most important issue in this work. Ab is the well-known molecule for the cause of Alzheimer’s disease. After hippocampal primary culture got network activity, Ab was applied to the culture media. Ab has no acute effect on the cultured neuron activity. In several days, though, Ab diminished the presynaptic size both of excitatory and inhibitory synapse. Network activity is not changed at 37C, but changed at 28C. These results indicate temperature-sensitive homeostatic plasticity rescued from the toxicity of Ab in the experimental condition. In addition, BDNF might completely eliminate the toxicity of Ab, so there was no network activity change.
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