| Project/Area Number |
25460893
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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 internal medicine(including psychosomatic medicine)
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| Research Institution | University of Fukui |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Naiki Hironobu 福井大学, 医学部, 教授 (10227704)
Shirafuji Norimichi 福井大学, 医学部附属病院, 医員 (40529319)
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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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アルツハイマー病 / タウ蛋白 / タウオリゴマー / 神経細胞死 / ピオグリタゾン / オリゴマー / GSK3β |
|---|
| Outline of Final Research Achievements |
One of the pathological hallmarks of Alzheimer’s disease (AD) is neurofibrillary tangle (NFT) which is composed of highly phosphorylated tau protein. It was shown that oligomeric tau causes neuronal cell death. We have demonstrated that neuronal cell models which express the wild type tau protein via TET OFF induction shows 120 kDa, 180 kDa, and 240 kDa oligomeric tau in sarkosyl insoluble fraction which was shown by Western blotting. It was also shown that oligomeric tau activates caspase3, and induces neuronal cell death. We have also determined that pioglitazone, PPARgamma agonist, decreased phosphorylated tau, as well as oligomeric tau.
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