| Project/Area Number |
13671445
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
MORIOKA Motohiro Kumamoto University School of Medicine, Department of Neurosurgery, Instructor, 医学部附属病院, 助手 (20295140)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Satoshi Kumamoto University School of Medicine, Department of Neurosurgery, Associate Professor, 医学部, 助教授 (50240916)
HAMADA Jun-ichiro Kumamoto University School of Medicine, Department of Neurosurgery, Assistant Professor, 医学部附属病院, 講師 (40253752)
USHIO Yukitaka Kumamoto University School of Medicine, Department of Neurosurgery, Professor, 医学部, 教授 (20028583)
YANO Shigetoshi Kumamoto University School of Medicine, Department of Neurosurgery, Instructor, 医学部附属病院, 助手 (60332871)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | HIPPOCAMPUS / ISCHEMIA / TAR FACTOR / PHOSPHORYLATION / NEURONAL CELL DEATH / 燐酸化反応 |
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| Research Abstract |
Tau factor is cytoskeletal protein, which regulated by phosphorylation reaction. Recently, hyperphosphorylated tau factor is known to be involved in the mechanism of Alzheimer Disease. We examined the phosphorylation state of tau factor in the hippocampus after transient forebrain ischemia. The hyperphosphorylation of serin199/202 was transiently found in CA1 subfield, while the phosphorylation of serin396 did not change. Furthermore, we prepared 199/202-dephosphorylated form-tau factor by the site directed mutagenesis combined with TAT protein. Intraventricle injection of this dephosphorylated form-tau prevented ischemic neuronal cell death, while normal form-tau did not. It is concluded that the hyperphosphorylation of serin199/202 play an important role for neuronal cell death after transient ischemia.
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