| Project/Area Number |
16591136
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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 |
Psychiatric science
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| Research Institution | OSAKA UNIVERSITY |
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Principal Investigator |
TANAKA Toshihisa Osaka University, Graguate School of Medicine, Assistant Professor, 医学系研究科, 講師 (10294068)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEDA Masatoshi Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (00179649)
KUDO Takashi Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (10273632)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Alzheimer disease / Tau Protein / Apoptosis |
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| Research Abstract |
Neurofibrillary tangles (NFTs) are neuropathological hallmarks of Alzheimer disease (AD) and abnormally hyperphosphorylated tau is the major protein component of NFTs. According to our previous studies on the regulation of phosphorylation of tau protein, an involvement of intrinsic anti-apoptotic factor in neurodegenerative process in AD, is speculated. Therefore XIAP (X chromosome-linked inhibitor of apoptosis), one of intrinsic anti-apoptotic proteins, was investigated in this study. First, transfected XIAP protected COS cells from death and increased phosphorylation of tau protein in cells treated with 1 μM of wortmannin, an inhibitor to phosphatidylinositol 3-kinase. Second, the binding of XIAP with N-terminal tau sequence was observed only when the first methionine was deleted. These results suggest that XIAP might be involved in neurodegenerative process of AD or tauopathy, that is slowly progressive.
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