| Project/Area Number |
06807056
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Tottori University |
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Principal Investigator |
SHIMOMURA Tokio Tottori University, Associate Professor, 医学部, 助教授 (00216136)
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| Co-Investigator(Kenkyū-buntansha) |
URAKAMI Katsuya Tottori University, Lecturer, 医学部, 講師 (30213507)
高橋 和郎 鳥取大学, 医学部, 教授 (10031965)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Superoxide dismutase (SOD) / G-protein / Neurotransmitter / Intracellular calcium / Point mutation / Mitochondria / Gsa / エクソン9 / Gsa / GTP結合蛋白 / アルツハイマー病 / SOD / ラジカルスカベンジャー / mRNA / DNA / PCR / SSCP |
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| Research Abstract |
We investigated concentration of Cu, Zn superoxide dismutase (SOD1) in fibroblasts in patients with senile dementia of the Alzheimer type (SDAT). The levels of SOD1 in fibroblasts were significantly lower in the patients with SDAT than in the control subjects. The levels of mRNA of SOD1 in fibroblasts were significantly lower in the patients with SDAT than in the controls. In the patients with migraine, activities and concentrations of SOD1 in platelets were significantly lower than in the controls. None of the patients with SDAT had any mutations or deletions in the mitochondrial gene related to the pathophysiology of the disease. Twenty-five percent of the patients with migraine had a mutation in mitochondrial DNA.The mobilization of intracellular calcium (Ca^<2+>) was lower in the patients with SDAT than in the controls when platelets were stimulated with serotonin. It was not statistically significant. We investigated the gene of GTP coupling protein using polymerase chain reaction and single-strand conformation polymorphism, especially exon 8 and exon 9 in the gene of Gsalpha in the patients with SDAT.They had no mutations in the exon 8 and exon 9 in the gene of Gsalpha. It is suggested that low levels of SOD and mRNA of SOD may play an important role in the development of SDAT.In migraine, it is suggested that low platelet SOD levels may play a role in the etiology of migraine. We suggest a relation between low levels of SOD and mitochondrial dysfunction or mutation in mitocondrial gene in migraine.
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