| Project/Area Number |
09470152
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Gunma University |
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Principal Investigator |
OKAMOTO Koichi Gunma University, Department of Neurology, Professor, 医学部, 教授 (00124652)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Makoto Gunma University, Department of Neurology, Associate Professor, 医学部, 講師 (40143226)
水野 裕司 群馬大学, 医学部, 助手 (20282395)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 1998: ¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 1997: ¥7,000,000 (Direct Cost: ¥7,000,000)
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| Keywords | amyotrophic lateral sclersois / spinocerebellar ataxia / Alzheimer's disease / Golgi apparatus / 病理 / Golgi装置 / 免疫染色 |
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| Research Abstract |
We did the morphological, immnocytochemical and molecular researches for amyotrophic lateral scleosis (ALS) spinocerebellar ataxia and Alzheimer's disease. The main results are follows. (1) We made polyclonal antibodies against peptides of MG 160 and human trans-Golgi network, and staining pattern of both antibodies were almost similar to original anti-MG 160 antibody. We are now doing immunohistochemical study of Golgi appatatus in the neurons of many neurodegenerative disordes using these antibodies. (2)In 16 ALS patients, 13.2% of counted Betz cells had fragmented Golgi apparatus in contrast to 0.6% in the 10 non-ALS controls. (3)The temporal lobes of 30 clinically and pathologically confirmed patients with ALS were examined, and we disclosed the characteristic pathology of dementia with ALS.(4)We disclosed that autopsied cases of dementia with ALS were not rarely present in UK.(5)We reported that combination assay for CSF tau, amyloid beta 1-40 and amyloid beta1-42(43) in CSF is a biological marker of Alzheimer's disease. (6) We analysed 13 patients with spinocerebellar ataxia type 2 in Gunma prefecture. (7)We also analysed 16 spinocerebellar ataxia type 6 patients. (8) We reported a Japanese family with adrenoleukodystrophy with a three base deletion (delGAG29l) in the gene. (9) We also reported a familial spinocerebellar ataxia, which has clinical featutes slimar to Friedreich's ataxia. (10) We reported that activated microglia cause iron-dependent lipid peroxidation in the presence of ferritin.
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