| Project/Area Number |
08670695
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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 |
Neurology
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| Research Institution | University of Tokyo |
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Principal Investigator |
KUSUNOKI Susumu University of Tokyo, Graduate School of Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (90195438)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | ganglioside / neuropathy / peripheral nerve / Guillain-Barre syndromo / glycolipid / ataxia / 末梢神経 / 感覚神経 |
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| Research Abstract |
Antiganglioside antibodies are frequently elevated in sera from patients with autoimmune neuropathies. They may be involved in the pathogenetic mechanisms as autoantibodies. We have reported induction of experimental sensory ataxic neuropathy by sensitization of rabbits with ganglioside GD1b, which are localized in the primary sensory neurons. Axonal degeneration of the primary sensory neurons conveying deep sensation was observed pathologically. Elevation of anti-GD1b antibody in high titer and absence of lymphocytic infiltration suggested that anti-GD1b antibody is the crucial factor for induction of this expermental neuropathy. Lymphocytic infiltration was not detected even in the early preclinical period. Anti-GD1b antibody of IgM class reached the peak level in four weeks after the first immunization. The elevation of the IgG antibody followed that. The neurological signs developed after that. GD1b-positive primary sensory neurons were with large diameters. One rabbit which were followed for 5 months after the neurological onset improved and again worsened. THe anti-GD1b antibody decreased and increased in association with the clinical course. In the three affected rabbits from which blood was taken frequently, the antibody titer decreased and the clinical findings improved markedly. The binding of the anti-GD1b antibody(especially the IgG class)to the large primary sensory neurons, which convey deep sensation, therefore may be the important step in the pathogenesis of this experimental neuropathy. Removal of anti-GD1b antibody may be effective for the treatment of this neuropathy.
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