| Project/Area Number |
05670551
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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 | University of Tokyo |
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Principal Investigator |
KUSUNOKI Susumu Department of Neurology, Faculty of Medicine University of Tokyo, Research Associate, 医学部(医), 助手 (90195438)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Guillain-Barre' syndrome / Ganglioside / Glycolipid / Galactocerebroside / Mycoplasma pneumoniae / Myelin / Demyelination / Neuropathy / フィッシャー症候群 / GQ1b / GM1 / シァリダーゼ / GalNAc-GD1a / GQ16 / GD16 |
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| Research Abstract |
Because of the effectiveness of plasmapheresis, humoral factors including autoantibodies may function in the pathogenetic process of Guillain-Barre' syndrome (GBS). Serum antibodies against several glycolipids have been reported in patients in the acute phase sera of GBS,their titers decreasing with clinical improvement. Because minor unidentified glycolipids also may be targets of antibodies in GBS sera, we assayd serum antibody against a crude ganglioside fraction using thin-layr chromatogram (TLC) immunostaining. Antibody activity was detected against a band that migrated just below GD1a in 6 of the 50 patients with GBS tested. The unidentified glycolipid was isolated by DEAE-Sephadex A-25 column chromatography, sialidase treatment, and Iatrobeads column chromatography. Fast atom bombardment-mass spectra showed it to be GalNAc-GD1a. All 6 patients had suffered gastrointestinal infection before the neurological onset of GBS and showed low amplitudes for the compound muscle action pot
… More
entials and normal or only slightly decreased nerve conduction velocities. Therefore, this antibody may be raised in GBS with axonal damage or demyelinative change in the most distal sites of the peripheral nerve. Future study is necessary for determining localization of GalNAc-GD1a. Mycoplasma pneumoniae is one agent of the infections preceding GBS.Four of 82 patients with GBS suffered from mycoplasma infection before onset of GBS.All four patients had antibody against galactocerebroside (Gal-C). Two of 78 patients with GBS without mycoplasma infection had anti-Gal-C antibody but none of the disease or normal controls had it. Thus anti-Gal-C antibody may be characteristically raised in GBS subsequent to mycoplasma infection. Gal-C is known to be an important antigen in myelin, and sensitization to Gal-C has been reported to cause antibody-mediated demyelinative neuropathy in rabbit. The anti-Gal-C antibodies may function in the pathophysiologic mechanism of demyelinative neuropathy in patients with GBS subsequent to mycoplasma infection. Less
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