Volume 35, Issue 5 pp. 570-576
Original Article
Full Access

N-acetylgalactosaminyl GD1a is a target molecule for serum antibody in Guillain-Barré syndrome

Susumu Kusunoki MD

Corresponding Author

Susumu Kusunoki MD

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Japan

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113 JapanSearch for more papers by this author
Atsuro Chiba MD

Atsuro Chiba MD

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Japan

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Kazuo Kon

Kazuo Kon

Department of Membrane Biochemistry, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan

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Susumu Ando MD, PhD

Susumu Ando MD, PhD

Department of Membrane Biochemistry, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan

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Kazuko Arisawa

Kazuko Arisawa

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Japan

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Asako Tate

Asako Tate

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Japan

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Ichiro Kanazawa MD

Ichiro Kanazawa MD

Department of Neurology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Japan

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First published: May 1994
Citations: 153

Abstract

Serum antibodies against such major glycolipids as GM1, GD1b, and LM1 have been reported in patients in the acute phase of Guillain-Barré syndrome (GBS). Because minor unidentified glycolipids also may be targets of antibodies in GBS sera, we assayed serum antibody against a crude ganglioside fraction using thin-layer chromatogram immunostaining. Antibody activity was detected against a band that migrated just below GD1a in 6 of the 50 patients with GBS tested. Antibody titer, as determined by enzyme-linked immunosorbent assay, decreased during the course of the disease. All 6 patients had suffered gastrointestinal infection before the neurological onset of GBS and showed low amplitudes for the compound muscle action potentials and normal or only slightly decreased nerve conduction velocities. Thin-layer chromatogram immunostaining did not show this antibody activity in any of the 16 normal and 119 disease controls. 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 N-acetyl-galactosaminyl GD1a.

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