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Animal model of axonal Guillain‐Barré syndrome induced by sensitization with GM1 ganglioside
Author(s) -
Yuki Nobuhiro,
Yamada Mitsunori,
Koga Michiaki,
Odaka Masaaki,
Susuki Keiichiro,
Tagawa Yumi,
Ueda Shuichi,
Kasama Takeshi,
Ohnishi Akio,
Hayashi Shintaro,
Takahashi Hitoshi,
Kamijo Mikiko,
Hirata Koichi
Publication year - 2001
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.1012
Subject(s) - guillain barre syndrome , wallerian degeneration , sensitization , pathogenesis , ganglioside , medicine , pathology , immunogen , antibody , immunology , peripheral neuropathy , neuroscience , biology , endocrinology , biochemistry , monoclonal antibody , diabetes mellitus
Some humans develop the axonal form of Guillain‐Barré syndrome after receiving bovine brain ganglioside. On sensitization with the ganglioside mixture, all of a group of rabbits injected developed high anti‐GM1 IgG antibody titers, flaccid limb weakness of acute onset, and a monophasic illness course. Pathological findings for the peripheral nerves showed predominant Wallerian‐like degeneration, with neither lymphocytic infiltration nor demyelination. IgG was deposited on the axons of the anterior roots, and GM1 was proved to be present on the axons of peripheral nerves. Sensitization with purified GM1 also induced axonal neuropathy, indicating that GM1 was the immunogen in the mixture. A model of human axonal Guillain‐Barré syndrome has been established that uses inoculation with a bovine brain ganglioside mixture or isolated GM1. This model may help to clarify the molecular pathogenesis of the syndrome and to develop new treatments for it.