Certain species of anti-ganglioside antibodies are associated with specific
clinical features in various neurologic diseases. Serum autoantibodies to
these minor gangliosides were investigated in a number of neurological dise
ases in order to examine the biological functions of GD1 alpha and GQ1 beta
. Eleven patients with Guillain-Barre syndrome had remarkably high IgG anti
-GD1 alpha antibody titers, but no GD1 alpha was detected in human peripher
al nerve. An absorption study showed that IgG anti-GD1 alpha antibodies fro
m eight of the 11 patients were significantly absorbed by GD1a and GM1b, in
dicative that the IgG anti-GD1 alpha antibodies cross-react with GD1a and G
M1b. Both GDla and CM1b have been reported to be target molecules for serum
antibodies in certain patients with Guillain-Barre syndrome. GD1 alpha may
induce the production of IgG anti-GD1 alpha antibody which cross-reacts wi
th GD1a or GM1b, and subsequently functions in the development of Guillain-
Barre syndrome. The IgGs from six patients with Fisher's syndrome who had t
he anti-GQ1 beta antibody had anti-GQ1b activity as well. All the patients
had external ophthalmoplegia, but no GQ1 beta was detected in the human ocu
lomotor nerve, further evidence that GQ1b, not GQ1 beta, is the molecule ta
rgeted by the autoantibody in Fisher's syndrome. (C) 1999 Elsevier Science
B.V. All rights reserved.