Complex gangliosides as autoantibody targets at the neuromuscular junction in Miller Fisher syndrome: a current perspective

O'Hanlon, G.M., Bullens, R.W.M., Plomp, J.J. and Willison, H.J. (2002) Complex gangliosides as autoantibody targets at the neuromuscular junction in Miller Fisher syndrome: a current perspective. Neurochemical Research, 27(7-8), pp. 697-709. (doi:10.1023/A:1020284302718)

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Publisher's URL: http://dx.doi.org/10.1023/A:1020284302718

Abstract

Glycosphingolipid biology has increasingly interfaced with the field of human autoimmune neuropathy over the last two decades. There are currently over 20 distinct glycolipids that have been identified as autoantibody targets in a wide range of clinical neuropathy syndromes. This review sets out the clinical and experimental background to one interesting example of anti-glycolipid antibody-associated neuropathy termed Miller Fisher syndrome. This syndrome, comprising the triad of ataxia, areflexia, and ophthalmoplegia, correlates highly with the presence of serum anti-GQ1b antibodies, arising through molecular mimicry with microbial oligosaccharides. Anti-GQ1b antibodies mediate neural injury through binding to GQ1b-enriched sites in the peripheral nervous system, including extraocular nerves. Animal experimental evidence, along with a hypothetical background, indicates the motor nerve terminal may be a key site for anti-GQ1b antibody binding with consequent defects in synaptic transmission, as occurs in botulism and other toxinopathies. Our work in recent years on this hypothesis is summarized.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Willison, Professor Hugh
Authors: O'Hanlon, G.M., Bullens, R.W.M., Plomp, J.J., and Willison, H.J.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Neurochemical Research
ISSN:0364-3190
ISSN (Online):1573-6903

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