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Autoantibodies to glutamate receptor subunit GluR2 in nonfamilial olivopontocerebellar degeneration

From Geriatric Research, Education and Clinical Center (GRECC), VA Medical Center, Salt Lake City, UT (Drs. Gahring and Rogers); the Program in Human Molecular Biology and Genetics, Eccles Institute of Genetics (Drs. Gahring, Rogers, and Twyman); Huntsman Cancer Institute (Drs. Gahring, Rogers, and Twyman); Department of Medicine, Division of Geriatrics (Dr. Gahring); the Department of Neurobiology and Anatomy (Dr. Rogers); and the Departments of Neurology and Pharmacology (Dr. Twyman), University of Utah School of Medicine, Salt Lake City, UT.
Supported by an award from the Huntsman Cancer Institute and by NIH NINDS grant NS30990, the Esther A. and Joseph Klingenstein Foundation, and the PEW Charitable Trust to S.W.R.; by a VA Merit Review Grant and the American Federation for Aging Research to L.C.G., and by NIH NINDS grant NS31519 and the Mallinckrodt Foundation to R.E.T.
Received March 12, 1996. Accepted in final form May 23, 1996.
Address correspondence and reprint requests to Dr. Gahring, HMBG, Bldg. 533, Rm. 4220, University of Utah School of Medicine, Salt Lake City, UT 84112.

Article abstract-We describe a 63-year-old man with a 5-year history of progressive sporadic olivopontocerebellar atrophy (OPCA) who exhibits high serum titers of IgM autoantibodies to the neuronal glutamate receptor subunit GluR2. Immunohistochemistry revealed intense staining of mouse cerebellar Purkinje cells and cells in the pontine nuclei and olivary complex. Glutamate receptor currents were activated in a subset of cultured mouse neurons by an anti-GluR2 IgM fraction, and they were blocked by the competitive AMPA-type glutamate receptor antagonist CNQX and by a synthetic peptide to a specific epitope region of GluR2 (AA 369-393). The patient was treated with nine courses of plasmapheresis with little improvement of symptomatology. However, IgM titers to GluR2 decreased approximately 8-fold and the serum functional activity decreased proportionally. These findings may suggest a role for autoimmunity to glutamate receptors in the pathophysiology of certain forms of progressive nervous system degeneration.

NEUROLOGY 1997;48: 494-500

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