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NEUROLOGY 2005;65:1802-1804
© 2005 American Academy of Neurology


Brief Communications

{alpha}7-Acetylcholine receptor antibodies in two patients with Rasmussen encephalitis

R. Watson, DPhil, J.E.C. Jepson, BSc, I. Bermudez, PhD, S. Alexander, BSc, Y. Hart, MD, FRCP, K. McKnight, MRCP, A. Roubertie, MD, F. Fecto, J. Valmier, MD, PhD, D. B. Sattelle, ScD, D. Beeson, PhD, A. Vincent, FRCPath and B. Lang, PhD

From the Neurosciences Group (Drs. Watson, McKnight, Beeson, Vincent, and Lang, S. Alexander and F. Fecto), Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital; MRC Functional Genetics Unit (Dr. Sattelle, J.E.C. Jepson), Department of Human Anatomy and Genetics, University of Oxford; School of Biomedical Sciences (Dr. Bermudez), Oxford Brookes University; Department of Clinical Neurology (Dr. Hart), Radcliffe Infirmary, Oxford, UK; and INSERM U-583 (Drs. Roubertie and Valmier), Institut des Neurosciences de Montpellier, Université Montpellier II, Montpellier, France.

Address correspondence and reprint requests to Dr. B. Lang, Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Ox-ford, John Radcliffe Hospital, Oxford OX3 9DS, UK; e-mail: blang{at}hammer.imm.ox.ac.uk

Rasmussen encephalitis (RE) sera were screened for antibodies to human {alpha}7 nicotinic acetylcholine receptors (nAChRs) using electrophysiology, calcium imaging, and ligand binding assays. Sera from two of nine patients with RE blocked ACh-induced currents through {alpha}7 nAChRs and the ACh-induced rise in intracellular free calcium ([Ca2+]i) and inhibited 125I-{alpha}-bungarotoxin binding in cells expressing {alpha}7 nAChRs. Thus, the {alpha}7 nAChR is a potential target for pathogenic antibodies in patients with RE.


Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the December 13 issue to find the title link for this article.

Editorial, see page 1688

See also pages 1701 and 1730

Supported by the Medical Research Council of the United Kingdom (R.W., K.McK., D.B.S., D.B.), Biotechnology and Biological Sciences Research Council (J.E.C.J.), the Wellcome Trust (B.L., I.B., S.A.), and the Muscular Dystrophy Campaign (D.B.).

Disclosure: The authors report no conflicts of interest.

Received May 10, 2005. Accepted in final form October 11, 2005.


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