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Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

Authors

  • Antonio L. Teixeira Jr MD, PhD,

    1. Movement Disorders Clinic, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil
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  • Melissa M. Guimarães MSc,

    1. Laboratory of Neuropharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil
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  • Marco Aurélio Romano-Silva MD, PhD,

    1. Laboratory of Neuropharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil
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  • Francisco Cardoso MD, PhD

    Corresponding author
    1. Movement Disorders Clinic, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil
    • Movement Disorders Clinic, Hospital das Clínicas, UFMG, Av. Pasteur 89/1107, 30150–290, Belo Horizonte MG, Brazil
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Abstract

The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca2+ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca2+ levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti–basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction. © 2005 Movement Disorder Society

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