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Pathogenic role of glial cells in Parkinson's disease

Authors

  • Peter Teismann PhD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Kim Tieu PhD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Oren Cohen MD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Dong-Kug Choi PhD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Du Chu Wu MD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Daniel Marks,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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    • Daniel Marks is a student at the Mamaroneck High School, Mamaroneck, New York, USA.

  • Miquel Vila MD, PhD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Vernice Jackson-Lewis PhD,

    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
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  • Serge Przedborski MD, PhD

    Corresponding author
    1. Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
    2. Department of Pathology, Columbia University, New York, New York, USA
    • BB-307 Columbia University, 650 West 168th Street, New York, NY 10032
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Abstract

An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;19:119).

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of these neurons is associated with a glial response composed mainly of activated microglial cells and, to a lesser extent, of reactive astrocytes. This glial response may be the source of trophic factors and can protect against reactive oxygen species and glutamate. Alternatively, this glial response can also mediate a variety of deleterious events related to the production of pro-oxidant reactive species, and pro-inflammatory prostaglandin and cytokines. We discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how those factors may contribute to the pathogenesis of this disease. © 2002 Movement Disorder Society

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