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Brain Advance Access originally published online on July 11, 2007
Brain 2007 130(8):1978-1980; doi:10.1093/brain/awm161
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© The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Scientific Commentary

Schwann cells and their precursors for repair of central nervous system myelin

Jeffery D. Kocsis and Stephen G. Waxman

Department of Neurology,
Yale University School of Medicine,
New Haven, Connecticut 06510; and
Rehabilitation Research Center,
Veterans Affairs Connecticut Healthcare System,
West Haven, Connecticut 06516, USA

E-mail: jeffery.kocsis@yale.edu

The first 150 words of the full text of this article appear below.

In multiple sclerosis (MS), axons of the central nervous system lose their myelin sheaths, and there is also death of oligodendrocytes. Although some demyelinated axons rebuild their membranes so that they can conduct action potentials in the absence of myelin insulation, others do not; and loss of the myelin thus impairs impulse conduction either temporarily or permanently. Mounting evidence also suggests that loss of central myelin may have the secondary consequence of making axons more sensitive to damage or may, in itself, produce changes that impair axonal integrity, thereby leading to cumulative loss of axons that culminates in irreversible neurological deficits (Waxman, 2006Go). While a number of treatments such as the beta interferons (IFN-ß) and glatirimer acetate (GA) are now available for the treatment of MS, and clinical studies using autologous haematopoietic stem cell transplantation (HSCT) and monoclonal antibody interventions in MS patients have shown profound suppression of inflammatory . . . [Full Text of this Article]


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