• Chao Zhao, Stephen P J Fancy, Mark R Kotter, Wen-Wu Li, and Robin J M Franklin.
• Cambridge Centre for Brain Repair and Neuroregeneration Laboratory, Department of Veterinary Medicine, Madingley Road, University of Cambridge, Cambridge CB3 0ES, UK.
• J. Neurol. Sci. 2005 Jun 15;233(1-2):87-91.

AbstractThere are two components to the treatment of multiple sclerosis (MS); the first is to prevent damage occurring, and the second is to repair the residual damage. While considerable progress has been made in the recent years with the former through the development of anti-inflammatory and immunomodulatory therapies, there are currently no effective repair therapies routinely used in MS patients. This represents a significant gap in the MS clinician's therapeutic armoury. In this article we argue that a clear understanding of the repair mechanisms following CNS demyelination is fundamental to filling this gap. We discuss (1) the cellular events involved in remyelination, (2) changes in transcription factor expression within oligodendrocyte precursor cells associated with their activation in response to demyelination, (3) the role of platelet derived growth factor in the OPC recruitment phase of remyelination, and (4) the significance of the inflammatory response associated with demyelination in creating a signalling environment that favours remyelination.

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