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Neurodegeneration in multiple sclerosis

Defining the problem

From the Division of Neuroimmunology, Department of Neurology, Department of Immunology and Microbiology, and the Multiple Sclerosis Center, Wayne State University School of Medicine and the Detroit Medical Center, Detroit, Michigan.

Address correspondence and reprint requests to Dr. Robert P. Lisak, Department of Neurology, Wayne State University School of Medicine, 8D University Health Center, 4201 St Antoine, Detroit, MI 48201 rlisak{at}med.wayne.edu

It is increasingly apparent that neurodegeneration in multiple sclerosis (MS) begins earlier in the course of the disease than was previously believed. The loss of axons, which results in permanent deficits, is distributed beyond regions of abnormal-appearing CNS white matter, and a constant background of neuron loss continues to take place while clinical symptoms wax and wane. It is therefore important to precisely define the scope of neurodegeneration so that experimental and clinical approaches to providing neuroprotective therapies can be devised that will halt and reverse neuron damage. Some of the complexities involved in cellular interactions in the normal-appearing and obviously affected CNS are reviewed here as a starting point for the consideration of approaches to neuroprotective strategies.

This supplement was supported by an educational grant from Teva Neuroscience. BioScience Communications contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.

Disclosure: R.P.L. has received grant support and consulting fees from Teva Neuroscience.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represents the opinions of the authors and is not endorsed by nor does it reflect the views of the American Academy of Neurology, Editorial Board, Editor-in-Chief, or Associate Editors of Neurology.

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