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Volume 2011 (2011), Article ID 248758, 1 page
1Department of Clinical Neurology, University of Oxford, Oxford OX3 9DU, UK
2Department of Medical Genetics, University of Calgary, Calgary, AB, T2N 4N1, Canada
3Department of Neuroimmunology, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London E1 2AT, UK
4Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8581, Japan
Received 21 March 2011; Accepted 21 March 2011
Copyright © 2011 Sreeram Ramagopalan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Multiple sclerosis (MS) is the commonest disease of the central nervous system (CNS) to cause permanent disability in young adults. Based on strong circumstantial evidence, MS is considered to be an organ-specific autoimmune disorder, but the exact cause is as yet unknown. It appears that the disease develops in a genetically susceptible population as a result of environmental exposures.
The incidence of MS has been documented to be increasing across the globe. The focus of this issue was therefore on studies with a goal of further understanding the aetiology of the disease. We were pleased to have received submissions on a wide variety of topics including the immunology of MS (research papers on the roles of Fc receptors by X. Z. Hu et al. and tumor necrosis factor- (TNF-) related apoptosis-inducing ligand (TRAIL) by A. L. O. Hebb and colleagues) and the genetics and epigenetics of MS (reviews on the future of MS genetics by S. V. Ramagopalan and D. A. Dyment and microRNAs in MS by K. U. Tufekci and coworkers). The potential role of vitamin D deficiency influencing susceptibility to and the clinical course of MS is gaining interest, and to this end, we have a review paper on this topic by J. Smolders and a research paper describing the novel role of a vitamin D receptor modulator on experimental autoimmune encephalomyelitis by S. Na et al. The role of mitochondria as potentially underlying CNS damage is reviewed by G. R. Campbell and D. J. Mahad, and J. Witherick and colleagues review a potential treatment measure, namely, mesenchymal stem cells. Finally, we have a perspective piece regarding the potential role of human endogenous retroviruses in MS by B. Krone and J. M. Grange, and finally G. Disanto and colleagues try to address the complex issue of heterogeneity of multiple sclerosis.
We hope that you enjoy reading this special issue as much as we enjoyed putting it together.