This Article Full Text (PDF) All Versions of this Article: 1352458508091370v1 14/8/1013    most recent References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Wilkins, A Articles by Scolding, N Search for Related Content PubMed PubMed Citation Articles by Wilkins, A Articles by Scolding, N Social Bookmarking                         What's this?

Protecting axons in multiple sclerosis

Department of Neurology, Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, UK alastair.wilkins{at}bristol.ac.uk

N Scolding

Department of Neurology, Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, UK

Typically patients with multiple sclerosis (MS) experience acute episodes of neurological dysfunction, which recover followed, at a later stage, by slow and insidious accumulation of disability (disease progression). Disease progression reflects axon damage and loss within the central nervous system. However, the precise mechanism of axon injury in MS is not clear. Inflammation occurring during acute relapses undoubtedly causes some degree of acute axon damage, but epidemiological data and treatment studies have suggested that inflammation alone is not the sole cause of axonopathy. Indeed, there appears to be dissociation between inflammation and disease progression once a certain level of clinical disability has been reached because immune suppression in patients who have established disease progression does not halt the slow decrease of function. The slow and insidious loss of neurological function that occurs during the progressive phase of the disease implies a degenerative process. Whether axon drop-out occurs at these later stages because of previous inflammatory damage to axons; because of low grade inflammation causing damage to already vulnerable demyelinated axons; because of loss of trophic environment for axons to survive; or as part of a completely independent neurodegenerative process is not clear. Understanding disease mechanisms involved in the axonopathy of MS allows for the development of rational therapies for disease progression.

Key Words: axonal loss • demyelination • progressive

This version was published on September 1, 2008

Multiple Sclerosis, Vol. 14, No. 8, 1013-1025 (2008)
DOI: 10.1177/1352458508091370


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				M Hutchinson Predicting and preventing the future: actively managing multiple sclerosis Practical Neurology, June 1, 2009; 9(3): 133 - 143. [Abstract] [Full Text] [PDF]

				J. Alix Axons and multiple sclerosis Multiple Sclerosis, February 1, 2009; 15(2): 278 - 278. [PDF]