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Axon damage and repair in multiple sclerosis

Record type: Article

It is well known that within long-standing multiple sclerosis (MS) lesions there is axonal loss but whether it is an early or late event has been more difficult to establish. The use of immunocytochemical methods that reveal axonal end-bulbs is a valuable approach to investigating acute axonal injury in human pathological material. The application of these techniques to multiple sclerosis tissue reveals evidence of axonal injury in acute lesions; the distribution of the end-bulbs in acute and active-chronic lesions is associated with regions of maximal density of infiltrating macrophages. Axon injury within the MS lesion will result in both Wallerian degeneration of the axon and also retrograde degeneration of the cell body. The functional consequences of the axon injury will depend upon numbers of axons injured and the topographical organization of the fibres coursing through the lesion. The molecular mechanisms by which the recruited leucocytes damage or transect the axons are not known. However, investigations in the Wld mutant mouse with very slow Wallerian degeneration demonstrate that axon degeneration is not simply a passive disintegration of the axon but has clear parallels with the active processes of programmed cell death. The presence of early axon injury and the consequences of an ever increasing load of neuronal damage has important implications not only for when therapy should be initiated in MS but also the therapeutic target.

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Citation

Perry, V.H. and Anthony, D.C. (1999) Axon damage and repair in multiple sclerosis Philosophical Transactions A, 354, (1390), pp. 1641-1647.

More information

Published date: 29 October 1999

Identifiers

Local EPrints ID: 56466
URI: http://eprints.soton.ac.uk/id/eprint/56466
ISSN: 0962-8436
PURE UUID: f81453d3-84a6-49c9-97dc-f56791c7649c

Catalogue record

Date deposited: 22 Aug 2008
Last modified: 17 Jul 2017 14:30

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Contributors

Author: V.H. Perry
Author: D.C. Anthony

University divisions


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