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Axon pathology in neurological disease: a neglected therapeutic target

Record type: Article

In the C57BL/WldS mouse, a dominant mutation dramatically delays Wallerian degeneration in injury and disease, possibly by influencing multi-ubiquitination. Studies on this mouse show that axons and synapses degenerate by active and regulated mechanisms that are akin to apoptosis. Axon loss contributes to neurological symptoms in disorders as diverse as multiple sclerosis, stroke, traumatic brain and spinal cord injury, peripheral neuropathies and chronic neurodegenerative diseases, but it has been largely neglected in neuroprotective strategies. Defects in axonal transport, myelination or oxygenation could trigger such mechanisms of active axon degeneration. Understanding how these diverse insults might initiate an axon-degeneration process could lead to new therapeutic interventions.

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Citation

Coleman, M.P. and Perry, V.H. (2002) Axon pathology in neurological disease: a neglected therapeutic target Trends in Neurosciences, 25, (10), pp. 532-537. (doi:10.1016/S0166-2236(02)02255-5).

More information

Published date: 1 October 2002
Keywords: axon degeneration, slow Wallerian degeneration, multiple sclerosis, amyotrophic lateral sclerosis, axonal transport, ubiquitin proteasome pathway, WldS

Identifiers

Local EPrints ID: 56428
URI: http://eprints.soton.ac.uk/id/eprint/56428
PURE UUID: 6b75cbb0-6ef5-42a7-b216-3df8f33cc805

Catalogue record

Date deposited: 08 Aug 2008
Last modified: 17 Jul 2017 14:30

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Contributors

Author: M.P. Coleman
Author: V.H. Perry

University divisions


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