Axon pathology in neurological disease: a neglected therapeutic target

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).


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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.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1016/S0166-2236(02)02255-5
Keywords: axon degeneration, slow Wallerian degeneration, multiple sclerosis, amyotrophic lateral sclerosis, axonal transport, ubiquitin proteasome pathway, WldS
ePrint ID: 56428
Date :
Date Event
1 October 2002Published
Date Deposited: 08 Aug 2008
Last Modified: 16 Apr 2017 17:41
Further Information:Google Scholar

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