Coleman, M.P. and Perry, V.H.
Axon pathology in neurological disease: a neglected therapeutic target
Trends in Neurosciences, 25, (10), . (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.
|Digital Object Identifier (DOI):
||axon degeneration, slow Wallerian degeneration, multiple sclerosis, amyotrophic lateral sclerosis, axonal transport, ubiquitin proteasome pathway, WldS
|1 October 2002||Published|
||08 Aug 2008
||16 Apr 2017 17:41
|Further Information:||Google Scholar|
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