Brain Advance Access originally published online on January 5, 2005
Brain 2005 128(2):356-364; doi:10.1093/brain/awh355
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Brain Vol. 128 No. 2 © Guarantors of Brain 2005; all rights reserved
Sequential loss of myelin proteins during Wallerian degeneration in the human spinal cord
1 Department of Neurology, Aachen University Medical School, 2 Department of Neuropathology, Georg-August-Universität Gottingen, Germany, 3 Centre for Neuromuscular and Neurological Disorders, University of Western Australia, Australia, 4 Department of Neurosurgery, Sart Tilman Hospital, 5 Departments of Neurology and Neuropathology and 6 Center for Cellular and Molecular Neuroscience, University of Liège, Belgium, 7 Brain Research Institute, University of Zurich and 8 Department of Biology, ETH Zurich, Switzerland
Corresponding author: Armin Buss, Pauwelsstrasse 30, D-52074 Aachen, Germany E-mail: arminbuss{at}hotmail.com
Axons undergo Wallerian degeneration (WD) distal to a point of injury. In the lesioned PNS, WD may be followed by successful axonal regeneration and functional recovery. However, in the lesioned mammalian CNS, there is no significant axonal regeneration. Myelin-associated proteins (MAPs) have been shown to play significant roles in preventing axonal regeneration in the CNS. Since relatively little is known about such events in human CNS pathologies, we performed an immunohistochemical investigation on the temporal changes of four MAPs during WD in post-mortem spinal cords of 22 patients who died 2 days to 30 years after either cerebral infarction or traumatic spinal cord injury. In contrast to experimental studies in rats, the loss of myelin sheaths is greatly delayed in humans and continues slowly over a number of years. However, in agreement with animal data, a sequential loss of myelin proteins was found which was dependent on their location within the myelin sheath. Myelin proteins situated on the peri-axonal membrane were the first to be lost, the time course correlating with the loss of axonal markers. Proteins located within compact myelin or on the outer myelin membrane were still detectable 3 years after injury in degenerating fibre tracts, long after the disappearance of the corresponding axons. The persistence of axon growth-inhibitory proteins such as NOGO-A in degenerating nerve fibre tracts may contribute to the maintenance of an environment that is hostile to axon regeneration, long after the initial injury. The present data highlight the importance of correlating the well documented, lesion-induced changes that take place in controlled laboratory investigations with those that take place in the clinical domain.
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