Journal Article

Sequential loss of myelin proteins during Wallerian degeneration in the human spinal cord

A. Buss, K. Pech, D. Merkler, B. A. Kakulas, D. Martin, J. Schoenen, J. Noth, M. E. Schwab and G. A. Brook

in Brain

Published on behalf of The Guarantors of Brain

Volume 128, issue 2, pages 356-364
Published in print February 2005 | ISSN: 0006-8950
Published online January 2005 | e-ISSN: 1460-2156 | DOI:
Sequential loss of myelin proteins during Wallerian degeneration in the human spinal cord

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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.

Keywords: Wallerian degeneration; spinal cord; oligodendrocyte; myelin; NOGO-A; CST = corticospinal tract; MAG = myelin-associated glycoprotein; MBP = myelin basic protein; MOG = myelin oligodendrocyte glycoprotein; PLP = proteolipoprotein; SCI = spinal cord injury; WD = Wallerian degeneration

Journal Article.  5211 words.  Illustrated.

Subjects: Neurology ; Neuroscience

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