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Sequential loss of myelin proteins during Wallerian degeneration in the human spinal cord
Open accessAbstract
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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“Immediately after injury the spinal cord undergoes massive cellular and molecular changes, including increased cell death [64, 65], infiltration of inflammation cells in the lesion [2–6], axon degeneration [7–10], and OL and myelin loss [13–16, 66, 67].”
From Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury (2020) · cites this paper as [7]
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Metadata
- Authors
- Buss, A.
- Affiliations
- University of Göttingen (DE)
- Corresponding author
- Buss, A.
- ORCID
- Buss, A.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-12-22
- Volume
- 128
- Issue
- 2
- Pages
- 356-364
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2131832510
- Cited by
- 111
- References
- 41
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 4 · 2023: 5 · 2022: 12 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 5 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 3 · 2013: 9 · 2012: 9
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- reroDoc Digital Library (submittedVersion)
- Open Repository and Bibliography (University of Liège) (submittedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- ETH Zürich Research Collection
- Zurich Open Repository and Archive (University of Zurich)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
- Keywords
- Wallerian degeneration, myelin proteins, spinal cord injury, cerebral infarction, axon regeneration, myelin sheath, Nogo-A, compact myelin, axon growth inhibition, human spinal cord
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Astrocytes, Cell Count, Cerebral Infarction, Humans, Middle Aged, Myelin Proteins, Nerve Fibers, Oligodendroglia, Spinal Cord, Spinal Cord Injuries, Time Factors, Wallerian Degeneration
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