By studying axonal pathology in human multiple sclerosis and its models, we observed that myelin ensheathment itself can be detrimental for axonal survival. We hypothesize that oligodendroglial support is disrupted under inflammatory conditions, with the most severe consequences for the axons that remain physically isolated from the extracellular milieu by myelin.
References
Trapp, B. D. & Nave, K.-A. Multiple sclerosis: an immune or neurodegenerative disorder? Annu. Rev. Neurosci. 31, 247–269 (2008). This review discusses the role of neurodegeneration and axonal damage in MS.
Nikić, I. et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat. Med. 17, 495–499 (2011). This paper reports that axonal injury is an early feature in MS and EAE and is observed prior to myelin loss.
Nave, K. A. Myelination and support of axonal integrity by glia. Nature 468, 244–252 (2010). This review discusses the concept of axonal support by oligodendrocytes.
Fünfschilling, U. et al. Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity. Nature 485, 517–521 (2012). This paper reports axonal metabolic support by myelinating oligodendrocytes.
Stassart, R. M., Möbius, W., Nave, K. A. & Edgar, J. M. The axon-myelin unit in development and degenerative disease. Front. Neurosci. 12, 467 (2018). This review discusses the axon–glia unit and its relevance for axonal integrity.
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This is a summary of: Schäffner, E. et al. Myelin insulation as a risk factor for axonal degeneration in autoimmune demyelinating disease. Nat. Neurosci. https://doi.org/10.1038/s41593-023-01366-9 (2023).
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Lack of myelin improves axon survival in inflammatory lesions in the CNS. Nat Neurosci 26, 1145–1146 (2023). https://doi.org/10.1038/s41593-023-01372-x
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DOI: https://doi.org/10.1038/s41593-023-01372-x
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