The possible role of neural cell apoptosis in multiple sclerosis

Kennedy, P. G. E., George, W. and Yu, X. (2022) The possible role of neural cell apoptosis in multiple sclerosis. International Journal of Molecular Sciences, 23(14), 7584. (doi: 10.3390/ijms23147584) (PMID:35886931)

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Abstract

The etiology of multiple sclerosis (MS), a demyelinating disease affecting the central nervous system (CNS), remains obscure. Although apoptosis of oligodendrocytes and neurons has been observed in MS lesions, the contribution of this cell death process to disease pathogenesis remains controversial. It is usually considered that MS-associated demyelination and axonal degeneration result from neuroinflammation and an autoimmune process targeting myelin proteins. However, experimental data indicate that oligodendrocyte and/or neuronal cell death may indeed precede the development of inflammation and autoimmunity. These findings raise the question as to whether neural cell apoptosis is the key event initiating and/or driving the pathological cascade, leading to clinical functional deficits in MS. Similarly, regarding axonal damage, a key pathological feature of MS lesions, the roles of inflammation-independent and cell autonomous neuronal processes need to be further explored. While oligodendrocyte and neuronal loss in MS may not necessarily be mutually exclusive, particular attention should be given to the role of neuronal apoptosis in the development of axonal loss. If proven, MS could be viewed primarily as a neurodegenerative disease accompanied by a secondary neuroinflammatory and autoimmune process.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Kennedy, Professor Peter
Creator Roles:
Kennedy, P.Writing – original draft
Authors: Kennedy, P. G. E., George, W., and Yu, X.
College/School:College of Medical Veterinary and Life Sciences > School of Psychology & Neuroscience
Journal Name:International Journal of Molecular Sciences
Publisher:MDPI
ISSN:1661-6596
ISSN (Online):1422-0067
Published Online:08 July 2022
Publisher Policy:Reproduced under a Creative Commons Licence

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