A Ceramide Theory of Multiple Sclerosis

Ari Rappoport

doi:10.20944/preprints202409.1854.v1

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preprints.org > biology and life sciences > neuroscience and neurology > doi: 10.20944/preprints202409.1854.v1

Preprint Article Version 1 This version is not peer-reviewed

A Ceramide Theory of Multiple Sclerosis

Ari Rappoport

Version 1 : Received: 23 September 2024 / Approved: 23 September 2024 / Online: 24 September 2024 (12:28:45 CEST)

How to cite: Rappoport, A. A Ceramide Theory of Multiple Sclerosis. Preprints 2024, 2024091854. https://doi.org/10.20944/preprints202409.1854.v1 Rappoport, A. A Ceramide Theory of Multiple Sclerosis. Preprints 2024, 2024091854. https://doi.org/10.20944/preprints202409.1854.v1

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MDPI and ACS Style

Rappoport, A. A Ceramide Theory of Multiple Sclerosis. Preprints 2024, 2024091854. https://doi.org/10.20944/preprints202409.1854.v1

APA Style

Rappoport, A. (2024). A Ceramide Theory of Multiple Sclerosis. Preprints. https://doi.org/10.20944/preprints202409.1854.v1

Chicago/Turabian Style

Rappoport, A. 2024 "A Ceramide Theory of Multiple Sclerosis" Preprints. https://doi.org/10.20944/preprints202409.1854.v1

Abstract

This paper presents a new theory explaining the pathological mechanisms of multiple sclerosis (MS). MS is triggered by persistently activated immune cells, mainly B cells, as in reactivated Epstein-Barr virus infection. Activated immune cells release cytokines, the main one here being TNFa. A major role of TNFa is to support immune cell motility and tissue penetration, by promoting the breakdown of ceramide products that stabilize membranes (sphingomyelin (SPM) and galactosylceramide (GalCer)), by stimulating membrane breakdown via ceramide 1-phosphate-induced liberation of arachidonic acid, and by promoting the production of sphingosine 1-phosphate, a ceramide product that promotes immune motility. These ceramide products are expressed in endothelial cells, including the blood-brain barrier, and have a large presence in myelin. Thus, excessive cytokine release both allows immune penetration into the brain, and impairs existing myelin sheaths. SPM and GalCer are essential for myelin maintenance but not for its synthesis, explaining the dominant relapsing-remitting nature of the disease. The theory is supported by diverse evidence, and supports modern B cell-based treatment directions.

Keywords

multiple sclerosis; demyelination; ceramide; sphingomyelin; galactosylceramide

Subject

Biology and Life Sciences, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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