What is it about?
The discussion is old: Is multiple sclerosis a classical, primary autoimmune disorder OR are neurodegenerative processes triggering the disease? While this is still an unresolved question, we know that the suppression of the om, while effective during the initial disease phase, losses its effectiveness once the disease progresses. In this study, we can demonstrate that Siponimod (Mayzent®), an approved drug for treating active multiple sclerosis patients, ameliorates tissue damage in a non-inflammatory MS model. Furthermore, our results suggest that Siponimod directly protects the oligodendrocytes, which are the main target in MS. Experiments using genetically modified mice demonstrated that this protective effect is mediated via the so-called "Sphingosine-1 Phosphate receptor 5".
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Photo by Pawel Czerwinski on Unsplash
Why is it important?
Our studies revealed that the Sphingosine-1 Phosphate receptor signaling cascade is an attractive target for developing new drugs effective during primary and secondary progressive multiple sclerosis. Beyond, our results help to understand the positive effects of Mayzent® in recent clinical trials.
Perspectives
Since oligodendrocytes are protected by Siponimod, we now will focus on other neurodegenerative disorders, investigating whether the modification of the Sphingosine-1 Phosphate receptor signaling cascade might be a therapeutic option.
Markus Kipp
Universitat Rostock
Read the Original
This page is a summary of: Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5, Proceedings of the National Academy of Sciences, September 2022, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2204509119.
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