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Cells 2019, 8(1), 24;

Mechanism of Siponimod: Anti-Inflammatory and Neuroprotective Mode of Action

Department of Anatomy II, Ludwig-Maximilians-University of Munich, 80336 Munich, Germany
Department of Anatomy, University Medical Center, 39071 Rostock, Germany
Author to whom correspondence should be addressed.
Received: 12 December 2018 / Revised: 28 December 2018 / Accepted: 28 December 2018 / Published: 7 January 2019
(This article belongs to the Special Issue The Molecular and Cellular Basis for Multiple Sclerosis)
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Multiple sclerosis (MS) is a neuroinflammatory disorder of the central nervous system (CNS), and represents one of the main causes of disability in young adults. On the histopathological level, the disease is characterized by inflammatory demyelination and diffuse neurodegeneration. Although on the surface the development of new inflammatory CNS lesions in MS may appear consistent with a primary recruitment of peripheral immune cells, questions have been raised as to whether lymphocyte and/or monocyte invasion into the brain are really at the root of inflammatory lesion development. In this review article, we discuss a less appreciated inflammation-neurodegeneration interplay, that is: Neurodegeneration can trigger the formation of new, focal inflammatory lesions. We summarize old and recent findings suggesting that new inflammatory lesions develop at sites of focal or diffuse degenerative processes within the CNS. Such a concept is discussed in the context of the EXPAND trial, showing that siponimod exerts anti-inflammatory and neuroprotective activities in secondary progressive MS patients. The verification or rejection of such a concept is vital for the development of new therapeutic strategies for progressive MS. View Full-Text
Keywords: multiple sclerosis; neurodegeneration; inflammation; siponimod; progressive multiple sclerosis; neurodegeneration; inflammation; siponimod; progressive

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Behrangi, N.; Fischbach, F.; Kipp, M. Mechanism of Siponimod: Anti-Inflammatory and Neuroprotective Mode of Action. Cells 2019, 8, 24.

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