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REVIEW article
Front. Pharmacol.
Sec. Neuropharmacology
Volume 15 - 2024 |
doi: 10.3389/fphar.2024.1450493
This article is part of the Research Topic Innovative Therapies Against Neurodegenerative Disorders: from New Active Molecules to Novel Drug Delivery Systems View all 3 articles
The Leukotriene Receptor Antagonist Montelukast as a Potential Therapeutic Adjuvant in Multiple Sclerosis -A Review
Provisionally accepted- 1 IntelGenx Corp., Saint-Laurent, Quebec, Canada
- 2 Department of Clinical Neuroscience, Karolinska Institutet (KI), Stockholm, Stockholm, Sweden
- 3 Paracelsus Medical University, Salzburg, Austria
Multiple Sclerosis (MS) is a multifactorial autoimmune disease of the central nervous system (CNS). It is characterized by a heightened activation of the immune system with ensuing inflammation, demyelination and neurodegeneration with consequences such as motor, sensory, cognitive, as well as autonomic dysfunctions. While a range of immune-modulatory drugs have shown certain efficacy in alleviating pathology and symptoms, none of the currently available therapeutics regenerates the damaged CNS to restore function. There is emerging evidence for leukotrienes and leukotriene receptors being involved in the various aspects of the MS pathology including neuroinflammation and de/remyelination. Moreover, leukotriene receptor antagonists such as the asthma drug montelukast diminish inflammation and promote regeneration / remyelination. Indeed, montelukast has successfully been tested in animal models of MS and a recent retrospective case-control study suggests that montelukast treatment reduces relapses in patients with MS. Therefore, we propose montelukast as a therapeutic adjuvant to the standard immune-modulatory drugs with the potential to reduce pathology and promote structural and functional restoration. Here, we review the current knowledge on MS, its pathology, and on the potential of leukotriene receptor antagonists as therapeutics for MS.
Keywords: Regeneration, restoration, Drug Development, remyelination, Neuroinflammation
Received: 17 Jun 2024; Accepted: 27 Aug 2024.
Copyright: © 2024 Pietrantonio, Serreqi, Zerbe, Svenningsson and Aigner. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Frank Pietrantonio, IntelGenx Corp., Saint-Laurent, QC H4S 1Y2, Quebec, Canada
Ludwig Aigner, Paracelsus Medical University, Salzburg, Austria
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