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BRIEF RESEARCH REPORT article

Front. Neurol.

Sec. Neuromuscular Disorders and Peripheral Neuropathies

Volume 16 - 2025 | doi: 10.3389/fneur.2025.1513501

This article is part of the Research Topic Neurology and Connective Tissue View all 18 articles

Experimental Autoimmune Encephalomyelitis Causes Skeletal Muscle Dysfunction in Mice

Provisionally accepted
Julian Boesch Julian Boesch Pamela Ramseier Pamela Ramseier Sarah Tisserand Sarah Tisserand Eliane Pierrel Eliane Pierrel Giuseppe Locatelli Giuseppe Locatelli Serge Summermatter Serge Summermatter *
  • Novartis Institutes for BioMedical Research, Basel, Switzerland

The final, formatted version of the article will be published soon.

    Multiple sclerosis (MS) is a neuroinflammatory disease affecting the brain and spinal cord and characterized by demyelination, neurodegeneration and chronic inflammation. More than 90% of people with MS present with peripheral muscle dysfunction and a progressive decline in mobility. Current treatments attenuate the inflammatory processes but do not prevent disease progression. Therefore, there remains an unmet medical need for new and/or additional therapeutic approaches that specifically improve muscle function in this patient population.The development of novel treatments targeting skeletal muscle dysfunction in MS will depend on suitable preclinical models that can mimic the human musculoskeletal manifestations of MS. Using a non-invasive approach to assess muscle function, we demonstrate in vivo that Experimental Autoimmune Encephalomyelitis (EAE) impairs skeletal muscle strength. Our data reveal a 28.3% (p<0.0001) lower muscle force in animals with EAE compared to healthy control mice during electrically evoked tetanic muscle contractions that occur at intervals of 0.25 seconds and thus mimic fatiguing tasks.As we conduct force measurements by direct transcutaneous muscle stimulation in anesthetized animals, our setup allows for the repeated evaluation of muscle function, and in the absence of primary fatigue or reduced nerve input which constitute important confounding factors in MS. Taken together, our data highlight important similarities between MS in humans and EAE in mice with regards to skeletal muscle contractile impairments, and provide first evidence for a non-invasive in-vivo setup that will enable the preclinical profiling of novel drug candidates directed at specifically improving muscle function in MS.

    Keywords: skeletal muscle dysfunction, Motor fatigability, Multiple Sclerosis, Experimental autoimmune encephalomyelitis, Translatability

    Received: 22 Nov 2024; Accepted: 27 Mar 2025.

    Copyright: © 2025 Boesch, Ramseier, Tisserand, Pierrel, Locatelli and Summermatter. 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: Serge Summermatter, Novartis Institutes for BioMedical Research, Basel, Switzerland

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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