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Peer-reviewedCC BYFrontiers in molecular neuroscience

Combining pharmacological and non-invasive brain stimulation strategies to promote remyelination in multiple sclerosis.

  • Thomas Jonathan Scheinok1,2,3
  • Dimitri De Bundel2
  • Tim Vanmierlo4,5
  • Jeroen Van Schependom1,6
6 affiliations
  1. 1AIMS Lab, Center for Neurosciences (C4N), UZ Brussel, Vrije Universiteit Brussel, Brussels, Belgium.
  2. 2Laboratory of Pharmaceutical Chemistry, Drug Analysis and Drug Information (FASC), Research Group Experimental Pharmacology (EFAR), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Brussels, Belgium.
  3. 3NEUR Research Group, Center for Neurosciences (C4N), Vrije Universiteit Brussel, Brussels, Belgium.
  4. 4Division of Translational Neuroscience, Department of Psychiatry and Neuropsychology, Mental Health and Neuroscience Research Institute (MHeNS), Maastricht University, Maastricht, Netherlands.
  5. 5Department of Neuroscience, Biomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.
  6. 6Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Brussels, Belgium.
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Abstract

Remyelination in multiple sclerosis (MS) fails for several, partly overlapping reasons. The differentiation of oligodendrocyte precursor cells into myelin-producing oligodendrocytes is impaired both by intrinsic factors and by the surrounding lesion environment, which becomes increasingly inflammatory and senescent with age. Pharmacological strategies acting on a single target to promote oligodendrocyte lineage progression have been successful in animal models but have yet to produce meaningful clinical benefit in people with MS (pwMS). In this perspective paper, we argue that simultaneously targeting several of the mechanisms underlying this failure is a more promising route to repairing myelin lesions in pwMS. We outline how non-invasive brain stimulation (NIBS) might be leveraged to shift the glial microenvironment towards a pro-regenerative, remyelinating state, and how this can be paired with targeted pharmacological agents that enhance oligodendrocyte differentiation. We also discuss how the expected effect of such a combination may depend on age and lesion stage. This framework may offer a rational route beyond the translational failures of single-target remyelination therapies.

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Cite

BibTeXRIS
BibTeX
@article{scheinok2026combining,
  title = {{Combining pharmacological and non-invasive brain stimulation strategies to promote remyelination in multiple sclerosis.}},
  author = {Thomas Jonathan Scheinok and Dimitri De Bundel and Tim Vanmierlo and Jeroen Van Schependom},
  journal = {Frontiers in molecular neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnmol.2026.1980126},
  url = {https://europepmc.org/article/MED/42952812},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Combining pharmacological and non-invasive brain stimulation strategies to promote remyelination in multiple sclerosis.
AU  - Thomas Jonathan Scheinok
AU  - Dimitri De Bundel
AU  - Tim Vanmierlo
AU  - Jeroen Van Schependom
PY  - 2026
DA  - 2026/10/14
JO  - Frontiers in molecular neuroscience
DO  - 10.3389/fnmol.2026.1980126
UR  - https://europepmc.org/article/MED/42952812
AB  - Remyelination in multiple sclerosis (MS) fails for several, partly overlapping reasons. The differentiation of oligodendrocyte precursor cells into myelin-producing oligodendrocytes is impaired both by intrinsic factors and by the surrounding lesion environment, which becomes increasingly inflammatory and senescent with age. Pharmacological strategies acting on a single target to promote oligodendrocyte lineage progression have been successful in animal models but have yet to produce meaningful clinical benefit in people with MS (pwMS). In this perspective paper, we argue that simultaneously targeting several of the mechanisms underlying this failure is a more promising route to repairing myelin lesions in pwMS. We outline how non-invasive brain stimulation (NIBS) might be leveraged to shift the glial microenvironment towards a pro-regenerative, remyelinating state, and how this can be paired with targeted pharmacological agents that enhance oligodendrocyte differentiation. We also discuss how the expected effect of such a combination may depend on age and lesion stage. This framework may offer a rational route beyond the translational failures of single-target remyelination therapies.
SN  - 1662-5099
ER  -