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EDITORIAL article

Front. Immunol., 18 September 2025

Sec. Multiple Sclerosis and Neuroimmunology

Volume 16 - 2025 | https://doi.org/10.3389/fimmu.2025.1699850

This article is part of the Research TopicNovel CNS targeting Molecules, Methods, and Therapeutics in Multiple SclerosisView all 6 articles

Editorial: Novel CNS targeting molecules, methods, and therapeutics in multiple sclerosis

Rune Alexander Aamodt Hglund*Rune Alexander Aamodt Høglund1*Stella E. Tsirka*Stella E. Tsirka2*Makoto Inoue*Makoto Inoue3*
  • 1Department of Neurology, Akershus University Hospital, Lørenskog, Norway
  • 2Department of Pharmacological Sciences, Renaissance School of Medicine at Stony Brook University, Stony Brook, NY, United States
  • 3Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Champaign, IL, United States

Multiple sclerosis (MS) is a chronic autoimmune and neurodegenerative disease of the central nervous system (CNS), affecting nearly three million people worldwide. Understanding the progression of pathogenic alterations in the CNS during MS is critical for identifying therapeutic targets and improving diagnostic approaches. Novel drugs aimed at CNS pathology hold promise for enhancing treatment efficacy and reducing adverse effects. This Research Topic highlights recent advances in MS autoimmunity, with the goal of showcasing the development of targeted therapies and diagnostic strategies.

Chen et al. investigated the relationship between microglial activation and remyelination status in MS. Microglia play a dual role: they facilitate clearance of myelin debris and promote the recruitment of oligodendrocyte precursor cells (OPCs) to lesion sites, but they also contribute to neuroinflammation, death of oligodendrocytes, and neuronal damage. The authors compared microglial subtypes and early-stage oligodendrocytes in remyelinated regions of MS patients, identifying differences between efficiently and poorly remyelinating individuals.

Hoffrogge et al. reported that antagonism of the purinergic P2X7 receptor (P2X7R) ameliorates experimental autoimmune encephalomyelitis (EAE) by suppressing microglial activation without affecting the peripheral immune system. P2X7R, a ligand-gated ion channel activated by extracellular ATP, is strongly upregulated in reactive astrocytes and microglia within MS lesions. Sustained P2X7R activation contributes to lesion formation, suggesting that P2X7R antagonists hold therapeutic potential in MS.

Sindi et al. demonstrated that positive allosteric modulators of AMPA-type glutamate receptors (AMPA-PAMs) protect against demyelination in the EAE and cuprizone models. AMPA-PAMs enhance synaptic transmission without causing excitotoxicity and exhibit neuroprotective effects. Notably, they increase OPC numbers, suggesting their potential in promoting remyelination.

Neupokoeva et al. proposed a novel diagnostic method for MS using blood serum surface-enhanced Raman scattering (SERS) combined with machine learning analysis. Compared to MRI, the current gold standard for detecting CNS demyelination, but with practical limitations, SERS offers exceptionally high specificity and sensitivity for diagnosing MS patients.

Anandan et al. reviewed the potential of brain-derived blood biomarkers in MS. The authors provide a comprehensive summary of all biomarkers of the past, present, and future, including brain-derived extracellular vesicles, which may serve as valuable tools for diagnosis, prognosis, monitoring, and personalized treatment.

Altogether, this Research Topic advances our understanding of CNS-targeted therapies and diagnostic innovations in MS, helping to shape future research agendas toward improving patient care.

Author contributions

RH: Writing – review & editing. ST: Writing – review & editing. MI: Writing – original draft.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

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The author(s) declare that no Generative AI was used in the creation of this manuscript.

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Publisher’s note

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.

Keywords: CNS therapeutics, diagnostic method, biomarker, neurogenesis, remyelination, neuronal progenitor cells, oligodedrocyte progenitor cells

Citation: Høglund RAA, Tsirka SE and Inoue M (2025) Editorial: Novel CNS targeting molecules, methods, and therapeutics in multiple sclerosis. Front. Immunol. 16:1699850. doi: 10.3389/fimmu.2025.1699850

Received: 05 September 2025; Accepted: 09 September 2025;
Published: 18 September 2025.

Edited and reviewed by:

Robert Weissert, University of Regensburg, Germany

Copyright © 2025 Høglund, Tsirka and Inoue. 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) and the copyright owner(s) 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: Rune Alexander Aamodt Høglund, ci5hLmEuaG9nbHVuZEBtZWRpc2luLnVpby5ubw==; Stella E. Tsirka, c3R5bGlhbmktYW5uYS50c2lya2FAc3Rvbnlicm9vay5lZHU=; Makoto Inoue, bWFrb3RvaUBpbGxpbm9pcy5lZHU=

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.