ReviewNature reviews. Neurology2025
Multiple sclerosis: an immune attack on astrocyte-mediated ion and water homeostasis.
Review in Nature reviews. Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Aegle marmelos neuroprotective potential in demyelination rat model through modulation of BDNF, GDNF, HSP-90 and HSP-60.Inflammopharmacology · 2026Article
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- From insights to innovations: evaluating preclinical paradigms in demyelinating disease therapeutics.Lab animal · 2026Review
- Astrocyte Functional Heterogeneity in Multiple Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Myelin sheaths in the central nervous system can withstand damage and dynamically remodel.Science (New York, N.Y.) · 2026Article
- Multiple sclerosis patients under treatment with interferon β1-a or ocrelizumab exhibit different T and B cell responses to SARS-CoV-2 vaccine.Frontiers in immunology · 2026Article
- Astrocyte-blood-brain barrier crosstalk in cerebral small vessel disease: linking barrier dysfunction to neurovascular failure.Frontiers in neurology · 2026Review
- Article
- Sex-Specific Effects ofInternational journal of molecular sciences · 2025Article
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS. The chain of events that results in demyelinating lesions is not understood, although most theories assume a primary immune attack on myelin. However, the glial cell adhesion molecule GlialCAM, which forms part of a protein complex in astrocytic endfeet that is crucial for brain ion and water homeostasis, was recently identified as a target for autoimmunity in patients with MS. This complex also includes the astrocytic transmembrane protein MLC1, the water channel aquaporin 4 (AQP4) and the potassium channel KIR4.1. Autoimmunity against AQP4 underlies another demyelinating disorder, neuromyelitis optica, and autoimmunity against KIR4.1 has been implicated in a subtype of MS. Genetic defects in any of these proteins cause leukodystrophies with disruption of brain ion and water homeostasis, which is regulated by astrocytes and secondarily affects myelin. In this Perspective, we argue that an immune attack on the ion and water homeostasis machinery in astrocytic endfeet, rather than directly on myelin, is the primary event in MS and that myelin damage is a consequence of astrocyte dysfunction. This hypothesis is supported by pathological studies on tissue from people with MS and has important implications for disease models and therapy targets.
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Registered trials
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