ArticleNeurology(R) neuroimmunology & neuroinflammation2025
Extracellular Vesicle Marker Changes Associated With Disease Activity in Relapsing-Remitting Multiple Sclerosis.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Crossroads of Neuroinflammation and Biomarkers in Multiple Sclerosis: A Systematic Review.Cells · 2026Pooled it
- Biomarkers for myelin oligodendrocyte glycoprotein-associated disease: recent advances and future.Frontiers in immunology · 2026Review
- Small Extracellular Vesicles in Neurodegenerative Disease: Emerging Roles in Pathogenesis, Biomarker Discovery, and Therapy.International journal of molecular sciences · 2025Review
- In-Depth Characterization of L1CAMInternational journal of molecular sciences · 2025Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesMultiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are autoimmune disorders of the CNS causing severe neurologic impairment. Evidence suggests that extracellular vesicles (EVs) may play a disease-specific role in the orchestration of the immune cell response of MS, NMOSD, and MOGAD. In addition, EVs are considered as a potential source of biomarkers that may allow us to establish molecular signatures for these diseases and perhaps as well to follow treatment effects and disease progression. The aim of this study was to analyze the composition of EVs in patients with relapsing-remitting MS (RRMS) (n = 52), NMOSD (n = 19), and MOGAD (n = 10) and healthy controls ([HCs], n = 15).
methodsThe concentrations of neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were determined in plasma using single-molecule array (SIMOA). The size and concentration of tetraspanin-presenting EVs were evaluated in plasma samples with a single-particle interferometric resonance imaging sensor (SP-IRIS). Tetraspanin-independent analyses were performed by nanoparticle-tracking analysis (NTA) after EV isolation by size exclusion (SmartSEC) and cryo-electron microscopy observations. EV epitopes were analyzed by extended multiplex analysis using flow cytometry.
resultsThe plasma concentration of NfL and GFAP was significantly higher in patients with RRMS than in HCs. For patients with NMOSD, only GFAP increased. The density of EVs assessed by NTA was lower in plasma of patients with RRMS than in HC plasma. In addition, the 3 disease groups presented increased mean EV sizes in comparison with HCs. Tetraspanin-based EV analyses by SP-IRIS allowed us to observe a modest difference in the level of CD81 in RRMS EVs. In patients with RRMS, but not in those with NMOSD and MOGAD, multiplex/flow cytometry analyses revealed changes in the EV levels of CD29, CD31, and CD69 associated with the time elapsed since the last relapse. The negative correlations established between the vesicular levels of CD31, CD40, CD44, CD49c, CD69, and NfL or GFAP z-scores suggest a negative relationship specifically in RRMS. DISCUSSION: We speculate that the higher release of EVs containing CD29, CD31, CD40, CD44, CD49c, and CD69 in plasma, at low levels of circulating NfL/GFAP, may be associated with reduced immune cell activity in RRMS. These EV markers may characterize patients with RRMS in disease stabilization.
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