ArticleFrontiers in immunology2026
Disease-specific patterns of glymphatic-related dysfunction between multiple sclerosis and neuromyelitis optica spectrum disorder.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Glymphatic dysfunction has been reported in multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), yet disease-specific patterns of glymphatic-related impairment and their structural and cognitive consequences remain poorly characterized. Methods: This study enrolled 196 MS patients, 88 NMOSD patients, and 108 healthy controls (HC). Glymphatic-related function was assessed using diffusion tensor image analysis along the perivascular space (DTI-ALPS) and periventricular diffusivity (PVeD). Between-group differences, partial correlations with structural and clinical outcomes, AQP4 subgroup comparisons, mediation analyses, and subcortical atrophy-based subgroup analyses were performed to characterize disease-specific glymphatic-related impairment patterns. Results: MS showed more extensive glymphatic-related impairment than NMOSD, with significant reductions in both DTI-ALPS and PVeD compared to HC (all p<0.001). PVeD was significantly reduced in NMOSD compared to HC in both cohorts (p ≤ 0.008), whereas DTI-ALPS differences in NMOSD relative to HC were inconsistent across cohorts, reaching significance only in the GE replication cohort. In MS, PVeD showed widespread structural and cognitive associations; in NMOSD, associations were restricted to ventricular and choroid plexus volumes. A parallel multiple mediation model showed that subcortical gray matter atrophy, but not lesion volume, independently mediated the association between PVeD and Symbol Digit Modalities Test performance in MS, a pattern absent in NMOSD. Stratified subgroup analysis showed a pattern consistent with a glymphatic-cognitive association specific to patients with greater subcortical atrophy in MS, although formal interaction tests did not reach statistical significance; no such association was observed in either atrophy subgroup in NMOSD. AQP4-seropositive, but not seronegative, NMOSD patients showed significantly lower glymphatic-related metrics than HC (p<0.001); direct comparison between the two subgroups was not significant. Conclusion: Glymphatic-related dysfunction exhibits distinct disease-specific patterns in MS and NMOSD, with PVeD showing broader sensitivity across both cohorts. These findings support PVeD as a promising complementary glymphatic-related diffusion marker in inflammatory demyelinating disease, though causal and disease-mechanistic interpretations await validation in longitudinal and mechanistic studies.
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