2026-07-09 | Neutrophil extracellular traps exacerbate blood-brain barrier disruption in neuromyelitis optica spectrum disorder.

Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS) characterized by recurrent optic neuritis and myelitis. Blood-brain barrier (BBB) disruption is a key pathological feature of NMOSD, but the role of neutrophil extracellular traps (NETs) in this process remains poorly defined. Serum proteomic profiling in patients with acute NMOSD revealed enrichment of the NET formation pathway. Neutrophils from these patients showed an increased propensity for NETosis, accompanied by elevated myeloperoxidase-DNA complexes, neutrophil elastase-DNA complexes, and cell-free DNA in serum, as well as increased neutrophil elastase-DNA complex levels in cerebrospinal fluid. In a murine NMOSD model, neutrophil depletion, peptidylarginine deiminase 4 inhibition (Cl-amidine), and NET degradation (DNase I) each attenuated astrocyte loss, demyelination, neuroinflammation, and BBB disruption. In vitro, patient-derived NETs downregulated tight junction proteins in bEnd.3 endothelial cells through mechanisms associated with myeloperoxidase and neutrophil elastase, while c-Jun N-terminal kinase inhibition mitigated NET-induced endothelial barrier disruption. Together, these findings suggest that aberrant NETosis may contribute to BBB disruption in acute NMOSD and support further investigation of NET-associated pathways as potential therapeutic targets.

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2026-07-06 | Quality of life and its influencing factors in patients with neuromyelitis optica spectrum disorder.

Neuromyelitis optica spectrum disorder (NMOSD) imposes a significant burden on health-related quality of life (HRQoL). However, comprehensive studies examining HRQoL and its biopsychosocial determinants in Chinese NMOSD patients remain scarce. In this cross-sectional study, 216 Chinese patients with NMOSD underwent clinical evaluation for neurological disability (EDSS) and completed a battery of standardized self-report measures. These scales assessed HRQoL (SF-36), basic activities of daily living (BADL), depressive symptoms (PHQ-9), anxiety (GAD-7), sleep quality (PSQI), psychological resilience (CD-RISC), perceived social support (PSSS), general alienation (GAS), and social avoidance and distress (SAD). Multiple stepwise linear regression analyses were employed to identify independent associated factors of the Physical (PCS) and Mental (MCS) Component Summaries of the SF-36. The cohort (median age 37, 85.2% female) showed significantly reduced median PCS (55.5) and MCS (51.0), with role-physical (25.0) and role-emotional (33.3) most impaired. In multivariate analysis, older age (β = -0.194), depressive symptoms (PHQ-9; β = -0.290), social avoidance (SAD; β = -0.128), and poor sleep (PSQI; β = -0.282) independently associated worse PCS (adjusted R 2 = 0.402). For MCS (adjusted R 2 = 0.576), depressive symptoms (β = -0.439), social avoidance (β = -0.135), poor sleep quality (β = -0.267), and lower resilience (CD-RISC; β = 0.127) were significant associated factors. (all p < 0.05). Psychosocial factors critically influence HRQoL in Chinese NMOSD patients. Multidimensional, culturally sensitive interventions targeting mental health, sleep, and social functioning may provide insights for improving patient outcomes.

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2026-07-03 | Bridging to low-dose corticosteroids after satralizumab discontinuation in unplanned pregnancy: Two cases of AQP4-positive NMOSD.

Satralizumab is effective for relapse prevention in AQP4-positive neuromyelitis optica spectrum disorder (NMOSD), but its safety during pregnancy has not been established. While several cases have reported continued satralizumab use in planned pregnancies, the management of unplanned pregnancy in patients already on satralizumab remains undefined. We report two AQP4-positive NMOSD patients (aged 32 and 21 years) who conceived unexpectedly during satralizumab maintenance therapy (8 and 7 months of treatment, respectively). Upon pregnancy confirmation, satralizumab was discontinued. Both patients received low-dose corticosteroid monotherapy throughout gestation as bridging maintenance: one with methylprednisolone 4 mg/day, the other with prednisolone 10 mg/day. No NMOSD relapses occurred during pregnancy. Both delivered healthy full-term neonates without congenital anomalies. Satralizumab was resumed immediately postpartum, with no relapses during follow-up. Among two AQP4-IgG-positive NMOSD patients with sustained pre-conception remission who experienced unplanned pregnancy during satralizumab maintenance, switching to low-dose corticosteroid monotherapy after drug cessation coincided with relapse-free gestation. The strategy avoids fetal exposure to satralizumab with unconfirmed gestational safety, yet the benign clinical course cannot be solely attributed to steroid bridging. Persistent residual satralizumab activity, inherent long-term disease quiescence, and pregnancy-mediated immune shifts all likely contributed to the stable disease state. These paired clinical observations only generate preliminary hypotheses and cannot support broad clinical recommendations for pregnant NMOSD patients.

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