ArticleActa neuropathologica communications2025
Complement inhibition rapidly blocks lesion extension and facilitates remyelination in neuromyelitis optica.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A novel limited-dose C5 inhibitor add-on as rescue therapy for refractory NMOSD attacks: a practical alternative to conventional multi-dose regimens.BMC neurology · 2026Article
- Complement Inhibition for Acute Neuromyelitis Optica Spectrum Disorder Attacks: Insights From an International Case Series.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Eculizumab as a rescue therapy in acute-phase aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder.Journal of neurology · 2026Article
- Complement C5 inhibitor as a rescue therapy for acute NMOSD attacks: a multicenter retrospective cohort study in China.Frontiers in immunology · 2026Article
- Complement C5 inhibitors as add-on rescue treatment in severe AQP4-antibody neuromyelitis optica spectrum disorder attacks: a case series and literature review.Therapeutic advances in neurological disorders · 2026Article
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Cumulative disability in neuromyelitis optica spectrum disorder (NMOSD) results from incomplete recovery following inflammatory, demyelinating attacks. Retrospective case studies and current clinical practice indicate that rapid treatment of acute attacks with apheresis limits injury and improves recovery. We evaluated the effects of apheresis and complement inhibition on lesion progression and recovery in a murine ex vivo cerebellar explant model of NMOSD injury. While both strategies reduced lesion formation relative to vehicle treatment, we observed that anti-C5 complement inhibition with eculizumab rapidly halted astrocyte destruction and immediately curtailed lesion extension; whereas an experimental mimic of immunoadsorption (IA), allowed for continued low level astrocyte destruction. During lesion recovery, C5 complement inhibition resulted in a faster rate of oligodendrocyte repopulation and improved myelin repair compared to IA. Complement inhibition may offer multiple benefits for the treatment of acute NMOSD attacks.
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