ReviewWiener medizinische Wochenschrift (1946)2024
Treatment of neuromyelitis optica spectrum disorder: revisiting the complement system and other aspects of pathogenesis.
Review in Wiener medizinische Wochenschrift (1946), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- A novel recombinant anti-cluster of differentiation 20 humanized monoclonal antibody (B001) for the treatment of neuromyelitis optica spectrum disorder: a phase 1, multicenter randomized, double-blind trial.Frontiers in immunology · 2026Trial
- Apheresis for the treatment of relapses in MS and NMOSD: reduced antibody reactivities, gene expression changes and potential clinical response indicators.Frontiers in immunology · 2025Article
- Autoimmune neurology-a rapidly evolving field.Wiener medizinische Wochenschrift (1946) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) represents a rare neuroimmunological disease causing recurrent attacks and accumulation of permanent disability in affected patients. The discovery of the pathogenic IgG‑1 antibody targeting a water channel expressed in astrocytes, aquaporin 4, constitutes a milestone achievement. Subsequently, multiple pathophysiological aspects of this distinct disease entity have been investigated. Demyelinating lesions and axonal damage ensue from autoantibodies targeting an astroglial epitope. This conundrum has been addressed in the current disease model, where activation of the complement system as well as B cells and interleukin 6 (IL-6) emerged as key contributors. It is the aim of this review to address these factors in light of novel treatment compounds which reflect these pathophysiological concepts in aiming for attack prevention, thus reducing disease burden in patients with NMOSD.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.