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Related Concept Videos

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Related Experiment Video

Updated: Nov 19, 2025

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Targeting the complement system in neuromyelitis optica spectrum disorder.

Nithi Asavapanumas1, Lukmanee Tradtrantip2, Alan S Verkman2

  • 1Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.

Expert Opinion on Biological Therapy
|January 29, 2021
PubMed
Summary

Neuromyelitis optica spectrum disorder (NMOSD) involves central nervous system inflammation. Complement activation plays a key role in AQP4-IgG seropositive NMOSD, with eculizumab showing efficacy.

Keywords:
Aquaporin-4NMOSDastrocyteautoimmunitycomplementneuroinflammation

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Area of Science:

  • Neuroimmunology
  • Complement system biology
  • Autoimmune disorders

Background:

  • Neuromyelitis optica spectrum disorder (NMOSD) is a severe autoimmune disease of the central nervous system (CNS).
  • Aquaporin-4 immunoglobulin G (AQP4-IgG) autoantibodies are key drivers in seropositive NMOSD, targeting astrocyte water channels.
  • Complement activation is increasingly recognized as a critical mediator of tissue injury in AQP4-IgG seropositive NMOSD.

Purpose of the Study:

  • To review evidence for complement-dependent and independent mechanisms in AQP4-IgG seropositive NMOSD.
  • To discuss complement targets and potential therapeutic strategies.
  • To evaluate the role of complement inhibition in NMOSD treatment.

Main Methods:

  • In vitro studies
  • Animal models of NMOSD
  • Analysis of human clinical data

Main Results:

  • Preclinical data suggest complement activation is central to NMOSD pathogenesis.
  • Clinical data for eculizumab, a C5 inhibitor, support the importance of complement-dependent mechanisms.
  • Multiple drug candidates targeting various complement pathways are under investigation.

Conclusions:

  • Complement-dependent mechanisms are likely predominant in AQP4-IgG seropositive NMOSD.
  • Complement inhibitors offer therapeutic potential, but their optimal use requires further clarification.
  • The development of targeted therapies for NMOSD is advancing, with ongoing research into alternative mechanisms of action.