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Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.

Siqi Qiu1, Yingyu Zhang1, Xiaoshuang Wang1

  • 1Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China.

Frontiers in Immunology
|May 4, 2026
PubMed
Summary

Neuromyelitis optica spectrum disorder (NMOSD) research uses animal models to study autoimmune attacks on astrocytes targeting aquaporin-4 (AQP4). These models offer insights into disease mechanisms but have limitations in fully replicating human NMOSD.

Keywords:
animal modelsaquaporin-4neuromyelitis optica spectrum disorderspathogenesistranslational medicine

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Area of Science:

  • Neuroimmunology
  • Autoimmune Diseases
  • Demyelinating Disorders

Background:

  • Neuromyelitis optica spectrum disorder (NMOSD) is a CNS demyelinating disease driven by autoimmune inflammation.
  • Antibody-mediated injury of astrocytes, targeting aquaporin-4 (AQP4), is a key pathogenic mechanism in NMOSD.
  • Developing accurate animal models for NMOSD is challenging due to immune tolerance limitations.

Purpose of the Study:

  • To review and analyze experimental systems modeling NMOSD pathogenesis.
  • To evaluate how well current models recapitulate key pathological features of NMOSD.
  • To identify limitations of existing models and propose priorities for next-generation models.

Main Methods:

  • Survey of experimental systems across four mechanistic themes: immune tolerance breakdown, T-B cell collaboration, antibody-mediated injury, and pro-inflammatory milieus.
  • Evaluation of model design rationale, pathological feature representation, and interpretational limitations.
  • Discussion of how animal study findings inform therapeutic target discovery.

Main Results:

  • Existing NMOSD models capture complementary, partially overlapping aspects of pathogenesis.
  • These platforms provide a mechanism-oriented framework for understanding disease drivers.
  • Significant discrepancies remain between experimental systems and the heterogeneous, dynamic course of human NMOSD.

Conclusions:

  • Animal models are crucial for NMOSD research but do not fully replicate human disease complexity.
  • Understanding model limitations is key to advancing therapeutic development for NMOSD.
  • Future research should focus on developing next-generation models with enhanced translational relevance for NMOSD.