ArticleJournal of neuroinflammation2014
Experimental mouse model of optic neuritis with inflammatory demyelination produced by passive transfer of neuromyelitis optica-immunoglobulin G.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- PPAR-γ activation by pioglitazone inhibits microglia-mediated neuroinflammation and alleviates disease in neuromyelitis optica spectrum disorders.Acta neuropathologica communications · 2025Article
- Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Aquaporin-4 Peptide Injection in Mice Induces Retinal and Optic Nerve Alterations That Simulate Those of Neuromyelitis Optica Spectrum Disorder.Translational vision science & technology · 2025Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- NMOSD IgG Impact Retinal Cells in Murine Retinal Explants.Current issues in molecular biology · 2023Article
- Modeling MOG Antibody-Associated Disorder and Neuromyelitis Optica Spectrum Disorder in Animal Models: Visual System Manifestations.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- TREM2 deficiency inhibits microglial activation and aggravates demyelinating injury in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2023Article
- A novel aquaporin-4-associated optic neuritis rat model with severe pathological and functional manifestations.Journal of neuroinflammation · 2022Article
- Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives.International journal of molecular sciences · 2022Review
- In utero exposure to maternal anti-aquaporin-4 antibodies alters brain vasculature and neural dynamics in male mouse offspring.Science translational medicine · 2022Article
- Mesenchymal Stem Cell-Derived Extracellular Vesicles and Their Therapeutic Use in Central Nervous System Demyelinating Disorders.International journal of molecular sciences · 2022Review
- The changing landscape of optic neuritis: a narrative review.Journal of neurology · 2022Review
- Neuromyelitis optica (NMO)-IgG-driven organelle reorganization in human iPSC-derived astrocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- An Experimental Model of Neuromyelitis Optica Spectrum Disorder-Optic Neuritis: Insights Into Disease Mechanisms.Frontiers in neurology · 2021Article
- High-throughput investigation of molecular and cellular biomarkers in NMOSD.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- Experimental animal models of aquaporin-4-IgG-seropositive neuromyelitis optica spectrum disorders: progress and shortcomings.Brain pathology (Zurich, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAlthough optic neuritis (ON) is a defining feature of neuromyelitis optica (NMO), appropriate animal models of NMO ON are lacking. Most NMO patients are seropositive for immunoglobulin G autoantibodies (NMO-IgG) against the astrocyte water channel aquaporin-4 (AQP4).
methodsSeveral approaches were tested to develop a robust, passive-transfer mouse model of NMO ON, including NMO-IgG and complement delivery by: (i) retrobulbar infusion; (ii) intravitreal injection; (iii) a single intracranial injection near the optic chiasm; and (iv) 3-days continuous intracranial infusion near the optic chiasm.
resultsLittle ON or retinal pathology was seen using approaches (i) to (iii). Using approach (iv), however, optic nerves showed characteristic NMO pathology, with loss of AQP4 and glial fibrillary acidic protein immunoreactivity, granulocyte and macrophage infiltration, deposition of activated complement, demyelination and axonal injury. Even more extensive pathology was created in mice lacking complement inhibitor protein CD59, or using a genetically modified NMO-IgG with enhanced complement effector function, including significant loss of retinal ganglion cells. In control studies, optic nerve pathology was absent in treated AQP4-deficient mice, or in wild-type mice receiving control (non-NMO) IgG and complement.
conclusionPassive transfer of NMO-IgG and complement by continuous infusion near the optic chiasm in mice is sufficient to produce ON with characteristic NMO pathology. The mouse model of NMO ON should be useful in further studies of NMO pathogenesis mechanisms and therapeutics.
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