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Modeling MOG Antibody-Associated Disorder and Neuromyelitis Optica Spectrum Disorder in Animal Models: Visual System

Jana Remlinger1, Maud Bagnoud1, Ivo Meli1

  • 1From the Department of Neurology (J.R., M.B., I.M., M.M., R.H., A.C., A.S.), Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Switzerland; Graduate School for Cellular and Biomedical Sciences (J.R., M.M.), University of Bern, Switzerland; Institute of Infection (C.L.), Immunity and Inflammation, University of Glasgow, UK; Departments of Neurology and Ophthalmology (J.L.B.), Programs in Neuroscience and Immunology, University of Colorado Anschutz Medical Campus, Aurora; and Department of Ophthalmology (V.E.), Inselspital, Bern University Hospital and Department for BioMedical Research (DBMR), University of Bern, Switzerland.

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|July 10, 2023
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Visual acuity declines in aquaporin 4 antibody (AQP4-IgG) and myelin oligodendrocyte glycoprotein antibody (MOG-IgG) diseases. Optic nerve inflammation begins earlier in AQP4-IgG disease, while retinal ganglion cell loss correlates with mobility impairment in both.

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Area of Science:

  • Neuroimmunology
  • Ophthalmology
  • Neurology

Background:

  • Mechanisms of visual impairment in aquaporin 4 antibody (AQP4-IgG) seropositive neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disorder (MOGAD) are not fully understood.
  • The distinct roles of optic nerve demyelination and retinal neurodegeneration in these conditions require investigation in animal models.

Purpose of the Study:

  • To investigate the differential impact of optic nerve demyelination and retinal neurodegeneration in animal models of AQP4-IgG-seropositive NMOSD and MOG-IgG-associated disorder (MOGAD).
  • To longitudinally assess visual acuity, retinal structure, and optic nerve pathology in response to MOG-IgG and AQP4-IgG administration.

Main Methods:

  • Experimental autoimmune encephalomyelitis (EAE) was induced in mice, followed by administration of monoclonal MOG-IgG or recombinant AQP4-IgG.
  • Longitudinal assessments included visual acuity testing (optomotor reflex) and optical coherence tomography (OCT) for retinal layer thickness.
  • Histopathological analysis of optic nerves and retinas examined immune cell infiltration, demyelination, and neuronal/glial changes.

Main Results:

  • Both MOG-IgG and AQP4-IgG EAE models showed decreased visual acuity and reduced retinal ganglion cell counts.
  • Optic nerve inflammation, characterized by immune cell infiltration, was evident earlier in the AQP4-IgG EAE model.
  • Reduced retinal ganglion cell complex (GCC) thickness and counts correlated with increased mobility impairment in the chronic disease phase.

Conclusions:

  • Animal models of MOGAD and NMOSD exhibit distinct patterns of optic nerve and retinal involvement, with earlier optic nerve inflammation in AQP4-IgG pathophysiology.
  • Retinal atrophy, indicated by GCC thickness and RGC counts, serves as a potential marker for neurodegeneration and correlates with functional deficits.
  • Further research is needed to fully elucidate the differential mechanisms driving visual impairment in MOGAD and NMOSD.