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Updated: Jun 25, 2025

Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
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MOG antibody-associated optic neuritis.

Niroshan Jeyakumar1,2, Magdalena Lerch1, Russell C Dale3,4,5

  • 1Translational Neuroimmunology Group, Kids Neuroscience Centre and Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia.

Eye (London, England)
|May 23, 2024
PubMed
Summary
This summary is machine-generated.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) often presents as optic neuritis (MOG-ON). Early diagnosis relies on specific clinical and MRI features, aiding differentiation from other demyelinating disorders.

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Area of Science:

  • Neuroimmunology
  • Ophthalmology
  • Neurology

Background:

  • Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a distinct demyelinating disorder.
  • MOGAD frequently manifests as optic neuritis (MOG-ON), differing from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD).

Purpose of the Study:

  • To review key clinical and radiological features for expediting MOGAD diagnosis.
  • To discuss ancillary investigations and their diagnostic utility in MOG-ON.
  • To highlight current management strategies and research priorities for MOG-ON.

Main Methods:

  • Review of clinical presentations and characteristic MRI findings in MOG-ON.
  • Discussion of diagnostic assays, including serum MOG immunoglobulin G detection via live cell-based assay.
  • Analysis of ancillary investigations: visual fields, visual evoked potentials, CSF analysis, and optical coherence tomography (OCT).

Main Results:

  • Bilateral optic neuritis, disc swelling, and longitudinally extensive optic nerve hyperintensity with perineuritis on MRI are key diagnostic indicators.
  • Serum MOG IgG detection using live cell-based assays is highly specific for MOGAD diagnosis.
  • OCT can detect acute optic nerve swelling and chronic atrophy, potentially serving as a diagnostic and prognostic biomarker.

Conclusions:

  • MOG-ON diagnosis is supported by specific clinical and radiological findings and confirmed by MOG IgG testing.
  • Corticosteroids are the primary acute treatment, but relapses are common, especially with rapid tapering.
  • Further research is needed to optimize acute therapy, establish long-term immunotherapy protocols, and identify relapse predictors.