MOG antibody disease: the determinants of clinical phenotype and disease activity

Understanding genetic and environmental factors will promote more focussed treatment approaches

The significance of antibodies to myelin oligodendrocyte glycoproteins (anti-MOGIgG1) in demyelinating disorders of the central nervous system was initially drawn around neuromyelitis optica spectrum disorders (NMOSDs), particularly in those patients that did not express antibodies to aquaporin four (AQP4IgG). As further research studies and clinical observations have emerged, it now seems likely myelin oligodendrocyte glycoproteins (MOG)-related disease is a separate entity, with wider and more variable clinical and radiological presentations. This tenet applies whether considering NMOSD, isolated or recurrent optic neuritis, long or short transverse myelitis, brainstem or Acute dissaminated encephalomyelitis (ADEM)-like presentations, encephalitis or rarely isolated cranial nerve involvement.1 To reinforce such an hypothesis, recent reports have been published to establish that the histopathological changes in MOG antibody associated disease(MOGAD) are different from those observed in AQP4IgG-positive NMOSD and multiple sclerosis.2 Ongoing research in…

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