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MOG antibody disease: the determinants of clinical phenotype and disease activity
  1. Shahd H M Hamid
  1. Neurology, The Walton Centre NHS Foundation Trust, Liverpool, Liverpool, UK
  1. Correspondence to Dr Shahd H M Hamid, Neurology, The Walton Centre NHS Foundation Trust, Liverpool L9 7LJ, UK; shahd.hamid{at}thewaltoncentre.nhs.uk

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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 …

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  • Twitter @HamidShahd

  • Contributors Invited manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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