Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD

Yaping Yan1, Yujing Li2, Ying Fu2

  • 1Departments of Neurology and Immunology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. yaping.yan@tmu.edu.cn.

Insights

Neuromyelitis optica spectrum disorder (NMOSD) patients with both aquaporin-4 (AQP4) and myelin-oligodendrocyte glycoprotein (MOG) autoantibodies showed severe disease. Those with only MOG autoantibodies had an intermediate phenotype between NMOSD and multiple sclerosis (MS).

Area of Science:

  • Neuroimmunology
  • Autoimmune neurological disorders
  • Neuromyelitis Optica Spectrum Disorder (NMOSD)

Background:

  • Neuromyelitis optica spectrum disorder (NMOSD) is a severe autoimmune condition affecting the central nervous system.
  • Autoantibodies against aquaporin-4 (AQP4) and myelin-oligodendrocyte glycoprotein (MOG) are key biomarkers in NMOSD.
  • The clinical and radiological phenotypes associated with dual positivity for AQP4 and MOG autoantibodies remain incompletely understood.

Purpose of the Study:

  • To characterize the clinical and radiological features of NMOSD patients with co-existing AQP4 and MOG autoantibodies.
  • To compare the disease course and disability in NMOSD patients with dual autoantibody positivity versus MOG autoantibody positivity alone.
  • To investigate the potential pathogenic role of MOG autoantibodies in NMOSD.

Main Methods:

  • Retrospective analysis of 125 NMOSD patients.
  • Serological testing for AQP4 and MOG autoantibodies.
  • Clinical data collection including disease course, relapse rate, and disability.
  • Magnetic Resonance Imaging (MRI) analysis of brain and spinal cord lesions.
  • Ophthalmic examination for retinal nerve fiber layer thickness and optic nerve atrophy.

Main Results:

  • 10% of NMOSD patients were double-positive for AQP4 and MOG autoantibodies; 11.2% were MOG-ab single positive.
  • Double-positive patients exhibited a multiphase disease course, high relapse rates, and severe disability, with MS-like brain lesions and severe spinal cord edema.
  • MOG-ab single-positive patients showed a predominantly monophasic course, milder disability, distinct MRI lesion patterns (spinal cord edema, periventricular brain lesions), and less optic nerve damage.

Conclusions:

  • NMOSD patients with both AQP4 and MOG autoantibodies present with a severe phenotype combining features of classic NMOSD and relapsing-remitting MS.
  • NMOSD patients with MOG autoantibodies only display an intermediate phenotype between NMOSD and MS.
  • The presence of MOG autoantibodies may indicate pathogenicity and influence disease management strategies in NMOSD.

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