Complement Activation Is a Prominent Feature of MOGAD
Christian W Keller1, Joseph A Lopez2,3,4,5, Eva-Maria Wendel6
1Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Myelin oligodendrocyte glycoprotein antibody-associated diseases (MOGADs) show increased systemic complement activation in both children and adults. This suggests complement inhibition may be a potential therapeutic strategy for MOGADs.
Area of Science:
- Neuroimmunology
- Neurology
- Complement System Biology
Background:
- Myelin oligodendrocyte glycoprotein antibody-associated diseases (MOGADs) are a significant cause of acquired demyelinating disorders in children and adults.
- The underlying pathogenesis and best treatment strategies for MOGADs remain unclear.
Purpose of the Study:
- To investigate and compare systemic complement activation patterns in patients with MOGADs against other demyelinating conditions and healthy controls.
- To assess complement activation across different age groups (pediatric and adult) and clinical presentations within MOGADs.
Main Methods:
- Systemic complement activation was profiled by measuring specific proteins.
- Patients with MOGADs (adult and pediatric) were compared with those having relapse-onset multiple sclerosis, neuromyelitis optica spectrum disorder, and healthy pediatric and adult controls.
Main Results:
- Proteins indicating both classical and alternative complement pathway activation were significantly elevated in MOGAD patients compared to all control groups.
- Increased complement activation was observed in both adult and pediatric MOGAD cases, irrespective of their specific clinical syndromes.
Conclusions:
- Systemic complement activation is a prominent feature of MOGADs in both pediatric and adult populations.
- These findings support the exploration of complement-targeting therapies for managing patients with MOGADs.
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