Investigating the Immunopathogenic Mechanisms Underlying MOGAD.

We read with interest the report by Keller et al1 describing increased levels of complement activation in the serum of patients with MOG-Ab associated disease (MOGAD), compared to multiple sclerosis (MS), aquaporin I - i 4 (AQP4), IgG I - i positive neuromyelitis optica spectrum disorder (NMOSD), and healthy controls. The authors suggest this supports complement activation contributing to central nervous system (CNS) tissue damage in MOGAD, and consequently that complement inhibition should be explored as a therapeutic option. [Extracted from the article]