Petzold, Axel;
(2025)
What does MOG autoimmunity teach us about post-inflammatory CNS diseases?
Presented at: 10th Istanbul MS Days, Istanbul, Turkey.
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Abstract
Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) provides a unique window into the mechanisms of post-inflammatory injury and repair within the central nervous system (CNS). MOG autoimmunity bridges infection, trauma, and other inflammatory triggers, producing a heterogeneous clinical spectrum distinct from multiple sclerosis and aquaporin-4 antibody disease. / Objective: To explore how MOG autoimmunity informs our understanding of post-inflammatory CNS disease, focusing on optic neuritis (MOG-ON) as a model. / Methods and Findings: Case-based evidence illustrates that MOG autoimmunity can follow diverse initiating events. The lecture will include infection, trauma, and even neurodegenerative processes such as genetic Creutzfeldt–Jakob disease. this suggests that MOG antibodies may arise as secondary or bystander responses in some contexts. Despite this heterogeneity, MOGAD is characteristically corticosteroid-responsive, and its course may be either transient or sustained, both clinically and immunologically. Optical coherence tomography (OCT) and serum neurofilament light chain offer valuable, though imperfect, tools for monitoring structural and neuroaxonal outcomes. / Conclusion: MOG autoimmunity exemplifies how a single antigenic target can link disparate CNS insults to common pathways of inflammation, demyelination, and repair. Its study underscores the need to treat early, interpret antibody titres dynamically, and refine paraclinical monitoring to better understand and manage post-inflammatory CNS diseases.
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