NMOSD is a relapse-driven, antibody-mediated astrocytopathy in which anti-aquaporin-4 antibodies and complement activation lead to targeted CNS damage, supporting the use of complement-inhibiting therapies.
Nikolaos Grigoriadis presents a keynote lecture on the pathophysiology of Neuromyelitis Optica Spectrum Disorder (NMOSD), focusing on the immunological mechanisms underlying disease activity. The session provides clinically relevant insights into how these mechanisms translate into relapse patterns and therapeutic targets.
Key Insights from the Lecture:
- NMOSD is a relapse-driven disease, with disability primarily resulting from acute attacks rather than progressive mechanisms
- Anti-aquaporin-4 antibodies are present in the majority of patients and play a central pathogenic role
- Aquaporin-4 is highly expressed in specific CNS regions, explaining the typical lesion distribution observed on MRI
- T cells contribute to disease initiation by facilitating blood–brain barrier disruption and supporting antibody production
- Complement activation, particularly the C5b pathway, leads to astrocyte damage and tissue injury
- NMOSD is primarily an astrocytopathy, with secondary effects on myelin and other CNS structures
- Targeting the complement cascade represents a key therapeutic strategy, with strong clinical response observed
“The immunopathological hallmarks of neuromyelitis optica spectrum disorder”.
Please subscribe to watch.
About the speaker:
Nikolaos Grigoriadis
Professor of Neurology at the Aristotle University of Thessaloniki
Media
Details
We value your opinion.
