Cognition

Astrocytes and myelin – Clinical aspects: available and future treatment

This webinar explores key differences between NMOSD and MOGAD, relating antibody targets to contrasting patterns of relapse recovery, disability, and treatment objectives. It emphasizes early diagnosis, timely relapse management, and tailored long-term therapy, alongside the need for MOGAD-specific evidence and biomarkers.

This lecture explains how antibody-mediated pathology translates into clinical phenotypes and treatment strategies in Neuromyelitis Optica Spectrum Disorder (NMOSD) and Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD). Melinda Magyari contrasts the core targets, astrocytes (aquaporin-4) in NMOSD versus myelin/oligodendrocytes (MOG) in MOGAD, and shows how these mechanisms drive differences in relapse recovery, long-term disability, and therapeutic priorities. A major emphasis is placed on early antibody testing to avoid misdiagnosis (particularly as Multiple Sclerosis) and on practical, stepwise treatment approaches for acute attacks and relapse prevention.

Key Insights from the Lecture:

S1P is a lipid-derived signaling molecule generated from membrane sphingolipids; it is regulated by kinases, phosphatases (reversible control), and lyase activity (irreDistinct pathophysiology: NMOSD (AQP4-IgG+) primarily targets astrocytes at the blood–brain barrier (often complement-mediated) with secondary demyelination, whereas MOGAD targets myelin/oligodendrocytes with primary demyelination.
Different clinical course: NMOSD disability is mainly relapse-driven with incomplete recovery; MOGAD often shows better remission and may be monophasic, especially in children.
Diagnosis is critical: Overlapping phenotypes require early, accurate antibody testing to avoid misdiagnosis as Multiple Sclerosis and inappropriate treatment.
Imaging clues: Differences in optic neuritis, brain/spinal lesion patterns, and possible red flags such as conus involvement may support MOGAD in some cases.
Acute treatment is urgent: High-dose IV corticosteroids are first-line; escalate to plasma exchange, IVIG, or immunoadsorption if response is insufficient, earlier treatment improves outcomes.
Maintenance strategy: Relapse prevention is central in NMOSD using approved biologics or off-label therapies depending on access and cost.
MOGAD remains less defined: No approved maintenance therapy; prevention is often considered after recurrent attacks, with IVIG showing promising real-world results and decisions guided by relapse risk factors.
Safety and practicality: Selection must balance efficacy with infection risk (including meningococcal risk with complement inhibition), teratogenicity (e.g., mycophenolate), and local availability/cost.
Pregnancy: Continuing effective therapy may be necessary to prevent severe relapse-related disability.
Unmet needs: MOGAD-specific trials, improved biomarkers, and more personalized immunotherapy are key priorities.

“Astrocytes and myelin – Clinical aspects: available and future treatment“.

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About the speaker:

Melinda Magyari

Director of the Danish Multiple Sclerosis Registry and consultant neurologist at department of Neurology, Rigshospitalet

Melinda Magyari is the director of The Danish Multiple Sclerosis Registry (link: www.dmsr.dk/) and a consultant neurologist at the Danish Multiple Sclerosis Center. Her major research area is in multiple sclerosis and other inflammatory disorders of the central nervous system with a special interest in the changing epidemiology and gender differences. Using nationwide population-based data sources, her research addresses questions on comorbidities, reproductive issues, risk factors and socioeconomic consequences in multiple sclerosis. She is involved in pharmacoepidemiological studies investigating the effectiveness and long-term safety of disease modifying therapies.