Myelin-oligodendrocyte glycoprotein antibody-associated disease

Romain Marignier*, Yael Hacohen, Alvaro Cobo-Calvo, Anne Katrin Pröbstel, Orhan Aktas, Harry Alexopoulos, Maria Pia Amato, Nasrin Asgari, Brenda Banwell, Jeffrey Bennett, Fabienne Brilot, Marco Capobianco, Tanuja Chitnis, Olga Ciccarelli, Kumaran Deiva, Jérôme De Sèze, Kazuo Fujihara, Anu Jacob, Ho Jin Kim, Ingo KleiterHans Lassmann, Maria Isabel Leite, Christopher Linington, Edgar Meinl, Jacqueline Palace, Friedemann Paul, Axel Petzold, Sean Pittock, Markus Reindl, Douglas Kazutoshi Sato, Krzysztof Selmaj, Aksel Siva, Bruno Stankoff, Mar Tintore, Anthony Traboulsee, Patrick Waters, Emmanuelle Waubant, Brian Weinshenker, Tobias Derfuss, Sandra Vukusic, Bernhard Hemmer

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review


Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently identified autoimmune disorder that presents in both adults and children as CNS demyelination. Although there are clinical phenotypic overlaps between MOGAD, multiple sclerosis, and aquaporin-4 antibody-associated neuromyelitis optica spectrum disorder (NMOSD) cumulative biological, clinical, and pathological evidence discriminates between these conditions. Patients should not be diagnosed with multiple sclerosis or NMOSD if they have anti-MOG antibodies in their serum. However, many questions related to the clinical characterisation of MOGAD and pathogenetic role of MOG antibodies are still unanswered. Furthermore, therapy is mainly based on standard protocols for aquaporin-4 antibody-associated NMOSD and multiple sclerosis, and more evidence is needed regarding how and when to treat patients with MOGAD.

Original languageEnglish
JournalThe Lancet Neurology
Issue number9
Pages (from-to)762-772
Publication statusPublished - Sept 2021

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