Myelin-oligodendrocyte glycoprotein antibody-associated disease
Tarih
2021Yazar
Derfuss, Tobias
Tintore, Mar
Traboulsee, Anthony
Waters, Patrick
Waubant, Emmanuelle
Weinshenker, Brian
Vukusic, Sandra
Hemmer, Bernhard
Amato, Maria-Pia
Asgari, Nasrin
Banwell, Brenda
Bennett, Jeffrey
Brilot, Fabienne
Capobianco, Marco
Chitnis, Tanuja
Ciccarelli, Olga
Deiva, Kumaran
De Seze, Jerome
Fujihara, Kazuo
Jacob, Anu
Kim, Ho Jin
Kleiter, Ingo
Lassmann, Hans
Leite, Maria-Isabel
Linington, Christopher
Meinl, Edgar
Palace, Jacqueline
Paul, Friedemann
Petzold, Axel
Pittock, Sean
Reindl, Markus
Sato, Douglas Kazutoshi
Selmaj, Krzysztof
Marignier, Romain
Hacohen, Yael
Cobo-Calvo, Alvaro
Probstel, Anne-Katrin
Aktas, Orhan
Alexopoulos, Harry
SİVA, Aksel
Stankoff, Bruno
Üst veri
Tüm öğe kaydını gösterÖzet
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 dinical 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.
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