| Literature DB >> 34418402 |
Romain Marignier1, Yael Hacohen2, Alvaro Cobo-Calvo3, Anne-Katrin Pröbstel4, Orhan Aktas5, Harry Alexopoulos6, Maria-Pia Amato7, Nasrin Asgari8, Brenda Banwell9, Jeffrey Bennett10, Fabienne Brilot11, Marco Capobianco12, Tanuja Chitnis13, Olga Ciccarelli2, Kumaran Deiva14, Jérôme De Sèze15, Kazuo Fujihara16, Anu Jacob17, Ho Jin Kim18, Ingo Kleiter19, Hans Lassmann20, Maria-Isabel Leite21, Christopher Linington22, Edgar Meinl23, Jacqueline Palace21, Friedemann Paul24, Axel Petzold25, Sean Pittock26, Markus Reindl27, Douglas Kazutoshi Sato28, Krzysztof Selmaj29, Aksel Siva30, Bruno Stankoff31, Mar Tintore3, Anthony Traboulsee32, Patrick Waters21, Emmanuelle Waubant33, Brian Weinshenker34, Tobias Derfuss4, Sandra Vukusic35, Bernhard Hemmer36.
Abstract
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.Entities:
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Year: 2021 PMID: 34418402 DOI: 10.1016/S1474-4422(21)00218-0
Source DB: PubMed Journal: Lancet Neurol ISSN: 1474-4422 Impact factor: 44.182