@article{3101979,
    title = "Myelin-oligodendrocyte glycoprotein antibody-associated disease",
    author = "Marignier, R. and Hacohen, Y. and Cobo-Calvo, A. and Pröbstel, A.-K. and Aktas, O. and Alexopoulos, H. and Amato, M.-P. and Asgari, N. and Banwell, B. and Bennett, J. and Brilot, F. and Capobianco, M. and Chitnis, T. and Ciccarelli, O. and Deiva, K. and De Sèze, J. and Fujihara, K. and Jacob, A. and Kim, H.J. and Kleiter, I. and Lassmann, H. and Leite, M.-I. and Linington, C. and Meinl, E. and Palace, J. and Paul, F. and Petzold, A. and Pittock, S. and Reindl, M. and Sato, D.K. and Selmaj, K. and Siva, A. and Stankoff, B. and Tintore, M. and Traboulsee, A. and Waters, P. and Waubant, E. and Weinshenker, B. and Derfuss, T. and Vukusic, S. and Hemmer, B.",
    journal = "The Lancet Neurology",
    year = "2021",
    volume = "20",
    number = "9",
    pages = "762-772",
    publisher = "The Lancet Publishing Group",
    doi = "10.1016/S1474-4422(21)00218-0",
    keywords = "corticosteroid;  immunoglobulin;  methylprednisolone;  autoantibody;  biological marker;  immunologic factor;  MOG protein, human;  myelin oligodendrocyte glycoprotein, adult;  antibody detection;  autoimmune disease;  child;  clinical feature;  clinical trial (topic);  human;  long term care;  myelin oligodendrocyte glycoprotein antibody associated disease;  myelin oligodendrocyte glycoprotein antibody associated disease;  neuroimaging;  nonhuman;  nuclear magnetic resonance imaging;  optical coherence tomography;  relapse;  Review;  adolescent;  blood;  demyelinating disease;  immunology;  middle aged;  pathology;  pathophysiology;  young adult, Adolescent;  Adult;  Autoantibodies;  Biomarkers;  Child;  Demyelinating Autoimmune Diseases, CNS;  Humans;  Immunologic Factors;  Middle Aged;  Myelin-Oligodendrocyte Glycoprotein;  Young Adult",
    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. © 2021 Elsevier Ltd"
}