Myelin oligodendrocyte glycoprotein-antibody-associated disease (MOGAD) is a demyelinating central nervous system disorder. We aimed to uncover immune pathways altered in MOGAD to predict disease progression. Using nanostring nCounter technology, we analyzed immune gene expression in PBMCs from MOGAD patients and compare it with healthy controls (HCs). We found 35 genes that distinguished MOGAD patients and HCs. We then validated those results in a larger cohort including MS and NMOSD patients. Expressions of HLA-DRA was significantly lower in MOGAD patients. This reduction in HLA-DRA, correlated with a monophasic disease course and greater brain volume, enhancing our ability to predict MOGAD progression.
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http://dx.doi.org/10.1016/j.jneuroim.2024.578351 | DOI Listing |
Ann Indian Acad Neurol
January 2025
Centre for Advanced Neurological Research, KS Hegde Medical Academy, Nitte University, Mangalore, Karnataka, India.
Myelin oligodendrocyte glycoprotein antibody-associated disease has been recently identified to be a distinct autoimmune central nervous system disorder. There is significant clinical and radiological overlap with multiple sclerosis and aquaporin-4-IgG-associated neuromyelitis optica spectrum disorders. Clinical course is variable in that patients may have a monophasic or relapsing course, disease severity is unpredictable, and unlike other idiopathic autoimmune inflammatory disorders, there is no gender predilection and it is more likely to affect pediatric population.
View Article and Find Full Text PDFMult Scler
January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Testing for myelin oligodendrocyte glycoprotein immunoglobulin G antibodies (MOG-IgG) is essential to the diagnosis of MOG antibody-associated disease (MOGAD). Due to its central role in the evaluation of suspected inflammatory demyelinating disease, the last 5 years has been marked by an abundance of research into MOG-IgG testing ranging from appropriate patient selection, to assay performance, to utility of serum titers as well as cerebrospinal fluid (CSF) testing. In this review, we synthesize current knowledge pertaining to the "who, what, where, when, why, and how" of MOG-IgG testing, with the aim of facilitating accurate MOGAD diagnosis in clinical practice.
View Article and Find Full Text PDFBMC Med
January 2025
Department of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Background: The clinical phenotypes of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) have been found to overlap with several other diseases. The new criteria proposed in 2023 were designed to better identify the disease but require validation across various populations to ascertain its clinical utility. We aimed to investigate the diagnostic performance in phenotypically diverse patients.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. At present, the mechanism underlying the disease is unknown.
View Article and Find Full Text PDFBMJ Case Rep
January 2025
Neurology, National Center for Child Health and Development, Setagaya-ku, Japan.
While advancements in the classification of acquired demyelinating syndromes have significantly benefited children with this condition, some cases present with overlapping features, posing diagnostic challenges. We describe an Asian girl of early childhood age with acute visual loss. Examination revealed right optic neuritis, left optic nerve atrophy and demyelinating lesions in the juxtacortical brain parenchyma.
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