1/22/2024 0 Comments Anti mog ms![]() However, not all individuals will recover fully. ![]() In patients with TM, the presence of MOG-Ab has also been associated with a better recovery from acute attacks, and really similar frequency of severe attacks at the onset to AQP4-Ab-associated disorders. Although, MOG-Ab-associated ON is usually a recurrent disease, visual recovery was good the outcome was better in MOG-than in AQP4-Ab-positive patients correlating with a better preserved retinal fiber layer thickness. MOG-Ab-positive patients less frequently suffer motor disability and have a better extended disability status scale (EDSS) score, compared to AQP4-Ab-positive patients. In several studies, MOG-Ab was associated with a favorable outcome. Cortical encephalitis was recently described in MOG-Ab-positive patients but not in AQP4-Ab NMOSD. In a large cohort of MOG-Ab–positive patients, ADEM (or an ADEM-like episode) was reported as the initial feature in 18%, primarily affecting children. Brainstem involvement and postrema area syndrome (persistent nausea, vomiting, or hiccups), which usually present in NMOSD (around 40%), has been reported in 6%–15% of MOG-Ab–positive patients as well. Among patients with TM, motor symptoms were frequent and included tetraparesis in 28%, paraparesis in 48%, and severe weakness in 21%. In the largest series, visual acuity was described to be <0.1 at least once in 69% of patients with ON. The first attack of TM or ON can be severe. Two independent groups have evaluated the categories of clinical phenotypes for MOGAD: ON was the major phenotype (41%–63%), followed by LETM (29%–31%), NMO (6%–24%), and encephalomyelitis (2%–6%), while in AQP4-Ab-positive patients, the reported phenotypes were NMO in approximately 60%, followed by LETM (in about 30%), and ON (in about 10%). Significantly, MOG-Ab alone did not induce inflammation or tissue destruction rather, their interdependence with T cells was required to develop their pathogenic potential. The ac cumulation of MOG-Ab has been described in CNS antigen-presenting cells with subsequent activation of autoreactive T cells, followed by the induction of peripheral autoreactive T cells. In addition, MOG-Ab belongs to the complement binding IgG1 subtype and has been found to activate the complement cascade, leading to complement-dependent destruction of MOG-expressing cells. Initial studies revealed a pathogenic effect of the humoral immune response against MOG (human MOG-Ab) these antibodies were able to induce the death of MOG-expressing cells as well as natural killer cell-mediated cell death, with the extent of cell damage dependent on antibody levels. Furthermore, purified IgG from MOG-IgG–positive patients, when incubated with oligodendrocytes in vitro, led to obvious cytoskeletal disorganization, further suggesting functional pathogenicity. In humans, high-titer MOG-immunoglobulin G (MOG-IgG) levels in serum samples seem to efficiently activate the complement cascade in vitro. Key words: Myelin oligodendrocyte glycoprotein, Demyelinating diseases, Neuromyelitis optica, Optic neuritis, Acute disseminated encephalomyelitis This review summarizes the data regarding MOG-Ab as an impending biological marker for discriminating between these diverse demyelinating CNS diseases and discusses recent developments, clinical applications, and findings regarding the immunopathogenesis of MOG-Ab-associated disorders. A humoral immune reaction against MOG was recently found in monophasic diseases and recurrent/multiphasic clinical progression, particularly in pediatric patients. Using specific cell-based assays, MOG-Ab is becoming a potential biomarker of inflammatory demyelinating disorders of the CNS. MOG-Ab is associated with a wider clinical phenotype not limited to neuromyelitis optica spectrum disorder, with most patients presenting with optic neuritis, acute disseminated encephalomyelitis (ADEM) or ADEM-like encephalitis with brain demyelinating lesions, and/or myelitis. Antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) have been found in some cases of these demyelinating diseases, particularly in children. Inflammatory or immune-mediated demyelinating central nervous system (CNS) syndromes include a broad spectrum of clinical phenotype and different overlapping diseases.
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