Treatment response varies between MOGAD patients, and immunosuppressive treatments including rituximab or mycophenolate mofetil, often result in incomplete disease control ( 10, 22– 24). Attacks are treated with steroids, and those with suboptimal response may be treated with plasma exchange or intravenous immunoglobulin. In addition, prognosis is typically favorable compared to both MS and NMOSD, and standard MS treatments such as beta interferon, natalizumab, and glatiramer acetate ( 20, 21) may exacerbate disease. Clinically and radiologically, MOGAD resembles ADEM and NMOSD ( 2, 10, 16, 17), although MOG-abs does not induce astrocyte injury like AQP4-abs, and MOGAD are considered milder and less relapsing ( 18, 19). ![]() ![]() The most common phenotype is ON, which is frequently bilateral, as well as ADEM in young children ( 14, 15). MOGAD are characterized by monophasic or relapsing optic neuritis (ON), myelitis, brainstem, and cerebral cortical encephalitis ( 1, 10, 11), and in children by monophasic acute disseminated encephalomyelitis (ADEM) and ADEM followed by recurrent ON, multiphasic disseminated encephalomyelitis or AQP4-ab-negative neuromyelitis optica spectrum disorders (NMOSD) ( 12, 13). MOG-abs have been mentioned in the literature for almost 30 years, although their role in demyelinating diseases has not been fully elucidated until this decade ( 8, 9). MOG peptides are known to elicit a demyelinating immune response in experimental models of inflammatory demyelinating diseases ( 6, 7). MOG is a component of the myelin sheath uniquely expressed in oligodendrocytes in the CNS, which has been described as a potential target of demyelinating diseases ( 4, 5). Myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) have been recognized in the past 10 years as distinct inflammatory demyelinating diseases of the central nervous system (CNS), characterized by the presence of immunoglobulin G (IgG) class 1 antibodies targeting MOG ( 1– 3). Our data highlight the need for repeated evaluation of MOG-abs in patients with acquired CNS demyelinating disorders, especially in children under 10 and adults between 31 and 40 years of age. The highest prevalence of seropositivity was observed in children aged younger than 10 years (25.5%), followed by those aged 31–40 years (16.6%).Ĭonclusions: MOGAD are distinct autoimmune diseases that occurs at all stages of life with a significantly higher prevalence in children the main clinical presenting phenotype in the entire cohort is ON and young children most often presented with ON or ADEM. ![]() The age range of MOG-abs seropositive patients was 1–66 years, with increased prevalence in children (19% compared to 6.7% in adults) ( p < 0.01). Results: Of 683 patients with demyelinating diseases tested for MOG-abs, 53 were positive (7.7%), with ON the most common presenting phenotype (68%). Methods: MOG-abs were identified in serum using a cell-based assay, and clinical data were collected from the patients' medical records. However, data on the disease course and disability outcomes of these patients are scarce.Īim: To describe clinical and paraclinical features associated with MOG antibodies (abs) in a cohort of patients in Israel, and to assess baseline prognostic features of MOG-ab-associated diseases after a first acute demyelinating event. Antibodies against MOG are found mostly in patients with optic neuritis (ON), acute disseminated encephalomyelitis (ADEM), and aquaporin-4 antibody (AQP4-abs)-seronegative neuromyelitis optica spectrum disorders (NMOSD). ![]() Introduction: Myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) have been recognized over the past 10 years as distinct inflammatory, demyelinating diseases of the central nervous system (CNS).
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