MOG antibody–associated encephalomyelitis/encephalitis
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Abstract:
Myelin oligodendrocyte glycoprotein (MOG) antibody disease is a rare autoimmune disorder with antibodies against the MOG predominantly involving the optic nerve and spinal cord leading to vision loss and paralysis. When MOG antibody disease involves the brain, the phenotype is similar to acute disseminated encephalomyelitis (ADEM). In this review, we discuss MOG-positive cases presenting with encephalitis, encephalopathy, or ADEM-like presentation based on recently published series.Keywords:
Myelin oligodendrocyte glycoprotein
Acute disseminated encephalomyelitis
Neuromyelitis Optica
Encephalomyelitis
Myelin oligodendrocyte glycoprotein
Neuromyelitis Optica
Optic neuritis
Aquaporin 4
Spectrum disorder
Demyelinating Disorder
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We report the case of a 5-year-old Japanese girl who initially had acute disseminated encephalomyelitis (ADEM) and was positive for the myelin oligodendrocyte glycoprotein (MOG) antibodies and developed unilateral optic neuritis (ON) 71 days after ADEM onset. The patient's serum was positive for the anti-MOG antibodies from the onset of ADEM to the development of ON. This phenotype has been reported in only two previous articles, and the specific mechanism of action of the anti-MOG antibodies is not yet understood. Our case suggests that the anti-MOG antibody can be associated with the pathogenesis of ADEM followed by ON. Thus, patients with ADEM who test positive for the anti-MOG antibody may be at risk of developing subsequent ON.
Acute disseminated encephalomyelitis
Myelin oligodendrocyte glycoprotein
Optic neuritis
Encephalomyelitis
Pathogenesis
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Myelin oligodendrocyte glycoprotein
Encephalomyelitis
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Abstract: Neuromyelitis optica (NMO) refers to an antibody mediated, inflammatory disorder of the central nervous system (CNS) characterized by recurrent or monophasic attacks of optic neuritis and myelitis. Most patients with NMO possess a specific serum immunoglobin, NMO-IgG, which can serve as a biomarker for NMO. The autoantibodies target aquaporin-4 (AQP4), the main water channel protein found in the CNS including the brain, spinal cord, and optic nerve. The remaining 10–25% of patients are seronegative for NMO-IgG despite meeting the diagnostic criteria for NMO. Recent studies have shown that a subset of these patients is seropositive for antibodies against myelin oligodendrocyte glycoprotein (MOG). This paper will provide an overview of the current English scientific literature published regarding the history, epidemiology, AQP4 biomarker, MOG biomarker, diagnosis, clinical features, related diseases in NMO spectrum disorder (NMOSD), and treatments of NMO.
Neuromyelitis Optica
Myelin oligodendrocyte glycoprotein
Optic neuritis
Spectrum disorder
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Myelin oligodendrocyte glycoprotein
Demyelinating disease
Myelin proteolipid protein
Encephalomyelitis
Proteolipid protein 1
Pathogenesis
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Multiple Sclerosis (MS) is a chronic autoimmune inflammatory disease affecting the central nervous system (CNS). It is characterized by different prevalence in the sexes, affecting more women than men, and different outcomes, showing more aggressive forms in men than in women. Furthermore, MS is highly heterogeneous in terms of clinical aspects, radiological, and pathological features. Thus, it is necessary to take advantage of experimental animal models that allow the investigation of as many aspects of the pathology as possible. Experimental autoimmune encephalomyelitis (EAE) represents one of the most used models of MS in mice, modeling different disease features, from the activation of the immune system to CNS damage. Here we describe a protocol for the induction of EAE in both male and female C57BL/6J mice using myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) immunization, which leads to the development of a chronic form of the disease. We also report the evaluation of the daily clinical score and motor performance of these mice for 28 days post immunization (28 dpi). Lastly, we illustrate some basic histological analysis at the CNS level, focusing on the spinal cord as the primary site of disease-induced damage.
Myelin oligodendrocyte glycoprotein
Encephalomyelitis
Demyelinating disease
Experimental pathology
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Neuromyelitis Optica
Myelin oligodendrocyte glycoprotein
Spectrum disorder
Demyelinating Disorder
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Citations (1)
Abstract Experimental autoimmune encephalomyelitis (EAE), an inflammatory demyelinating disease of the CNS, is regarded as an experimental model for multiple sclerosis. The complement has been implicated in the pathogenesis of multiple sclerosis. To clarify the role of C in mouse EAE, we immunized mice deficient in C3 (C3−/−) and their wild-type (C3+/+) littermates with myelin oligodendrocyte glycoprotein peptide 35–55. C3−/− mice were susceptible to EAE as much as the C3+/+ mice were. No differences were found for the production of IL-2, IL-4, IL-12, TNF-α, and IFN-γ between C3+/+ and C3−/− mice. This finding shows that C3, a key component in C activation, is not essential in myelin oligodendrocyte glycoprotein peptide-induced EAE in mice.
Myelin oligodendrocyte glycoprotein
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Myelin oligodendrocyte glycoprotein
Immunosuppression
Microchimerism
Autoimmune thyroiditis
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Abstract Background and purpose We aimed to characterize hypothalamic involvement in myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD) and compare it with neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). Methods A retrospective study was performed to identify hypothalamic lesions in patients diagnosed with MOGAD, NMOSD, or MS from January 2013 to May 2020. The demographic, clinical, and radiological features were recorded. Hypothalamic dysfunction and prognosis were assessed through physical examination, biochemical testing, sleep monitoring, and magnetic resonance imaging. Results Hypothalamic lesions were observed in seven of 96 patients (7.3%) with MOGAD, 34 of 536 (6.3%) with NMOSD, and 16 of 356 (4.5%) with MS ( p = 0.407). The time from disease onset to development of hypothalamic lesions was shortest in MOGAD (12 months). The frequency of bilateral hypothalamic lesions was the lowest in MOGAD ( p = 0.008). The rate of hypothalamic dysfunction in MOGAD was 28.6%, which was lower than that in NMOSD (70.6%) but greater than that in MS patients (18.8%; p = 0.095 and p = 0.349, respectively). Hypothalamic dysfunction in MOGAD manifests as hypothalamic–pituitary–adrenal axis dysfunction and hypersomnia. The proportion of complete regression of hypothalamic lesions in MOGAD (100%) was much greater than that in NMOSD (41.7%) and MS patients (18.2%; p = 0.007 and p = 0.001, respectively). An improvement in hypothalamic dysfunction was observed in all MOGAD patients after immunotherapy. Conclusions MOGAD patients have a relatively high incidence of asymptomatic hypothalamic lesions. The overall prognosis of patients with hypothalamic involvement is good in MOGAD, as the lesions completely resolve, and dysfunction improves after immunotherapy.
Neuromyelitis Optica
Myelin oligodendrocyte glycoprotein
Spectrum disorder
Optic neuritis
Demyelinating Disorder
Demyelinating disease
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