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Anti-MOG antibodies have been described in some patients with NMOSD [15] [16] who were negative for the aquaporin 4 (AQP-4) antibody. However, most NMOSD is an astrocytopathy, specifically an AQP4 antibody-associated disease, whereas MOG antibody-associated disease is an oligodendrocytopathy, suggesting that these are two separate pathologic entities. [2]
MOG-IgG levels coarsely correlate with disease severity, with levels being higher during active disease, and higher levels being associated with more severe disease manifestation. [1] Antibodies against MOG are considered mostly absent in similar diseases, such as MS. [28] Therefore, it can be said that anti-MOG diseases are grouped within AQP4 ...
See Anti-neurofascin demyelinating diseases. Some anti-neurofascin demyelinating diseases were previously considered a subtype of Multiple Sclerosis but now they are considered a separate entity, as it happened before to anti-MOG and anti-AQP4 cases. Around 10% of MS cases are now thought to be anti-Neurofascin disease in reality. [34]
Several studies have shown a role for antibodies against MOG in the pathogenesis of MS, [8] [18] though most of them were written before the discovery of NMO-IgG and the NMO spectrum of diseases. Anti-MOG status is different depending whether it is measured by ELISA or by microarray . The proper way to identify it is by microarray, reacting ...
Encephalomyelitis is inflammation of the brain and spinal cord.Various types of encephalomyelitis include: Acute disseminated encephalomyelitis or postinfectious encephalomyelitis, a demyelinating disease of the brain and spinal cord, possibly triggered by viral infection.
Anti-AQP4 diseases, are a group of diseases characterized by auto-antibodies against aquaporin 4. After the discovery of anti-AQP4 autoantibody in neuromyelitis optica , it was found that it was also present in some patients with other clinically defined diseases, including multiple sclerosis variants like optic-spinal MS .
MOG antibody disease (MOGAD) was first described in the early 2000s as a subset of cases of neuromyelitis optica with antibodies to myelin oligocyte glycoprotein (MOG). [24] Banwell and colleagues worked to characterize pediatric MOGAD to determine methods of diagnosis, [25] treatment options, [26] and prognosis. [27]
As of 2019, the correlation between CRION and MOG antibody-associated encephalomyelitis is so high that now CRION is considered the most common phenotype related to myelin oligodendrocyte glycoprotein antibodies (MOG-IgG). [9] As of 2021, some reports point out a second kind of CRION due to anti-phospholipid antibodies. [10]
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