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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]
Optic neuritis or myelitis associated with lesions in specific brain areas such as the hypothalamus, periventricular nucleus, and brainstem [41] NMO-IgG negative NMO: AQP4 antibody-seronegative NMO poses a diagnostic challenge. [42] [43] Some cases could be related to anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies. [29]
The crystal structure of myelin oligodendrocyte glycoprotein was determined by x-ray diffraction at a resolution of 1.45 Angstroms, using protein from the Norway rat. This protein is 139 residues long, and is a member of the immunoglobulin superfamily. [ 13 ]
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]
Acute disseminated encephalomyelitis (ADEM), or acute demyelinating encephalomyelitis, is a rare autoimmune disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord. As well as causing the brain and spinal cord to become inflamed, ADEM also attacks the nerves of the central nervous system and damages their ...
Specifically, antibodies against myelin-associated glycoprotein (MAG) damage Schwann cells. While the disorder occurs in only 10% of those afflicted with peripheral neuropathy, people afflicted have symptoms such as muscle weakness, sensory problems, and other motor deficits usually starting in the form of a tremor of the hands or trouble walking.
As of 2019, three auto-antibodies have been found in atypical MS giving birth to separate diseases: Anti-AQP4 diseases, Anti-MOG and Anti-NF spectrums. [9] A LHON-associated MS [10] has also been reported, and in addition there have been inconclusive reports of TNF-α blockers inducing demyelinating disorders. [11]
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.
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