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Anti MOG vs MS

Vast Experience in rAbs R&D. Apply to Detection/Imaging/Diagnostics. Inquiry online! High Purity. Specific Bioactivity. Competitive Price. Fast Delivery. In Stock Discover best-sellers & new arrivals from top brands. Free delivery with Prime MOG antibodies were originally thought to be involved in multiple sclerosis (MS), but subsequent studies found it to be a distinct disease. MOGAD have many similarities to neuromyelitis optica but several studies have demonstrated they have unique clinical features, treatment response, and prognosis This is in consonance with the better recovery of some patients with anti-MOG syndromes as compared with NMOSD [119,131]. There are few pathological studies on anti-MOG syndromes [7,10]. A brain biopsy from a patient with MOG-antibody-associated encephalomyelitis revealed typical MS-type II histopathological features characterized by deposition.

The product of this gene is a membrane protein expressed on the

  1. Previously thought to be part of MS, it's actually different. Anti-MOG it seems is where a person has antibodies against Myelin Oligodendrocyte Glycoprotein. They tend to be absent in people with MS. The way the neurologists differentiate between the two is the shape of brain lesions. There seems to be a strong connection to optic neuritis
  2. Background: Whether antibody to myelin oligodendrocyte glycoprotein (MOG) can be a diagnostic marker for multiple sclerosis (MS) is still controversial. Recent studies suggested that serum specific anti-MOG epitope antibody might be an MS specific marker
  3. Neuromyelitis optica spectrum disorder (NMOSD) and anti-myelin oligodendrocyte glycoprotein (anti-MOG) syndromes are immune-mediated inflammatory conditions of the central nervous system that frequently involve the optic nerves and the spinal cord. Because of their similar clinical manifestations an
  4. And now, this second antibody — MOG — will be helpful because the presence of MOG antibodies indicates that a patient doesn't have MS. Dr. McKeon agrees and adds, The combination of these two tests — the AQP4 and MOG antibodies — allows for the most comprehensive evaluation for patients recently diagnosed with demyelinating.
  5. In cases associated with anti-MOG antibodies, it is considered that anti-MOG antibodies may trigger an attack on the myelin sheath resulting in demyelination. Symptoms are generally more severe after an NMO attack than an MS attack. NMO rarely has a secondary progressive stage as in MS; disabilities accumulate from repeated acute attacks

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Neuromyelitis optica (NMO) and multiple sclerosis (MS) are both immune system disorders that affect the nerves. Compare NMO vs. MS here, and learn more about their similarities and differences Multiple Sclerosis. N Engl J Med 2018;378:169-80. PubMed; Hardy TA, Reddel SW, Barnett MH et al. Atypical inflammatory demyelinating syndromes of the CNS. Lancet Neurol 2016; 15: 967-81. PubMed; Weber MS, Derfuss T, Metz I and Br ck W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination

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Myelin Oligodendrocyte Glycoprotein (MOG) Optic Neuritis is an antibody mediated demyelinating disease of the central nervous system (CNS) that is a distinct entity from other demyelinating processes of the CNS such as Multiple Sclerosis (MS) or AQP4-Ab-associated neuromyelitis optica spectrum disorder (NMOSD) Recently at The European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) annual meeting, there was a discussion about anti-MOG and whether it should be its own diagnostic category or another variant of NMOSD. Dr. Douglas Sato of the Brain Institute of the Rio Grande do Sul in Porte Allegre, Brazil, argued that there are. But anti-MOG has a much spottier record in multiple sclerosis, and the jury is still out on whether and how it is involved in demyelination (O'Connor et al., 2007; Mayer and Meinl, 2012). Some think its presence could be a sign of the disease rather than a feature of its pathogenesis Figure 1 shows that the risk of clinically definite multiple sclerosis was significantly lower among the patients who were seronegative for both anti-MOG and anti-MBP antibodies than among those. Overall, 32% of the children were positive for anti-MOG antibodies. Positivity was not associated with sex, but children with antibodies were significantly younger than those without (7 vs. 12 years). In fact, 77% of anti-MOG-positive children were younger than 11 years; just 15% of older children were positive for the antibodies

Even though rare, MOGAD is three times more frequent than AQP4-NMOSD in adults, and considered the second cause of inflammatory optic neuritis after MS. Distinguishing MOGAD from AQP4-NMOSD and MS is important because evolution and treatment regimens differ between the three conditions Terminology. Research in anti-MOG related diseases is rapidly evolving with new terminology being frequently proposed, including MOG-IgG-associated Optic Neuritis, Encephalitis, and Myelitis (MONEM), anti-MOG associated encephalomyelitis, anti-MOG encephalitis and other variations on this theme 1-4.. Epidemiology. MOGAD is primarily encountered in children and young adults 1 Neuromyelitis optica vs. multiple sclerosis: Causes. Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin, causing damage and thus exposing nerve fibers MS plaques can be further confirmed by the presence of abundant amounts of anti-myelin degradation products such as activation markers, anti-myelin oligodendrocyte glycoprotein (MOG), anti-myelin. Ten multiple sclerosis patients seropositive for anti-MOG-Ig antibodies (3 multiple sclerosis-R0, 4 multiple sclerosis-RR and 3 multiple sclerosis-CP patients) have been reinvestigated between 9 and 43 months (mean 21.2 ± 10.6 months) after first analysis

Anti-MOG antibodies are frequently associated with steroid

Overview of patient cohort, antibody status, and anti-MOG antibody levels. (A) Patient cohort and antibody status: The study comprised a total of 135 participants including patients with NMO/NMOSD (n = 48), relapsing-remitting multiple sclerosis (RR-MS) (n = 48), and healthy donors (n = 39).Of the NMO/NMOSD patients, 31 were positive for anti-AQP4 antibodies (AQP4+) with the cell-based assay. For many years, it was considered to be a subtype of multiple sclerosis, until the discovery of anti-aquaporin-4 antibodies at which time it was moved into its own disease category. It is now evident that a significant proportion of patients with clinical NMO do not have the anti-AQP4-antibody (some have anti-MOG-antibodies for example) and. The levels of anti-MOG antibody and the frequencies of patients positive to this antibody were also compared with those of anti-MBP antibody, which is known to be elevated nonspecifically in patients with MS. Our main finding is that patients with MS had higher CSF anti-MOG and anti-MBP antibody levels than controls The pathophysiological significance of MOG-specific autoantibodies in MS remains controversial, but study in a primate model of MOG-induced EAE showed that demyelination is mediated by MOG-specific antibodies directed against conformational rather than linear MOG epitopes, suggesting functional segregation of pathogenic vs nonpathogenic anti. Anti-MOG is an antibody to a component of myelin. It's already known to play a role in destroying myelin in mice with MS, reports Genain, but how it works in people is less clear. To better.

(PDF) Overlapping demyelinating syndrome (Neuromyelitis

MS and MOG Anitbody Disease Fact Sheet Cleveland Clini

The management of anti-MOG syndrome is thought to be similar to that of NMOSD. If a patient with known multiple sclerosis presents with monocular vision loss, what etiologies should be considered? Although optic neuritis is more common earlier in the course of MS, patients with MS can have optic neuritis at any point in their disease Importantly, however, MOG-EM and MS show a relevant phenotypic, i.e., clinical as well as radiological, overlap [3, 14]: like MS, MOG-EM follows a relapsing course in most cases [3, 6], at least in adults, and 33 and 15% of adult patients with MOG-EM meet McDonald's and Barkhof's criteria for MS, respectively, at least once over the course. Multiple Sclerosis. N Engl J Med 2018;378:169-80. PubMed; Hardy TA, Reddel SW, Barnett MH et al. Atypical inflammatory demyelinating syndromes of the CNS. Lancet Neurol 2016; 15: 967-81. PubMed; Weber MS, Derfuss T, Metz I and Br ck W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination anti-aquaporin-4 (AQP4-Ab)-positive, anti-myelin oligodendrocyte glycoprotein (MOG-Ab)-positive, MS and non-inflammatory neurological control groups. (B) Glial fibrillary acidic protein (GFAP) in the CSF of AQP4-Ab+, MOG-Ab+, multiple sclerosis (MS) and non-inflammatory neurological control groups

Neuromyelitis Optica Spectrum Disorder and Anti-MOG Syndrome

MOGFS : Neuromyelitis optica (NMO), sometimes called Devic disease or opticospinal multiple sclerosis (MS) is a severe, relapsing, autoimmune, inflammatory and demyelinating central nervous system disease (IDD) that predominantly affects optic nerves and spinal cord.(1) The disorder is now recognized as a spectrum of autoimmunity (termed NMO spectrum disorders: NMOSD).(1-3) Brain lesions are. However, MOG-IgG has also been found in association with other demyelinating disorders, including multiple sclerosis, acute disseminated encephalomyelitis, optic neuritis, and LETM . MOG-IgG binds to the MOG extracellular domains, which are highly expressed at the peripheral processes of oligodendrocytes, inducing myelin injury ( 92 )

Anti-MOG disease vs MS? - Everyday living - Foru

Serum antibodies to 25 myelin oligodendrocyte glycoprotein

for relapsing MS,6 and an overlap of pathologic MS and NMOSD features in a patient clinically classi-fied as ADEM, who also had anti-aquaporin-4 antibodies.7 Our cases imply that, although clinically and radiologically presenting as ADEM-like syndrome, MOG-abs-associated demyelinating disorders could pathologically resemble MS Neuromyelitis optica (NMO) and multiple sclerosis (MS) are often confused with each other because they share some similarities, but they are definitely two completely separate conditions with major differences. One thing they do share in common is that, unfortunately, both NMO and MS are fairly common, particularly in North America Table 1 Comparison of clinical, radiologic, and prognostic characteristics of MOG group with MS and AQP4 group MOG group MS group AQP4 group p Value MOG vs MS MOG vs AQP4 N 17 26 49 Sex, M:F 7:10 12:14 7:42 NS NS Age at onset, y, mean 6 SD (min-max) 42.69 6 19.3 (18.12- 70.69) 32.8 6 10.0 (19.2- 58.6) 43.41 6 13.96 (16.43- 75.3) NS N MOG antibodies have been reported without AQP4 antibodies in individuals with NMO and other non-multiple sclerosis demyelinating diseases. The presence of MOG antibodies in AQP4 antibody negative individuals can help differentiate between multiple sclerosis (MS) and non-MS demyelinating diseases and aid in clinical management decisions

CBAs have higher sensitivity (77% vs 63%-64% for indirect immunofluorescence or ELISA) and lower false-positive rates (0.1% among MS patients vs 0.5%-1.3% for ELISA). 1 MOG antibody tests reflex to titer; AQP4 antibody tests with and without reflex to titer are offered Based on clinical, immunological and histopathological evidence, MOG-IgG-associated encephalomyelitis (MOG-EM) has emerged as a distinct disease entity different from multiple sclerosis (MS) and aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder (NMOSD). MOG-EM is associated with a broader clinical phenotype including optic neuritis, myelitis, brainstem lesions and acute. 1.2. Structure and function of the MOG Ab. Myelin oligodendrocyte glycoprotein is a component of myelin and has a length of 245 amino acids with a molecular weight of approximately 26-28 kDa (Johns and Bernard, 1999).The human MOG gene is located on chromosome 6 within the human leukocyte antigen (HLA) complex (Pham-Dinh et al., 1993).MOG is located on the extracellular surface of myelin. Antibodies against conformation-dependent epitopes of myelin-oligodendrocyte-glycoprotein (MOG-abs) are present in subgroups of neuromyelitis optica spectrum disorder (NMOSD), recurrent optic neuritis (rON), multiple sclerosis (MS), and anti-NMDAR encephalitis. Using optical coherence tomography (OCT) we assessed whether MOG-abs might serve as potential marker of retinal axonal degeneration

Neuromyelitis Optica Spectrum Disorder and Anti-MOG

Copy article link. People with a demyelinating disease associated with antibodies against a myelin oligodendrocyte glycoprotein (MOG), most often develop episodes of optic neuritis (inflammation. Abstract: P306 Type: Poster Abstract Category: Clinical aspects of MS - 2 MS Variants Background: Recent studies indicate Anti-Myelin Oligodendrocyte Glycoprotein antibodies (MOG- IgG) as new serum biomarker of some forms of demyelinating diseases distinct both from classical Multiple sclerosis (MS) and from AQP4-IgG-mediated neuromyelitis optica spectrum disorders (NMOSD) Your doctor might test your blood for the autoantibody NMO-IgG, which helps doctors distinguish NMO from MS and other neurological conditions. This test helps doctors make an early diagnosis of NMO. A myelin oligodendrocyte glycoprotein (MOG-IgG) antibody test also might be used to look for another inflammatory disorder that mimics NMO Anti-MOG antibodies are present in a subgroup Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG (MOG vs. AQP4 vs. seronegative: 17 (3 to 32), Based on an observational prospective study of 16 patients with anti-myelin oligodendrocyte protein (MOG) disease and 29 anti-aquaporin-4 disease, the authors report lesser efficacy of rituximab in anti-MOG patients, characterized by higher occurrence of relapses in the anti-MOG group, even while the biological effect of rituximab on memory B-cell suppression was sustained

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Neuromyelitis optica (NMO) and NMO spectrum disorders (NMOSD) are clinical syndromes traditionally defined by the presence of myelitis and optic neuritis (ON). Aquaporin-4 (AQP4) is a water channel that is heavily expressed on astrocyte foot processes in the optic nerves, brainstem, and spinal cord. Antibodies to AQP4 are directly pathogenic. In MS, the inflammatory reaction in the brain is dominated by CD8 T-lymphocyte and CD20 B cells. Demyelination in MS appears to be triggered by soluble factors, produced by T cells and/or B cells, which are different from anti-MOG antibodies seen in EAE, and induce widespread MS like primary demyelination and tissue damage associated with. Objective To elucidate the differences in the source and in the level of intrathecal synthesis between anti-aquaporin-4 antibodies (AQP4-IgG) and anti-myelin oligodendrocyte glycoprotein antibodies (MOG-IgG). Methods Thirty-eight patients with MOG-IgG-associated disease and 36 with AQP4-IgG-positive neuromyelitis optica spectrum disorders (NMOSD) were studied for the antibody titers in. Transverse Myelitis. MOG-Ab associated acute transverse myelitis is a relatively common presentation of MOGAD in adults, and can be seen in children as well ().In some cases of MOG-TM, there is an antecedent history of infection or vaccination, but in most patients, no such history can be elicited (11, 18, 40).While MOG-TM is typically steroid-responsive with favorable long-term recovery.

Anti-TNF therapy says MS is one disease. Since their introduction in 1999, anti-tumour necrosis factor-α (anti-TNF-α) therapies have been suspected repeatedly to be associated with the occurrence of central nervous system (CNS) demyelinating disorders, including multiple sclerosis (MS). However, recent publications were restricted to. He proposed that instead of including MOG antibody disease into the neuromyelitis spectrum, it should be part of a new group: anti-MOG associated optic neuritis, encephalitis and myelitis (MONEM).. MOG is clearly associated with a set of disorders with distinct clinical phenotypes, which include myelitis and encephalitis, he said Results Levels of anti-MOG and anti-MBP antibodies measured in the same MS patients at different phases of disease (relapse vs remission)We found that levels of anti-MOG 1-26 ( Fig. 1) were significantly higher in MS patients in relapse phase than in remission (p<0.05) The clinical presentation of patients who are MOG ab + is characterized by a more frequent involvement of optic nerves than spinal cord. 63,88 Also a simultaneous affection of both optic nerves seems to be a hallmark of patients who are MOG ab + compared with NMO or MS. 66 Of interest, in patients with a clinically unilateral optic neuritis.

Neuromyelitis optica spectrum disorder (NMOSD), also known as Devic disease, is a chronic disorder of the brain and spinal cord dominated by inflammation of the optic nerve (optic neuritis) and inflammation of the spinal cord (myelitis). Classically, it was felt to be a monophasic illness, consisting of episodes of inflammation of one or both. Analyses were conducted with and without adjustment for serum titers of antibodies to the Epstein-Barr nuclear antigen (EBNA), which are an established risk factor for MS. RESULTS: The presence of anti-MOG IgG antibodies in serum was associated with an increase in risk of developing MS (relative risk for anti-MOG IgG+/IgM- vs seronegativity to. The authors of this prospective study examined the use of mycophenolate mofetil (MMF) for prevention of relapses associated with anti-MOG antibody disorders. The cohort included 79 patients; 54 patients were treated with MMF and 25 patients were not treated with MMF. MMF patients had a relapse rate of 7.4% compared with 44% in those without MMF. Given the pathogenic role of anti-MOG antibodies in MOG EAE and MS, 17 we assessed the potential variations in the number of donor splenic B cells by flow cytometry as well as serum levels of anti-MOG antibodies by ELISA. Flow cytometric results revealed similar proportions of B cells between mice treated with BMT only or in combination with.

[2,4]. In children, the anti-MOG humoral immune response has been shown to be specific for demyelinating CNS diseases and can differentiate them from viral encephalitis [10]. While it remains unclear if MOG-ab have demyelinating activity, the data suggests MOG-ab do not merely reflect myelin destruction [11] References 1.↵Ketelslegers IA, Van Pelt DE, Bryde S, et al. Anti-MOG antibodies plead against MS diagnosis in an acquired demyelinating syndromes cohort. Mult Scler 2015;12:1513-2030.OpenUrl 2.↵Hacohen Y, Absoud M, Deiva K, et al. Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children References 1.↵Ketelslegers IA, Van Pelt DE, Bryde S, et al. Anti-MOG antibodies plead against MS diagnosis in an Acquired Demyelinating Syndromes cohort. Mult Scler 2015;21:1513-1520.OpenUrlCrossRefPubMed 2.↵Rostasy K, Mader S, Schanda K, et al. Anti-myelin oligodendrocyte glycoprotein antibodies in pediatric patients with optic neuritis. Anti-MAG antibody titers are reduced by > 60%. Usually requires treatment with cyclophosphamide. Characteristics that increase the likelihood of a positive test: Age > 50. Gait disorder. Tremor. Functionally significant disability from motor or sensory loss. Demyelinating neuropathy: Usually slowly progressive

Recently, anti‐myelin oligodendrocyte glycoprotein (MOG) antibody has been detected in some patients with seronegative NMO and pediatric MS. 5, 6 Patients with anti‐MOG antibody should be treated in the same manner as NMO, and should avoid the use of DMD for MS even though the patient lacks characteristic NMO features. Early-onset (pediatric and adolescent) multiple sclerosis (MS) is a well-established demyelinating disease that accounts for approximately 3-5% of all MS cases. Thus, identifying potential biomarkers that can reflect the pathogenic mechanisms, disease course and prognosis, and therapeutic response in such patients is of paramount importance. Myelin oligodendrocyte glycoprotein (MOG) has. When excluding participants who met diagnostic criteria for MS, the occurrence of clinical relapses was more common among anti-MOG antibody-positive participants (9 of 71 [13%] vs 2 of 121 [2%]; P =.002), ie, 10 of 11 participants with relapsing non-MS disease (91%) were positive for anti-MOG antibody at presentation. Relapses in anti-MOG. Purpose: To evaluate the clinical differences between pediatric and adult patients with myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis (MOG-EM).Methods: We retrospectively reviewed the clinical features of pediatric and adult patients with MOG-EM in our center between November 2015 and October 2020.Results: Twenty-eight pediatric patients and 25 adults were admitted. Ordering now commercially available anti-MOG antibody testing in nearly all patients presenting with inflammatory demyelinating disease, particularly optic neuritis, appears to be warranted

Neuromyelitis Optica (NMO) National Multiple Sclerosis

Since anti-MOG antibodies are also found in pediatric MS and acute Anti-MOG reactivity is expressed as the geometric mean channel fluorescence (GMCF) ratio. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). The arrow indicates a clinical. Anti-MOG Optic Neuritis • Younger or even pediatric onset (25%) • MS-like Brain lesions or ADEM , positive OCB • Antibody level show fluctuating course (need to re-test to follow up) • Monophasic usually In contrast, anti-MOG is seen in patients with different disease entities such as childhood multiple sclerosis (MS), acute demyelinating encephalomyelitis (ADEM), anti-AQP4 negative NMO, and optic neuritis, but hardly in adult MS. A number of new candidate auto-antigens have been identified and await validation MS, is crucial as it harbors therapeutic implications. In contrast to MS, treatment (and even necessity of long-term treatment) of MOG-EM is thus far unclear as there are no established predic - tive markers to differentiate monophasic vs relapsing disease. Historically, MOG-IgG has been described as a potential part o

What is MOGAD? MOG Antibody Disease SRN

The investigators identified the myelin oligodendrocyte glycoprotein (MOG) antibody in their study of 535 children with central nervous system demyelinating disorders and encephalitis Participants 112 patients with NMOSD (31 AQP4-ab-positive, 21 MOG-ab-positive, 16 ab-negative) or MS (44) were selected from 3 centres (Oxford, Strasbourg and Liverpool) for the presence of brain lesions. Results MRI brain lesion distribution criteria were able to distinguish RRMS with a sensitivity of 90.9% and with a specificity of 87.1%.

Thus, Hacohen et al. proposed a diagnostic algorithm for relapsing ADS in children, identifying five categories of relapsing DS (MS, anti-AQP4-positive NMOSD, MOG antibody associated disorders, and antibody-negative RDS) and highlighting the importance of anti-MOG testing in the differential diagnosis of MS [97] Anti-MOG antibodies (MOGAb) recently emerged as potential biomarkers in a phenotypically-distinct group of patients with inflammatory demyelinating diseases (IDD). More described and defined forms of IDD include multiple sclerosis (MS) and aquaporin-4 (AQP4)-Ab associated neuromyelitis optica spectrum disorders (NMOSD), but a separate MOG-Ab. We suggest three rapid diagnostic tools for the analysis of MS patient sera to distinguish between pathogenic (e.g., anti-human MOG) and nonpathogenic (e.g., anti-rat MOG) antibodies: screening by (i) immunoblot against native (glycosylated) vs. nonglycosylated MOG, (ii) immunofluorescent microscopy against live vs. fixed, permeabilized OLs. MRI in children with demyelinating syndromes associated with MOG or AQP4 antibodies. (a, d): Brain and spinal cord MRI of a 13-year old girl with NMOSD and AQP4 antibodies.The sagittal MRI of the spinal cord shows hyperintensity involving more than 3 segments (a) whereas the brain axial T2-sequence shown in (d) is normal.(b, c, e, f): Coronal FLAIR-sequences of an 8-year old girl with an. The JC Virus and Risks for People with Multiple Sclerosis (MS) Medically reviewed by Deborah Weatherspoon, Ph.D., R.N., CRNA — Written by Kimberly Holland — Updated on February 4, 2019

MOGFS - Overview: Myelin Oligodendrocyte Glycoprotein (MOG

They were mostly identified in subgroups of NMO/NMOSD seronegative to auto antibodies against Aquaporin 4 (anti-AQP4): 8-39%, but also in MS (0-28%) ADEM and idiopathic ON. ON MOG + have a specific clinical presentation compare with ON associated with multiple sclerosis (SEP): older patient, less female preponderance, more often bilateral, more. Whilst an anti-MOG response and involvement of the complement system may increase the speed and severity of MS-like pathology, indicated by the more extensive demyelination in MOG immunised animals, it does not appear to be necessary for the development of chronic meningeal inflammation and accumulating neuronal loss, which were not.

clinically isolated syndromesMyelin injury without astrocytopathy in neuroinflammatoryThe Radiology Assistant : Spine - MyelopathyOptic Neuritis and OCT in Multiple SclerosisExperimental Autoimmune Encephalomyelitis (EAE) Model ofArchives des Neuro TV - Page 7 sur 12 - Neurologies

In a cohort of 47 patients with a clinically isolated syndrome, the baseline anti-MOG and anti-MBP antibody status was not associated with the risk of clinically definite multiple sclerosis after. Injection of MOG (myelin oligodendrocyte glycoprotein) along with transfer of anti-MOG lymphocytes can cause demyelination. While EAE proves that an autoimmune reaction can cause inflammation in the white matter, the analogy with MS stops there Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed on the surface of myelin sheaths and oligodendrocytes. 1,2 Anti-MOG antibodies (MOG-IgG) can cause demyelination in vitro and induce experimental autoimmune encephalomyelitis. 3,4 MOG-IgG are found in subtypes of central nervous system (CNS) acquired demyelinating syndromes (ADS) in both adult and paediatric patients, for example.