RARE DISEASE
Acute transverse myelitis with anti-MOG antibodies
Acute transverse myelitis with anti-MOG antibodies
Acute transverse myelitis with anti-MOG antibodies
Synonyms: Acute transverse myelitis with anti-myelin oligodendrocyte glycoprotein antibodies
Synonyms: Acute transverse myelitis with anti-myelin oligodendrocyte glycoprotein antibodies
Synonyms: Acute transverse myelitis with anti-myelin oligodendrocyte glycoprotein antibodies
Drug discovery
1
drug
With orphan designation
Overview
Acute transverse myelitis with anti-MOG antibodies is an immune-mediated demyelinating disorder affecting the spinal cord, characterized by acute/subacute motor, sensory, and autonomic dysfunction. Diagnosis relies on serum anti-MOG IgG positivity and MRI findings (longitudinally extensive lesions, H-shaped gray matter hyperintensity). Most patients show favorable recovery, though 30-50% experience relapses. Compared to AQP4-IgG+ NMOSD, MOGAD-TM has lower disability but higher bladder dysfunction risk [1][5][10][13].
Categories: rare neurological diseases
Research Papers
52 drug discovery papers about Acute transverse myelitis with anti-MOG antibodies, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
52 drug discovery papers about Acute transverse myelitis with anti-MOG antibodies, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
small molecules
2025-09-30 | Uncommon alliance between MOGAD and Behçet's disease.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a newly recognized demyelinating disease with diverse clinical and radiological manifestations that continue to expand over time. Its coexistence with Behçet's disease, a multisystem inflammatory disorder, has not been previously reported. We report a rare case of a 40-year-old female with Behçet's disease who was treated with colchicine and developed two attacks of longitudinal extensive transverse myelitis, associated with positive serum anti-MOG antibodies. During the first episode, the patient responded well to five days of intravenous methylprednisolone associated with two plasma exchange sessions. Although recommended, the patient declined Mycophenolate Mofetil treatment until the second episode. Since then, she has remained free of relapses during two years of follow-up, reinforcing the hypothesis that a background of autoimmune dysregulation may predispose patients to MOGAD and lead to its recurrence.
2025-09-04 | Hydrocephalus as an Initial Presentation of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-Associated Disease: A Case Report and Review of Tumor-Mimicking Demyelination.
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a demyelinating disease of the central nervous system (CNS) that manifests as optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cortical encephalitis. Some patients with MOGAD present with tumor-like brain lesions. However, hydrocephalus as an initial presentation is rare. We present the case of a 23-year-old Japanese man with an acute onset of headache, nausea, and diplopia, who was initially suspected of having a germinoma but was later diagnosed with MOGAD. Brain magnetic resonance imaging (MRI) revealed a tumor-like lesion with hyperintensity on fluid-attenuated inversion recovery (FLAIR) imaging and contrast enhancement on T1-weighted postcontrast images, extending from the midbrain to the thalamus with obstructive hydrocephalus. Neuroendoscopic third ventriculostomy and brain biopsy were performed. Histopathological analyses revealed demyelination, perivascular lymphocytic infiltration, and MOG loss. MOG antibody tests were positive, confirming MOGAD. The patient was treated with pulse steroid therapy (methylprednisolone 1,000 mg/day) and seven sessions of plasmapheresis, resulting in significant neurological improvement. He was discharged approximately two months after symptom onset, and at the six-month follow-up from discharge, he remained relapse-free with only mild diplopia. In this case, early diagnosis via pathological brain analysis and anti-MOG antibody testing allowed for timely treatment. We emphasize the importance of including MOGAD in the diagnostic workup of tumor-mimicking CNS lesions that can cause hydrocephalus.
2025-06-11 | French guidelines for the diagnosis and management of MOG antibody-associated disease.
MOG antibody-associated disease (MOGAD) is a new entity within the spectrum of autoimmune inflammatory diseases of the central nervous system. It is distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Although they share certain clinical characteristics, these 3 diseases differ in terms of their pathophysiology, disease course and response to treatment. MOGAD is a rare disease affecting both adults and children, with a higher frequency in the latter. The clinical presentation of MOGAD varies depending on age: in children under the age of 10, presentations of acute disseminated encephalomyelitis (ADEM) are frequently described, whereas in children over the age of 10 and in adults, unilateral or bilateral optic neuritis or acute myelitis is more often observed. Other, rarer presentations have also been reported, including encephalitic presentations with seizures. Radiologic findings can sometimes help guide the diagnosis: extensive anterior optic nerve involvement, perineuritis, extensive lesions of the spinal cord with involvement of the conus medullaris, and involvement of the pons, for example. Diagnosis is confirmed by measuring anti-MOG antibodies in the serum. In case of diagnostic doubt, the result must be confirmed in a reference laboratory (currently available in Lyon and Le Kremlin Bicêtre in France). The disease course is usually monophasic in children, but relapses are possible. In adults, the frequency of relapses seems higher than in children, estimated at more than 40% after 5 years. Visual, bladder/sphincter, cognitive and, to a lesser extent, motor sequelae may occur, but much less frequently than in NMOSD. In children and adults, attacks are treated with high-dose IV corticosteroids, which are often very effective, followed by an oral taper. In certain situations, long-term immunoactive therapy may be proposed, particularly when a relapse occurs, after discussion with a reference or expert center for Inflammatory diseases of the central nervous system. Long-term follow-up is proposed at the reference/expert center at least once a year. In between these appointments, follow-up with the referring pediatric neurologist, pediatrician, treating physician or referring neurologist is carried out every 6 months. It is important to check for the occurrence of a new attack and the onset of complications but also, in the case of long-term therapy, adherence to and tolerance of the treatment. Multidisciplinary management is essential and involves a variety of healthcare professionals (neurologist or pediatric neurologist, ophthalmologist, physiatrist, physiotherapist, speech therapist, occupational therapist, psychologist and social worker).
2024-10-25 | New insights into the use of high dose corticosteroids and plasmapheresis in persons with MOGAD and NMOSD.
Anti-myelin oligodendrocyte glycoprotein associated disease (MOGAD) and neuromyelitis optica spectrum disease (NMOSD) are antibody mediated diseases characterized by neurological symptoms including recurrent relapses of optic neuritis and/or myelitis, as well as other less frequent syndromes. The current treatment for acute attacks of NMOSD/MOGAD are based on clinical studies for other demyelinating diseases(i.e. Multiple Sclerosis). In NMOSD, high dose corticosteroids (HDS) are considered the standard first line therapy, with emerging evidence supporting the use of plasmapheresis (PLEX) as an acute therapy. In MOGAD, being a relatively new clinical syndrome, the consensus on acute treatments is yet to be reached. The objective of our study was to assess the efficacy of treatment regimens (no treatment vs. HDS vs. HDS and PLEX) on disability outcomes in persons with NMOSD and MOGAD-optic neuritis and myelitis. We retrospectively extracted data from the MuSicaL-NeMo database using a mixed Natural Language Processing followed by investigators verification. We assessed the change in Expanded Disability Status Scale (EDSS) and Visual Acuity (VA) following HDS and PLEX, in persons with MOGAD and NMOSD following myelitis and optic neuritis. We used the novel statistical measure Wilcoxon-Mann-Whitney Odd (WMW-Odd) to calculate the change through all the spectrum of each ordinal scale (VA and EDSS). Eleven myelitis and 12 optic neuritis in 22 persons with MOGAD and 30 myelitis and 12 optic neuritis in 20 persons with NMOSD were included(15 Aquaporin-4 seropositive). In persons with MOGAD-optic neuritis the group receiving HDS had a WMW-Odd of 15.33(p ≤ 0.001), however those not receiving treatment also tended to improve (WMW-Odd=3.17, p = 0.06). NMOSD-optic neuritis treated with HDS only improve 33.3 % of the times (p=NS). Persons with MOGAD-myelitis receiving HDS significantly improved (WMW-Odd=7.33, p = 0.002). Persons with NMOSD-myelitis treated with HDS had an WMW-Odd of 2.56 (p = 0.002) and those treated with PLEX plus HDS (PLEX+), had similar WMW-Odd of 2.51 (p = 0.03). When correcting for disease severity by restricting inclusion to persons with NMOSD with EDSS≥4, both treatments showed a higher WMW-Odd, however the group receiving HDS continued to show higher WMW-Odd than the PLEX+ group(WMW-Odd= 3.75, p = 0.002 vs. WMW-Odd =3.05, p = 0.02, respectvely) CONCLUSION: Our study suggests that persons with MOGAD-optic neuritis improve without acute treatments, however they have very marked improvement when using HDS, as previously suggested. Patient with MOGAD-myelitis are also very responsive to HDS, however, as compared to MOGAD-optic neuritis, they displayed less improvement, if not treated. In the NMOSD group the use of PLEX in addition to HDS did not demonstrate any significant difference in EDSS outcomes. Contrary to previous suggestions, when adjusting for group differences (by only including EDSS ≥4), the use of HDS and PLEX+ did not show better results than the group using HDS.
2024-06-10 | Extremely Longitudinally Extensive Transverse Myelitis in a Patient With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
Longitudinally extensive myelitis with 15 or more vertebrae in length is extremely rare, with limited evidence regarding clinical features and therapeutic response. We report a case of a 29-year-old male patient with extremely longitudinally extensive myelitis ultimately diagnosed as myelin oligodendrocyte glycoprotein-associated disease (MOGAD). The patient presented with an acute onset of meningismus, limb weakness, sensory disturbance below the C5 level, ataxia, and urinary retention. T2-weighted imaging on MRI showed an extremely longitudinally extensive spinal cord lesion ranging from C2 to the medullary conus, together with a left pontine lesion. Positive anti-myelin oligodendrocyte glycoprotein antibodies were serologically detected, which led to the diagnosis of MOGAD. Intravenous methylprednisolone followed by 1 mg/kg oral prednisolone with taper resulted in complete symptomatic and radiological resolution. The striking complete resolution despite the symptomatic and radiological severity observed in this case has been described in a few previously reported MOGAD cases. Extremely longitudinally extensive myelitis with excellent therapeutic response may be a characteristic presentation of MOGAD.
antibodies
2026-07-10 | Table 1_Anti-NMDA-receptor encephalitis and MOGAD associated optic neuritis: a case series.docx
Introduction Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a well-recognized autoimmune condition that often presents with neuropsychiatric symptoms and seizures. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) often manifests as optic neuritis and, less frequently, as acute demyelinating encephalomyelitis or transverse myelitis. The co-occurrence of anti-NMDAR encephalitis and MOGAD is becoming increasingly recognized, but clinical series remain limited. Description of cases We present three patients with anti-NMDAR encephalitis and MOGAD optic neuritis (ON): two men, aged 19 and 26, and one woman, aged 36. Clinical presentations, signs, investigations, and management of each case are discussed. The 26-year-old man presented with altered mental status and concurrent vision loss. The 36-year-old woman presented with altered mental status during the encephalitis episode and developed vision loss 4 months after encephalitis. The 19-year-old man with a prior history of altered mental status, diagnosed with NMDA encephalitis 9 years earlier, presented with headache and vision loss. Abnormal T2/FLAIR lesions in the brain and/or spinal cord during the encephalitis episode and unilateral or bilateral optic nerve enhancement during the optic neuritis episode were detected on brain and orbital magnetic resonance imaging (MRI) in all patients. All patients tested positive for cerebrospinal fluid (CSF) anti-NMDAR antibodies during the encephalitis episode and had positive serum MOG titers during the optic neuritis episode. Each patient presented with bilateral, asymmetrically reduced visual acuity and diminished color vision. One patient exhibited bilateral temporal optic nerve pallor, while two patients had bilateral optic nerve edema. The diagnostic work-up revealed positive serum MOG titers (1:100, 1:10,000, and 1:10,000 in the 36/F, 26/M, and 19/M, respectively). The 36-year-old woman was treated with intravenous (IV) steroids, plasma exchange (PLEX), and rituximab during the encephalitis episode. During the optic neuritis episode, she was treated with IV steroids, IV immunoglobulin (IVIG), and rituximab, followed by long-term rituximab maintenance therapy. The 19-year-old man was treated for encephalitis with IV steroids, IVIG, and rituximab. During his optic neuritis episode, he received IV steroids, IVIG, and tocilizumab, followed by long-term tocilizumab maintenance therapy. The 26-year-old man was treated with IV steroids, PLEX, and rituximab during the acute episode, followed by long-term IVIG maintenance therapy. After achieving 2 years of stability that prompted the discontinuation of IVIG, the patient experienced a MOG-IgG-positive relapse 5 months later. This relapse was marked by a seizure-like episode and the appearance of new lesions on MRI. The acute symptoms resolved after treatment with intravenous steroids and IVIG. Subsequently, the patient was initiated on an indefinite maintenance IVIG regimen. Visual acuity in all patients improved to their baseline levels following treatment. Conclusion This series highlights the emerging overlap between anti-NMDAR encephalitis and MOGAD optic neuritis. Optic neuritis may occur months to years after encephalitis, underscoring the need for careful monitoring of patients with anti-NMDAR encephalitis who develop new visual symptoms. Dual autoimmunity may represent a distinct phenotype with implications for long-term immunotherapy.
2026-02-07 | Overlapping autoimmunity and demyelination syndromes associated with TNF inhibitor therapy.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a demyelinating disorder of the central nervous system. We describe a case of a 31-year-old male with ankylosing spondylitis who developed optic neuritis and transverse myelitis accompanied by positive anti-MOG antibodies, and subsequently features consistent with systemic lupus erythematosus (SLE), beginning 3 months after initiating adalimumab. Adalimumab was discontinued, and the patient was treated with pulsed intravenous methylprednisolone followed by rituximab with significant improvement in clinical, imaging, and laboratory manifestations of the disease. This case highlights a rare constellation of overlapping autoimmune diseases, with both MOGAD and SLE emerging after anti-TNF antibody exposure in a patient with ankylosing spondylitis.
2025-07-03 | Anti-MOG Antibody Associated Disorders in Pakistan.
To present clinicopathological features and treatment outcomes of patients who tested positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in the catchment Pakistani population. Observational study. Place and Duration of the Study: Department of Immunology and Neurology, Shifa International Hospital / Shifa Tameer-e-Millat University, Islamabad, Pakistan, from January 2018 to December 2022. A review of patients referred for anti-MOG antibody testing was conducted. Indirect immunofluorescence was used to analyse all samples on EU 90 cells transfected with MOG genes. Patients who tested positive for anti-MOG antibodies were included in the study. Patients' medical records and interviews were used to gather clinical data, as per the objective. One hundred and fourteen patients out of 740 were tested positive for anti-MOG antibodies. A total of 59 patients were included for final analysis, and 78 (68.4%) of the seropositive population were male, with a mean age of 24 years ± 15.8 years (range 4-59 years). The most frequent clinical presentation was visual impairment in 39/59 (66%) patients, followed by muscle weakness in 36/59 (61%) and headache in 30/59 (50%) patients. Treatment included intravenous methylprednisolone, oral prednisolone, plasma exchange, rituximab, intravenous immunoglobulins, azathioprine, mycophenolate mofetil, cyclophosphamide, and methotrexate. The present study showed a higher percentage of males tested positive for anti-MOG antibodies. MOG-associated disorders can affect both children and adults. The most frequent clinical presentations of MOGAD in this study were visual impairment, followed by muscle weakness. The primary clinical phenotype identified was isolated transverse myelitis. Myelin oligodendrocyte glycoprotein, Optic neuritis, Myelitis, Acute disseminated encephalomyelitis, Demyelinating disease, Autoimmune disorder.
2025-05-15 | Coronavirus Disease 2019 Infection and Vaccination in Pediatric Demyelinating Diseases.
As compared to adults, less is known about the effects of SARS-CoV-2 infection in children with neuroinflammatory diseases, such as multiple sclerosis (MS), anti-myelin oligodendrocyte glycoprotein associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD). Moreover, the effects of SARS-CoV-2 vaccination on pediatric demyelinating diseases is also lesser known. Here, we examine the effects of SARS-CoV-2 infection and vaccination on children with demyelinating diseases. Retrospective chart review was performed at a single tertiary pediatric center, including 116 children with demyelinating diagnoses (MOGAD, MS, NMOSD, transverse myelitis-TM, and acute disseminated encephalomyelitis). Descriptive statistics and logistic regression were used. The diagnoses included: MS: 56/116 = 48%, MOGAD: 32/116 = 28%, NMOSD: 15/116 = 13%, acute disseminated encephalomyelitis: 12/116 = 10%, and TM: 1/116 = 1%. The known COVID infection rate was 26% = 30/116. Three of 30 (10%) of those with known infection were hospitalized. None of those hospitalized required intubation or ICU admission. Of the 30 with known infection, two (7%) had neuroinflammatory events that occurred within four weeks of infection, both of which were their first clinical events for MS. SARS-CoV-2 vaccination was not associated with any new onset or relapse neuroinflammatory events in our cohort. Demyelinating diagnosis and anti-CD20 mAbs were associated with known SARS-CoV-2 infection. Two participants had an initial clinical MS event associated with infection. However, we found no association with SARS-COV-2 vaccination or infection with relapses and no long-term adverse outcomes with SARS-CoV-2 vaccination or infection. Future larger multicenter studies should prospectively compare how infection and vaccination affects children and adults with demyelinating diseases.
2024-08-23 | [Modern pathogenetic treatment of rare demyelinating diseases].
Rare demyelinating diseases are a group of diseases whose pathogenesis is based on the process of demyelination. This group of diseases includes acute multiple encephalomyelitis (ADEM), opticoneuromyelitis spectrum diseases (NMOSD) and anti-myelin-oligodendrocyte glycoprotein-associated diseases (MOG-antibodies-associated diseases - MOGAD). Recently, new biological drugs for pathogenetic therapy have been developed, which have shown their effectiveness and good tolerability in comparison with therapy with first- and second-line drugs. Aim of the study - analysis of modern possibilities of pathogenetic treatment of patients with ADEM, seronegative and seropositive patients with NMOSD. The analysis was carried out on the basis of English-language publications in PubMed published over the past five years. This review summarizes current ideas about the possibilities of pathogenetic treatment of rare diseases. The advantages of using ravulizumab over other representatives of a new biological therapy associated with the use of monoclonal antibodies are shown. The analyzed data allow us to conclude that there is a significant development of pathogenetic treatment options for ZSONM. However, the effectiveness of new therapeutic biological drugs is still limited due to the lack of a large amount of clinical data to confirm, which creates the need to continue analyzing the experience of their use. Редкие демиелинизирующие заболевания представляют группу заболеваний, в основе патогенеза которых лежит процесс демиелинизации. К данной группе заболеваний относят острый рассеянный энцефаломиелит (ОРЭМ), заболевания спектра оптиконейромиелита (ЗСОНМ) и анти-миелин-олигодендроцитарный гликопротеин-ассоциированные заболевания (МОГАТАЗ). Разрабатываются новые биологические средства патогенетической терапии, которые показали более высокую эффективность и хорошую переносимость по сравнению с препаратами первой и второй линий. В статье представлен анализ современных возможностей патогенетического лечения пациентов с ОРЭМ, серонегативных и серопозитивных пациентов с ЗСОНМ. Проведен анализ англоязычных публикаций из базы PubMed, опубликованных за последние 5 лет. Суммированы современные представления о возможностях патогенетического лечения редких заболеваний. Показаны преимущества использования равулизумаба перед другими представителями новой биологической терапии, связанной с использованием моноклональных антител. Результаты анализа данных литературы позволяют сделать вывод о значительном развитии патогенетических вариантов лечения ЗСОНМ, однако данные об эффективности новых биологических препаратов по-прежнему ограничены из-за отсутствия достаточного количества клинических исследований для ее подтверждения, что диктует необходимость продолжить анализ опыта их использования.
cell therapies
2024-04-12 | An aggressive form of MOGAD treated with aHSCT: A case report.
Although myelin-oligodendrocyte-glycoprotein (MOG)-antibody-associated disease (MOGAD) has been considered a more favorable demyelinating central nervous system disorder, recent data evidence that some patients might experience severe relapses and high disability. Actual treatment-options are acquired mostly from anti-aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder and rely on clinical experience. Therefore, treatment of aggressive forms of MOGAD can be challenging. To describe a patient with an aggressive MOGAD treated with autologous hematopoietic stem cell transplantation (aHSCT). A 56-year-old man was diagnosed with MOGAD in 2017 because of right optic-neuritis and anti-MOG-antibody positivity. In the following 2 years, he experienced two optic neuritis with good recovery after high-dose steroid. At the end of 2019, he presented sensory and motor impairment at lower limbs with evidence of several spinal, longitudinally extended, tumefactive inflammatory lesions. Despite sequential treatment with rituximab and tocilizumab alongside high-dose steroid, intravenous immunoglobulins and plasma-exchange, he experienced several clinical relapses and exhibited persistent magnetic resonance activity. He was finally addressed to intense immunosuppression with myeloablative conditioning regimen followed by autologous hematopoietic stem cell transplantation (aHSCT). After 2 years follow-up, he is free from disease-activity. In a patient affected by aggressive, treatment-refractory MOGAD, aHSCT resulted as safe and was able to suppress disease-activity for over 2 years.
2020-08-20 | Regulatory B Cells and Its Role in Central Nervous System Inflammatory Demyelinating Diseases
Regulatory B (Breg) cells represent a population of suppressor B cells that participate in immunomodulatory processes and inhibition of excessive inflammation. The regulatory function of Breg cells has been demonstrated in mice and human with inflammatory diseases, cancer, after transplantation, and particularly in autoinflammatory disorders. In order to suppress inflammation, Breg cells produce anti-inflammatory mediators, induce death ligand-mediated apoptosis, and regulate many kinds of immune cells such as suppressing the proliferation and differentiation of effector T cell and increasing the number of regulatory T cells. Central nervous system Inflammatory demyelinating diseases (CNS IDDs) are a heterogeneous group of disorders, which occur against the background of an acute or chronic inflammatory process. With the advent of monoclonal antibodies directed against B cells, breakthroughs have been made in the treatment of CNS IDDs. Therefore, the number and function of B cells in IDDs have attracted attention. Meanwhile, increasing studies have confirmed that Breg cells play a role in alleviating autoimmune diseases, and treatment with Breg cells has also been proposed as a new therapeutic direction. In this review, we focus on the understanding of the development and function of Breg cells and on the diversification of Breg cells in CNS IDDs.
oligonucleotides
2024-03-11 | Administration methods and dosage of poly(lactic acid)-glycol intervention to myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalitis mice
Abstract Background Myelin oligodendrocyte glycoprotein-associated disorders (MOGAD) is an autoimmune central nervous system disease. Antigen-specific immune tolerance using nanoparticles such as Polylactic-co-glycolic acid (PLGA) have recently been used as a new therapeutic tolerization approach for CNS autoimmune diseases. We examined whether MOG 1-125 conjugated with PLGA could induce MOG-specific immune tolerance in an experimental autoimmune encephalitis (EAE) mouse model. EAE was induced in sixty C57BL/6 J wild-type mice using MOG 1-125 peptide with complete Freund’s Adjuvant. The mice were divided into 12 groups (n = 5 each) to test the ability of MOG 1-125 conjugated PLGA intervention to mitigate the severity or improve the outcomes from EAE with and without rapamycin compared to antigen alone or PLGA alone. EAE score and serum MOG-IgG titers were compared among the interventions.Kindly check and confirm the processed Affiliation “4” is appropriate.I confirmed the Aff 4.Affiliation: Corresponding author information have been changed to present affiliation. Kindly check and confirm.I checked and confirmed the Corresponding author's information. Results Mice with EAE that were injected intraperitoneally with MOG 1-125 conjugated PLGA + rapamycin complex showed dose-dependent mitigation of EAE score. Intraperitoneal and intravenous administration resulted in similar clinical outcomes, whereas 80% of mice treated with subcutaneous injection had a recurrence of clinical score worsening after approximately 1 week. Although there was no significant difference in EAE scores between unconjugated-PLGA and MOG-conjugated PLGA, serum MOG-IgG tended to decrease in the MOG-conjugated PLGA group compared to controls. Conclusion Intraperitoneal administration of PLGA resulted in dose-dependent and longer-lasting immune tolerance than subcutaneous administration. The induction of immune tolerance using PLGA may represent a future therapeutic option for patients with MOGAD.
small molecules
2025-09-30 | Uncommon alliance between MOGAD and Behçet's disease.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a newly recognized demyelinating disease with diverse clinical and radiological manifestations that continue to expand over time. Its coexistence with Behçet's disease, a multisystem inflammatory disorder, has not been previously reported. We report a rare case of a 40-year-old female with Behçet's disease who was treated with colchicine and developed two attacks of longitudinal extensive transverse myelitis, associated with positive serum anti-MOG antibodies. During the first episode, the patient responded well to five days of intravenous methylprednisolone associated with two plasma exchange sessions. Although recommended, the patient declined Mycophenolate Mofetil treatment until the second episode. Since then, she has remained free of relapses during two years of follow-up, reinforcing the hypothesis that a background of autoimmune dysregulation may predispose patients to MOGAD and lead to its recurrence.
2025-09-04 | Hydrocephalus as an Initial Presentation of Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-Associated Disease: A Case Report and Review of Tumor-Mimicking Demyelination.
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a demyelinating disease of the central nervous system (CNS) that manifests as optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cortical encephalitis. Some patients with MOGAD present with tumor-like brain lesions. However, hydrocephalus as an initial presentation is rare. We present the case of a 23-year-old Japanese man with an acute onset of headache, nausea, and diplopia, who was initially suspected of having a germinoma but was later diagnosed with MOGAD. Brain magnetic resonance imaging (MRI) revealed a tumor-like lesion with hyperintensity on fluid-attenuated inversion recovery (FLAIR) imaging and contrast enhancement on T1-weighted postcontrast images, extending from the midbrain to the thalamus with obstructive hydrocephalus. Neuroendoscopic third ventriculostomy and brain biopsy were performed. Histopathological analyses revealed demyelination, perivascular lymphocytic infiltration, and MOG loss. MOG antibody tests were positive, confirming MOGAD. The patient was treated with pulse steroid therapy (methylprednisolone 1,000 mg/day) and seven sessions of plasmapheresis, resulting in significant neurological improvement. He was discharged approximately two months after symptom onset, and at the six-month follow-up from discharge, he remained relapse-free with only mild diplopia. In this case, early diagnosis via pathological brain analysis and anti-MOG antibody testing allowed for timely treatment. We emphasize the importance of including MOGAD in the diagnostic workup of tumor-mimicking CNS lesions that can cause hydrocephalus.
2025-06-11 | French guidelines for the diagnosis and management of MOG antibody-associated disease.
MOG antibody-associated disease (MOGAD) is a new entity within the spectrum of autoimmune inflammatory diseases of the central nervous system. It is distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Although they share certain clinical characteristics, these 3 diseases differ in terms of their pathophysiology, disease course and response to treatment. MOGAD is a rare disease affecting both adults and children, with a higher frequency in the latter. The clinical presentation of MOGAD varies depending on age: in children under the age of 10, presentations of acute disseminated encephalomyelitis (ADEM) are frequently described, whereas in children over the age of 10 and in adults, unilateral or bilateral optic neuritis or acute myelitis is more often observed. Other, rarer presentations have also been reported, including encephalitic presentations with seizures. Radiologic findings can sometimes help guide the diagnosis: extensive anterior optic nerve involvement, perineuritis, extensive lesions of the spinal cord with involvement of the conus medullaris, and involvement of the pons, for example. Diagnosis is confirmed by measuring anti-MOG antibodies in the serum. In case of diagnostic doubt, the result must be confirmed in a reference laboratory (currently available in Lyon and Le Kremlin Bicêtre in France). The disease course is usually monophasic in children, but relapses are possible. In adults, the frequency of relapses seems higher than in children, estimated at more than 40% after 5 years. Visual, bladder/sphincter, cognitive and, to a lesser extent, motor sequelae may occur, but much less frequently than in NMOSD. In children and adults, attacks are treated with high-dose IV corticosteroids, which are often very effective, followed by an oral taper. In certain situations, long-term immunoactive therapy may be proposed, particularly when a relapse occurs, after discussion with a reference or expert center for Inflammatory diseases of the central nervous system. Long-term follow-up is proposed at the reference/expert center at least once a year. In between these appointments, follow-up with the referring pediatric neurologist, pediatrician, treating physician or referring neurologist is carried out every 6 months. It is important to check for the occurrence of a new attack and the onset of complications but also, in the case of long-term therapy, adherence to and tolerance of the treatment. Multidisciplinary management is essential and involves a variety of healthcare professionals (neurologist or pediatric neurologist, ophthalmologist, physiatrist, physiotherapist, speech therapist, occupational therapist, psychologist and social worker).
2024-10-25 | New insights into the use of high dose corticosteroids and plasmapheresis in persons with MOGAD and NMOSD.
Anti-myelin oligodendrocyte glycoprotein associated disease (MOGAD) and neuromyelitis optica spectrum disease (NMOSD) are antibody mediated diseases characterized by neurological symptoms including recurrent relapses of optic neuritis and/or myelitis, as well as other less frequent syndromes. The current treatment for acute attacks of NMOSD/MOGAD are based on clinical studies for other demyelinating diseases(i.e. Multiple Sclerosis). In NMOSD, high dose corticosteroids (HDS) are considered the standard first line therapy, with emerging evidence supporting the use of plasmapheresis (PLEX) as an acute therapy. In MOGAD, being a relatively new clinical syndrome, the consensus on acute treatments is yet to be reached. The objective of our study was to assess the efficacy of treatment regimens (no treatment vs. HDS vs. HDS and PLEX) on disability outcomes in persons with NMOSD and MOGAD-optic neuritis and myelitis. We retrospectively extracted data from the MuSicaL-NeMo database using a mixed Natural Language Processing followed by investigators verification. We assessed the change in Expanded Disability Status Scale (EDSS) and Visual Acuity (VA) following HDS and PLEX, in persons with MOGAD and NMOSD following myelitis and optic neuritis. We used the novel statistical measure Wilcoxon-Mann-Whitney Odd (WMW-Odd) to calculate the change through all the spectrum of each ordinal scale (VA and EDSS). Eleven myelitis and 12 optic neuritis in 22 persons with MOGAD and 30 myelitis and 12 optic neuritis in 20 persons with NMOSD were included(15 Aquaporin-4 seropositive). In persons with MOGAD-optic neuritis the group receiving HDS had a WMW-Odd of 15.33(p ≤ 0.001), however those not receiving treatment also tended to improve (WMW-Odd=3.17, p = 0.06). NMOSD-optic neuritis treated with HDS only improve 33.3 % of the times (p=NS). Persons with MOGAD-myelitis receiving HDS significantly improved (WMW-Odd=7.33, p = 0.002). Persons with NMOSD-myelitis treated with HDS had an WMW-Odd of 2.56 (p = 0.002) and those treated with PLEX plus HDS (PLEX+), had similar WMW-Odd of 2.51 (p = 0.03). When correcting for disease severity by restricting inclusion to persons with NMOSD with EDSS≥4, both treatments showed a higher WMW-Odd, however the group receiving HDS continued to show higher WMW-Odd than the PLEX+ group(WMW-Odd= 3.75, p = 0.002 vs. WMW-Odd =3.05, p = 0.02, respectvely) CONCLUSION: Our study suggests that persons with MOGAD-optic neuritis improve without acute treatments, however they have very marked improvement when using HDS, as previously suggested. Patient with MOGAD-myelitis are also very responsive to HDS, however, as compared to MOGAD-optic neuritis, they displayed less improvement, if not treated. In the NMOSD group the use of PLEX in addition to HDS did not demonstrate any significant difference in EDSS outcomes. Contrary to previous suggestions, when adjusting for group differences (by only including EDSS ≥4), the use of HDS and PLEX+ did not show better results than the group using HDS.
2024-06-10 | Extremely Longitudinally Extensive Transverse Myelitis in a Patient With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
Longitudinally extensive myelitis with 15 or more vertebrae in length is extremely rare, with limited evidence regarding clinical features and therapeutic response. We report a case of a 29-year-old male patient with extremely longitudinally extensive myelitis ultimately diagnosed as myelin oligodendrocyte glycoprotein-associated disease (MOGAD). The patient presented with an acute onset of meningismus, limb weakness, sensory disturbance below the C5 level, ataxia, and urinary retention. T2-weighted imaging on MRI showed an extremely longitudinally extensive spinal cord lesion ranging from C2 to the medullary conus, together with a left pontine lesion. Positive anti-myelin oligodendrocyte glycoprotein antibodies were serologically detected, which led to the diagnosis of MOGAD. Intravenous methylprednisolone followed by 1 mg/kg oral prednisolone with taper resulted in complete symptomatic and radiological resolution. The striking complete resolution despite the symptomatic and radiological severity observed in this case has been described in a few previously reported MOGAD cases. Extremely longitudinally extensive myelitis with excellent therapeutic response may be a characteristic presentation of MOGAD.
antibodies
2026-07-10 | Table 1_Anti-NMDA-receptor encephalitis and MOGAD associated optic neuritis: a case series.docx
Introduction Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a well-recognized autoimmune condition that often presents with neuropsychiatric symptoms and seizures. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) often manifests as optic neuritis and, less frequently, as acute demyelinating encephalomyelitis or transverse myelitis. The co-occurrence of anti-NMDAR encephalitis and MOGAD is becoming increasingly recognized, but clinical series remain limited. Description of cases We present three patients with anti-NMDAR encephalitis and MOGAD optic neuritis (ON): two men, aged 19 and 26, and one woman, aged 36. Clinical presentations, signs, investigations, and management of each case are discussed. The 26-year-old man presented with altered mental status and concurrent vision loss. The 36-year-old woman presented with altered mental status during the encephalitis episode and developed vision loss 4 months after encephalitis. The 19-year-old man with a prior history of altered mental status, diagnosed with NMDA encephalitis 9 years earlier, presented with headache and vision loss. Abnormal T2/FLAIR lesions in the brain and/or spinal cord during the encephalitis episode and unilateral or bilateral optic nerve enhancement during the optic neuritis episode were detected on brain and orbital magnetic resonance imaging (MRI) in all patients. All patients tested positive for cerebrospinal fluid (CSF) anti-NMDAR antibodies during the encephalitis episode and had positive serum MOG titers during the optic neuritis episode. Each patient presented with bilateral, asymmetrically reduced visual acuity and diminished color vision. One patient exhibited bilateral temporal optic nerve pallor, while two patients had bilateral optic nerve edema. The diagnostic work-up revealed positive serum MOG titers (1:100, 1:10,000, and 1:10,000 in the 36/F, 26/M, and 19/M, respectively). The 36-year-old woman was treated with intravenous (IV) steroids, plasma exchange (PLEX), and rituximab during the encephalitis episode. During the optic neuritis episode, she was treated with IV steroids, IV immunoglobulin (IVIG), and rituximab, followed by long-term rituximab maintenance therapy. The 19-year-old man was treated for encephalitis with IV steroids, IVIG, and rituximab. During his optic neuritis episode, he received IV steroids, IVIG, and tocilizumab, followed by long-term tocilizumab maintenance therapy. The 26-year-old man was treated with IV steroids, PLEX, and rituximab during the acute episode, followed by long-term IVIG maintenance therapy. After achieving 2 years of stability that prompted the discontinuation of IVIG, the patient experienced a MOG-IgG-positive relapse 5 months later. This relapse was marked by a seizure-like episode and the appearance of new lesions on MRI. The acute symptoms resolved after treatment with intravenous steroids and IVIG. Subsequently, the patient was initiated on an indefinite maintenance IVIG regimen. Visual acuity in all patients improved to their baseline levels following treatment. Conclusion This series highlights the emerging overlap between anti-NMDAR encephalitis and MOGAD optic neuritis. Optic neuritis may occur months to years after encephalitis, underscoring the need for careful monitoring of patients with anti-NMDAR encephalitis who develop new visual symptoms. Dual autoimmunity may represent a distinct phenotype with implications for long-term immunotherapy.
2026-02-07 | Overlapping autoimmunity and demyelination syndromes associated with TNF inhibitor therapy.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a demyelinating disorder of the central nervous system. We describe a case of a 31-year-old male with ankylosing spondylitis who developed optic neuritis and transverse myelitis accompanied by positive anti-MOG antibodies, and subsequently features consistent with systemic lupus erythematosus (SLE), beginning 3 months after initiating adalimumab. Adalimumab was discontinued, and the patient was treated with pulsed intravenous methylprednisolone followed by rituximab with significant improvement in clinical, imaging, and laboratory manifestations of the disease. This case highlights a rare constellation of overlapping autoimmune diseases, with both MOGAD and SLE emerging after anti-TNF antibody exposure in a patient with ankylosing spondylitis.
2025-07-03 | Anti-MOG Antibody Associated Disorders in Pakistan.
To present clinicopathological features and treatment outcomes of patients who tested positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in the catchment Pakistani population. Observational study. Place and Duration of the Study: Department of Immunology and Neurology, Shifa International Hospital / Shifa Tameer-e-Millat University, Islamabad, Pakistan, from January 2018 to December 2022. A review of patients referred for anti-MOG antibody testing was conducted. Indirect immunofluorescence was used to analyse all samples on EU 90 cells transfected with MOG genes. Patients who tested positive for anti-MOG antibodies were included in the study. Patients' medical records and interviews were used to gather clinical data, as per the objective. One hundred and fourteen patients out of 740 were tested positive for anti-MOG antibodies. A total of 59 patients were included for final analysis, and 78 (68.4%) of the seropositive population were male, with a mean age of 24 years ± 15.8 years (range 4-59 years). The most frequent clinical presentation was visual impairment in 39/59 (66%) patients, followed by muscle weakness in 36/59 (61%) and headache in 30/59 (50%) patients. Treatment included intravenous methylprednisolone, oral prednisolone, plasma exchange, rituximab, intravenous immunoglobulins, azathioprine, mycophenolate mofetil, cyclophosphamide, and methotrexate. The present study showed a higher percentage of males tested positive for anti-MOG antibodies. MOG-associated disorders can affect both children and adults. The most frequent clinical presentations of MOGAD in this study were visual impairment, followed by muscle weakness. The primary clinical phenotype identified was isolated transverse myelitis. Myelin oligodendrocyte glycoprotein, Optic neuritis, Myelitis, Acute disseminated encephalomyelitis, Demyelinating disease, Autoimmune disorder.
2025-05-15 | Coronavirus Disease 2019 Infection and Vaccination in Pediatric Demyelinating Diseases.
As compared to adults, less is known about the effects of SARS-CoV-2 infection in children with neuroinflammatory diseases, such as multiple sclerosis (MS), anti-myelin oligodendrocyte glycoprotein associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD). Moreover, the effects of SARS-CoV-2 vaccination on pediatric demyelinating diseases is also lesser known. Here, we examine the effects of SARS-CoV-2 infection and vaccination on children with demyelinating diseases. Retrospective chart review was performed at a single tertiary pediatric center, including 116 children with demyelinating diagnoses (MOGAD, MS, NMOSD, transverse myelitis-TM, and acute disseminated encephalomyelitis). Descriptive statistics and logistic regression were used. The diagnoses included: MS: 56/116 = 48%, MOGAD: 32/116 = 28%, NMOSD: 15/116 = 13%, acute disseminated encephalomyelitis: 12/116 = 10%, and TM: 1/116 = 1%. The known COVID infection rate was 26% = 30/116. Three of 30 (10%) of those with known infection were hospitalized. None of those hospitalized required intubation or ICU admission. Of the 30 with known infection, two (7%) had neuroinflammatory events that occurred within four weeks of infection, both of which were their first clinical events for MS. SARS-CoV-2 vaccination was not associated with any new onset or relapse neuroinflammatory events in our cohort. Demyelinating diagnosis and anti-CD20 mAbs were associated with known SARS-CoV-2 infection. Two participants had an initial clinical MS event associated with infection. However, we found no association with SARS-COV-2 vaccination or infection with relapses and no long-term adverse outcomes with SARS-CoV-2 vaccination or infection. Future larger multicenter studies should prospectively compare how infection and vaccination affects children and adults with demyelinating diseases.
2024-08-23 | [Modern pathogenetic treatment of rare demyelinating diseases].
Rare demyelinating diseases are a group of diseases whose pathogenesis is based on the process of demyelination. This group of diseases includes acute multiple encephalomyelitis (ADEM), opticoneuromyelitis spectrum diseases (NMOSD) and anti-myelin-oligodendrocyte glycoprotein-associated diseases (MOG-antibodies-associated diseases - MOGAD). Recently, new biological drugs for pathogenetic therapy have been developed, which have shown their effectiveness and good tolerability in comparison with therapy with first- and second-line drugs. Aim of the study - analysis of modern possibilities of pathogenetic treatment of patients with ADEM, seronegative and seropositive patients with NMOSD. The analysis was carried out on the basis of English-language publications in PubMed published over the past five years. This review summarizes current ideas about the possibilities of pathogenetic treatment of rare diseases. The advantages of using ravulizumab over other representatives of a new biological therapy associated with the use of monoclonal antibodies are shown. The analyzed data allow us to conclude that there is a significant development of pathogenetic treatment options for ZSONM. However, the effectiveness of new therapeutic biological drugs is still limited due to the lack of a large amount of clinical data to confirm, which creates the need to continue analyzing the experience of their use. Редкие демиелинизирующие заболевания представляют группу заболеваний, в основе патогенеза которых лежит процесс демиелинизации. К данной группе заболеваний относят острый рассеянный энцефаломиелит (ОРЭМ), заболевания спектра оптиконейромиелита (ЗСОНМ) и анти-миелин-олигодендроцитарный гликопротеин-ассоциированные заболевания (МОГАТАЗ). Разрабатываются новые биологические средства патогенетической терапии, которые показали более высокую эффективность и хорошую переносимость по сравнению с препаратами первой и второй линий. В статье представлен анализ современных возможностей патогенетического лечения пациентов с ОРЭМ, серонегативных и серопозитивных пациентов с ЗСОНМ. Проведен анализ англоязычных публикаций из базы PubMed, опубликованных за последние 5 лет. Суммированы современные представления о возможностях патогенетического лечения редких заболеваний. Показаны преимущества использования равулизумаба перед другими представителями новой биологической терапии, связанной с использованием моноклональных антител. Результаты анализа данных литературы позволяют сделать вывод о значительном развитии патогенетических вариантов лечения ЗСОНМ, однако данные об эффективности новых биологических препаратов по-прежнему ограничены из-за отсутствия достаточного количества клинических исследований для ее подтверждения, что диктует необходимость продолжить анализ опыта их использования.
cell therapies
2024-04-12 | An aggressive form of MOGAD treated with aHSCT: A case report.
Although myelin-oligodendrocyte-glycoprotein (MOG)-antibody-associated disease (MOGAD) has been considered a more favorable demyelinating central nervous system disorder, recent data evidence that some patients might experience severe relapses and high disability. Actual treatment-options are acquired mostly from anti-aquaporin-4-antibody-positive neuromyelitis optica spectrum disorder and rely on clinical experience. Therefore, treatment of aggressive forms of MOGAD can be challenging. To describe a patient with an aggressive MOGAD treated with autologous hematopoietic stem cell transplantation (aHSCT). A 56-year-old man was diagnosed with MOGAD in 2017 because of right optic-neuritis and anti-MOG-antibody positivity. In the following 2 years, he experienced two optic neuritis with good recovery after high-dose steroid. At the end of 2019, he presented sensory and motor impairment at lower limbs with evidence of several spinal, longitudinally extended, tumefactive inflammatory lesions. Despite sequential treatment with rituximab and tocilizumab alongside high-dose steroid, intravenous immunoglobulins and plasma-exchange, he experienced several clinical relapses and exhibited persistent magnetic resonance activity. He was finally addressed to intense immunosuppression with myeloablative conditioning regimen followed by autologous hematopoietic stem cell transplantation (aHSCT). After 2 years follow-up, he is free from disease-activity. In a patient affected by aggressive, treatment-refractory MOGAD, aHSCT resulted as safe and was able to suppress disease-activity for over 2 years.
2020-08-20 | Regulatory B Cells and Its Role in Central Nervous System Inflammatory Demyelinating Diseases
Regulatory B (Breg) cells represent a population of suppressor B cells that participate in immunomodulatory processes and inhibition of excessive inflammation. The regulatory function of Breg cells has been demonstrated in mice and human with inflammatory diseases, cancer, after transplantation, and particularly in autoinflammatory disorders. In order to suppress inflammation, Breg cells produce anti-inflammatory mediators, induce death ligand-mediated apoptosis, and regulate many kinds of immune cells such as suppressing the proliferation and differentiation of effector T cell and increasing the number of regulatory T cells. Central nervous system Inflammatory demyelinating diseases (CNS IDDs) are a heterogeneous group of disorders, which occur against the background of an acute or chronic inflammatory process. With the advent of monoclonal antibodies directed against B cells, breakthroughs have been made in the treatment of CNS IDDs. Therefore, the number and function of B cells in IDDs have attracted attention. Meanwhile, increasing studies have confirmed that Breg cells play a role in alleviating autoimmune diseases, and treatment with Breg cells has also been proposed as a new therapeutic direction. In this review, we focus on the understanding of the development and function of Breg cells and on the diversification of Breg cells in CNS IDDs.
oligonucleotides
2024-03-11 | Administration methods and dosage of poly(lactic acid)-glycol intervention to myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalitis mice
Abstract Background Myelin oligodendrocyte glycoprotein-associated disorders (MOGAD) is an autoimmune central nervous system disease. Antigen-specific immune tolerance using nanoparticles such as Polylactic-co-glycolic acid (PLGA) have recently been used as a new therapeutic tolerization approach for CNS autoimmune diseases. We examined whether MOG 1-125 conjugated with PLGA could induce MOG-specific immune tolerance in an experimental autoimmune encephalitis (EAE) mouse model. EAE was induced in sixty C57BL/6 J wild-type mice using MOG 1-125 peptide with complete Freund’s Adjuvant. The mice were divided into 12 groups (n = 5 each) to test the ability of MOG 1-125 conjugated PLGA intervention to mitigate the severity or improve the outcomes from EAE with and without rapamycin compared to antigen alone or PLGA alone. EAE score and serum MOG-IgG titers were compared among the interventions.Kindly check and confirm the processed Affiliation “4” is appropriate.I confirmed the Aff 4.Affiliation: Corresponding author information have been changed to present affiliation. Kindly check and confirm.I checked and confirmed the Corresponding author's information. Results Mice with EAE that were injected intraperitoneally with MOG 1-125 conjugated PLGA + rapamycin complex showed dose-dependent mitigation of EAE score. Intraperitoneal and intravenous administration resulted in similar clinical outcomes, whereas 80% of mice treated with subcutaneous injection had a recurrence of clinical score worsening after approximately 1 week. Although there was no significant difference in EAE scores between unconjugated-PLGA and MOG-conjugated PLGA, serum MOG-IgG tended to decrease in the MOG-conjugated PLGA group compared to controls. Conclusion Intraperitoneal administration of PLGA resulted in dose-dependent and longer-lasting immune tolerance than subcutaneous administration. The induction of immune tolerance using PLGA may represent a future therapeutic option for patients with MOGAD.
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Drug Discovery Landscape
1 orphan drug designation for Acute transverse myelitis with anti-MOG antibodies.
1 orphan drug designation for Acute transverse myelitis with anti-MOG antibodies.
Drug | Therapy type | Orphan designation | Clinical trial status | Sponsor |
|---|---|---|---|---|
satralizumab-mwge | antibodies | FDA | Genentech, Inc. |
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