Myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOGAD) is a neurological, immune-mediated disorder targeting MOG protein, located on the outermost myelin sheaths in the central nervous system. The diagnosis is confirmed when serum MOG antibody is found in patients in the context of inflammatory attacks of the central nervous system, usually with the brain, brainstem, optic nerve, and spinal cord. Although MOGAD manifestations can fulfill diagnostic criteria for Neuromyelitis optica disorder (NMOSD), evidence suggests that they have distinct immunological mechanisms. Similar to NMOSD, patients with persistent MOG antibodies are at risk for recurrent events. Recovery of MOGAD is generally reasonable. However, some patients get disability after a severe acute attack. Treatment for an acute attack is typically intravenous high-dose steroids, plasma exchange (PLEX), or intravenous immunoglobulin (IVIG). Maintenance therapy with immunosuppressants, i.e., azathioprine, mycophenolate, rituximab, etc., usually prevents future attacks, although they have long-term side effects. Therefore, it is still controversial how long treatment should be continued.
Previously MOGAD has been thought to be a subset of NMOSD. Indeed, about a third of patients fulfilling the diagnosis for AQP-4 seronegative NMOSD reveal the presence of MOG antibodies. Furthermore, studies have indicated that about half of the children diagnosed with ADEM are positive for the anti-MOG antibody. Although clinical presentations mimic those with NMOSD, studies show differences in demographic data, treatment response, and prognosis. While the neuroimmunological mechanism of MOGAD is not yet well understood, recent pathological findings tend to distinguish the two diseases as two distinct diagnostical entities.
Our goal is to help identify MOGAD from other demyelinating disorders and alert physicians of problematic issues in MOGAD.
In this research topic, we aim to provide up-to-date information on MOGAD regarding demographic data, neuroimmunological mechanism, clinical manifestations, diagnostic dilemma, and management of
MOGAD.
Thus, topic editors will welcome any types of manuscripts supported by the Journal – comprised of the research article, brief research article, review, and mini-review – pertaining, but not limited to the following themes:
• Epidemiology and genetic association of MOG Antibody-Associated Disorders (MOGAD)
• Pathology of MOGAD
• Neuroimmunology of MOGAD. Is it another entity from NMOSD?
• MOGAD associated myelitis
• MOGAD associated visual disturbance
• Age-Related Clinical Differences in MOGAD
• How to diagnose MOGAD?
• Serum and Cerebrospinal Fluid Biomarkers in MOGAD
• Optical Coherence Tomography (OCT) and Optical Coherence Tomography Angiography (OCTA) in MOGAD. What differs from other demyelinating diseases
• Neuroimaging findings in MOGAD–MRI
• MOG Antibody Disease (MOGAD) Prognosis & Management
We acknowledge the funding of the manuscripts published in this Research Topic by The Sumaira Foundation. We hereby state publicly that The Sumaira Foundation has had no editorial input in articles included in this Research Topic, thus ensuring that all aspects of this Research Topic are evaluated objectively, unbiased by any specific policy or opinion of The Sumaira Foundation.
Myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOGAD) is a neurological, immune-mediated disorder targeting MOG protein, located on the outermost myelin sheaths in the central nervous system. The diagnosis is confirmed when serum MOG antibody is found in patients in the context of inflammatory attacks of the central nervous system, usually with the brain, brainstem, optic nerve, and spinal cord. Although MOGAD manifestations can fulfill diagnostic criteria for Neuromyelitis optica disorder (NMOSD), evidence suggests that they have distinct immunological mechanisms. Similar to NMOSD, patients with persistent MOG antibodies are at risk for recurrent events. Recovery of MOGAD is generally reasonable. However, some patients get disability after a severe acute attack. Treatment for an acute attack is typically intravenous high-dose steroids, plasma exchange (PLEX), or intravenous immunoglobulin (IVIG). Maintenance therapy with immunosuppressants, i.e., azathioprine, mycophenolate, rituximab, etc., usually prevents future attacks, although they have long-term side effects. Therefore, it is still controversial how long treatment should be continued.
Previously MOGAD has been thought to be a subset of NMOSD. Indeed, about a third of patients fulfilling the diagnosis for AQP-4 seronegative NMOSD reveal the presence of MOG antibodies. Furthermore, studies have indicated that about half of the children diagnosed with ADEM are positive for the anti-MOG antibody. Although clinical presentations mimic those with NMOSD, studies show differences in demographic data, treatment response, and prognosis. While the neuroimmunological mechanism of MOGAD is not yet well understood, recent pathological findings tend to distinguish the two diseases as two distinct diagnostical entities.
Our goal is to help identify MOGAD from other demyelinating disorders and alert physicians of problematic issues in MOGAD.
In this research topic, we aim to provide up-to-date information on MOGAD regarding demographic data, neuroimmunological mechanism, clinical manifestations, diagnostic dilemma, and management of
MOGAD.
Thus, topic editors will welcome any types of manuscripts supported by the Journal – comprised of the research article, brief research article, review, and mini-review – pertaining, but not limited to the following themes:
• Epidemiology and genetic association of MOG Antibody-Associated Disorders (MOGAD)
• Pathology of MOGAD
• Neuroimmunology of MOGAD. Is it another entity from NMOSD?
• MOGAD associated myelitis
• MOGAD associated visual disturbance
• Age-Related Clinical Differences in MOGAD
• How to diagnose MOGAD?
• Serum and Cerebrospinal Fluid Biomarkers in MOGAD
• Optical Coherence Tomography (OCT) and Optical Coherence Tomography Angiography (OCTA) in MOGAD. What differs from other demyelinating diseases
• Neuroimaging findings in MOGAD–MRI
• MOG Antibody Disease (MOGAD) Prognosis & Management
We acknowledge the funding of the manuscripts published in this Research Topic by The Sumaira Foundation. We hereby state publicly that The Sumaira Foundation has had no editorial input in articles included in this Research Topic, thus ensuring that all aspects of this Research Topic are evaluated objectively, unbiased by any specific policy or opinion of The Sumaira Foundation.
