In June of 2021, The MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Project was joined by Dr. John Chen and Dr. Eoin Flanagan from the Mayo Clinic in our first of the MOGCast Series called MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease Diagnosis: Testing and Titers. Dr. Chen and Dr. Flanagan have answered 8 important community questions that we did not have time to ask during the MOGCast. OnInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. behalf of The MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Project and the MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease Community, we would like to thank Dr. Chen and Dr. Flanagan for taking the time to help the community understand the diagnosis of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , how to test and treat the disease, what the titers indicate, and all the research they continue to undertake onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Antibody-Associated Disorder.
You can view to the entire MOGCast here.
Blog Questions
Is there any hope of new treatment in the future?
Our understanding of MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease is growing. Many of our prior treatments were extensions of what we have done for NMOSDA disorder of the central nervous system that primarily affects the nerves of the eye and the spinal cord. Also known as Neuromyelitis Optica (NMO) or Devic’s Disease, but MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease is a different disease. maintenance IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment. may be an effective treatment for MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease . There are likely to be randomized clinical trials for new treatments coming soon.
If someone has MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. Optic NeuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. and they are high myopic, how does that affect the interpretation of the OCTA noninvasive imaging technology used to obtain high resolution cross-sectional images of the retina. The layers within the retina can be differentiated and retinal thickness can be measured to aid in the early detection and diagnosis of retinal diseases and conditions such as damage causd by optic neuritis in MOGAD. and Visual Field Test?
High refractive error, such as high myopia, will not influence visual field tests, but can alter the interpretation of the OCTs. OCTs are color coded as green (normal), yellow (mildly thin), and red (thin) when comparing a patient’s RNFL or GC-IPL thickness against the age-matched control database. However, the database of age-matched controls are from patients without much refractive error. Therefore, if a patient is highly myopic, the numbers do not match up with the age-matched controls (high myopia tends to have thinner RNFL). For this reason, it is helpful to have a baseline OCTA noninvasive imaging technology used to obtain high resolution cross-sectional images of the retina. The layers within the retina can be differentiated and retinal thickness can be measured to aid in the early detection and diagnosis of retinal diseases and conditions such as damage causd by optic neuritis in MOGAD. for an individual patient so changes can be followed over time rather than depending onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. a comparison of the thickness against the age-matched controls.
If you were reaching out to the public for awareness purposes, what age group would you target?
We would need to reach out to all ages because MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease can affect any age. Children and parents of children would also be very important because MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease likely accounts for about a quarter of demyelinatingThe process in which the protective coating of nerve tissue (i.e. myelin) becomes damaged or breaks down, causing nerve impulses to slow or halt that results in neurological problems. disease in children.
After stopping preventiveRefers to a medication or treatment that is administered to prevent future relapses (Also referred to as Preventative or Preventive Treatment). medications and negative for the MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system., how often should patients be retested in the remission phase? Do we ever stop retesting if they stop having attacks?
If a patient becomes seronegative for the MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system., this suggests a lower chance of relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community).. However, patients can still sometimes relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). despite becoming seronegative. We often retest MOG antibodiesA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. once a year, but part of this is for research purposes so we can get a better understanding of the importance of the MOGA type of protein involved in cell adhesion. Present throughout myelin sheaths. antibodiesA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system..
How crucial is identifying if a MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patient needs immunosuppressive treatment and an MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. patient needs immunomodulatory treatment for recovery and disability outcome?
For a patient with MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , we typically start chronic immunotherapy only in patients with relapsing disease. This is because only 50% will relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). and recovery is typically good, especially with early steroid treatment. Therefore, if we were to treat every MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patient with a single attack, we would be over-treating 50% of patients because they may not relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). even without treatment. For MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve., most patients need immunomodulatory treatment because patients can accumulate disability with relapsing-remitting disease and can progress to a secondary progressive phase.
For those who are steroid dependent and cannot get below a low dose without having an attack, is there a plan to allow them to transition off the steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency)? Is this answer different for children vs. adults?
For patients who continue to relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). when tapering the steroidsA type of medication typically given intraveneously or orally. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD) it is used as an immunosuppressant and anti-inflammatory to reduce disease activity and inflammation. In adults, it is sometimes used in high doses for acute attacks. In some adult patients, it may be used for 1-2 months after an acute attack to avoid a rapid onset of relapse. Higher doses (>10mg/day) are not recommended for an extended period of time but lower doses (<=10mg/day) may be used in some patients longer term. In children, it may be used after treatment of an acute attack, but it is not recommended long-term due to the profound effects of chronic steroids on a child’s health. Use of oral prednisone as a maintenance therapy in relapsing pediatric MOGAD patients is discouraged due to side effects in developing children, and other therapies such as monthly immune globulin are suggested. (To understand relapsing during steroid tapering, see Steroid Dependency), they will usually need chronic immunotherapy. Various medications are offered, including RituximabThe common brand for this drug is Rituxan. A therapeutic drug that suppresses the immune system often prescribed in certain autoimmune conditions. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this medication is used to suppress the immune system to reduce disease activity., AzathioprineBrand names include Imuran and AZT. A therapeutic drug that suppresses the immune system often prescribed in certain autoimmune conditions. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this medication is used to suppress the immune system to reduce disease activity., Mycophenolate, TocilizumabAn immunosuppressive drug that blocks the inflammatory protein IL-6. This may improve symptoms caused by inflammation. The common brand for this drug is Actemra. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this medication is used to suppress the immune system to reduce disease activity. May be given intraveneously or by subcutaneous injection., and maintenance IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment.. For children, we often use IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment. as first line therapy while in adults, we typically start with one of these other medications and reserve maintenance IVIGA human blood donor product made up of immunoglobulins (IgG and IgM antibodies) derived from plasma that can be administered intravenously (IVIG) or subcutaneously (SCIG). For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), it is used as an immunomodulator to reduce disease activity. Sometimes used for acute attacks or as an ongoing preventative treatment. for disease that breaks through some of these other treatments.
What studies have been done with children of MOG-AD? Is “remission” the accurate term if they’ve been testing negative with no relapsesWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). for a few years now?
There have been several large studies onInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. children with MOG-AD. Overall, children are more often monophasicA disease characterized by only one phase or attack. and have a higher tendency to become seronegative. If they become seronegative and have not had relapsesWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). for a few years, they could be called in remission (or be called monophasicA disease characterized by only one phase or attack. disease if there was only a single attack), but it is important to note that a relapseWhen you present to your doctor or hospital with new or worsening central nervous system symptoms. Generally, if your symptoms gradually worsen over 24-48 hours, there is heightened concern of a relapse. (Also referred to as a flare by the myelin oligodendrocyte glycoproten antibody disease (MOGAD) community). can occur many years after having quite a disease.
Thank you for your paper, “Steroid-Sparing Maintenance Immunotherapy for MOG-IgGRefers to the presence of immunoglobulin G (IgG) antibodies in the blood that are specifically targeted against myelin oligodendrocyte glycoprotein (MOG), a protein found in the central nervous system Associated Disorder (found here).” Do you know if there is a prospective randomized controlled study planned/in progress?
There are a couple of pharmaceutical sponsored randomized placebo controlled trials that will be starting in the next 1-2 years. We hope that these will provide proven treatments for MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease and a better understanding of the disease.
Key Takeaways from the MOGCast and Follow-Up Questions
- Live or inactivated cell-based assaysA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
should be used to test for the MOG antibodyA protective protein produced by your immune system that attaches to antigens (foreign substances), such as bacteria and toxins, and removes them from your body. In myelin oligodendrocyte glycoproten antibody disease (MOGAD), the body incorrectly produces an antibody that targets myelin oligodendrocyte glycoprotein, a component of the myelin sheath in the central nervous system. as they are reliable. However, live cell-based assaysA laboratory test used to: • Measure the presence or amount of a specific substance: in a sample, such as blood, urine, or tissue.
• Determine the potency or activity: of a drug or other substance.
• Analyze the purity: of a chemical compound.
• Identify and quantify: biomarkers related to a disease or condition.
tend to have more specificity and sensitivity. - A greater number of 1:1000 was a strong cut off for a patient who has true MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease , whilst majority of the false positives were at the 1:20 – 1:40 titer levels and a few at the 1:100 level. It’s up to the neurologist to put it all together and make sure that everything fits the diagnosis as some countries do not report titer levels but rather a positive or negative result.
- MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patients require immunosuppressive treatment after the second attack and not the first with the exception of those who have had a severe episode and poor recovery with the first attack.
- Due to MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease being a relatively new disease, the duration of treatment is not yet understood. Patients are being weaned off treatment after the 1-2 year mark unless they have poor outcomes and/or severe disability.
- B-cell depleting therapies such as RituximabThe common brand for this drug is Rituxan. A therapeutic drug that suppresses the immune system often prescribed in certain autoimmune conditions. For myelin oligodendrocyte glycoprotein antibody disease (MOGAD), this medication is used to suppress the immune system to reduce disease activity. and Ocrelizumab are used for MOG-like MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. presentations, particularly when it’s difficult for the neurologist to diagnose.
- Patients with a negative MRIA noninvasive imaging technique that uses strong magnetic fields to produce images of nearly any structure of the body. For MOGAD, it is typically used with and without contrast to identify disease activity in the central nervous system. should still be treated if their symptoms match the clinical picture and this can sometimes happen especially with optic neuritisInflammation of the optic nerve that may be classified as unilateral (affecting one eye) or bilateral (affecting both eyes) that may result in vision changes, vision loss, and/or pain with eye movement. as it remains a clinical diagnosis.
- MSAn autoimmune disease that attacks healthy cells in the myelin, the protective sheath that surrounds nerves in the central nervous system (CNS) leading to neurological symptoms originating from the brain, spinal cord, and/or optic nerve. patients require immunomodulatory therapy and MOG-ADOften referred to as MOGAD, Anti-MOG, MOG Ab+, MOG Antibody Disease, MOG Associated Antibody Disease, MOG positive disease patients need immunosuppressive therapy so a correct diagnosis is very crucial, especially in regards to moving forward with the right treatment plan.
