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The MOG Project Joins Global Genes Rare Foundation Alliance

Announcing our partnership with Global Genes as a member of their Rare Foundation Alliance!

We are now part of a network of over 700 RARE Foundation Alliance members which are committed to collaborating in order to create a stronger collective voice in the rare disease community. Through their resources and the sharing of other alliance member resources as well as our own, participation in Rare Foundation Alliance events and taking advantage of the ability to collaborate with other members, there is no limit to what we can do for this MOG-AD Community!

 

For more information on the Global Genes Rare Foundation Alliance, visit the Global Genes Rare Patient Alliance website.

Massachusetts General Hospital
Harvard University

Michael Levy, MD, PhD

Dr. Levy is an Associate Professor in Neurology who was recently recruited to lead the new Neuroimmunology Division at the Massachusetts General Hospital. His mission is to build a combined clinical and research neuroimmunology program to develop therapies for patients with autoimmune diseases of the central nervous system. Dr. Levy moved from Baltimore, MD, where he was one of the faculty at Johns Hopkins University since 2009 and Director of the Neuromyelitis Optica Clinic.

Clinically, Dr. Levy specializes in taking care of children and adults with rare neuroimmunological diseases including neuromyelitis optica, transverse myelitis, MOG antibody disease and acute disseminated encephalomyelitis. In addition to four monthly clinics, Dr. Levy is the principal investigator on several clinical studies and drug trials for these conditions.

In the laboratory, Dr. Levy’s research focuses on four main areas:
1. Development of animal models of neuromyelitis optica (NMO) with the goal of tolerization as a sustainable long term treatment: His team generated a mouse model of NMO based on pathogenic T cells reactive against the aquaporin-4 water channel. Now, they are using this mouse model to create a tolerization therapy to desensitize the immune response to aquaporin-4.
2. Genetic basis of transverse myelitis: His team discovered a genetic mutation in VPS37a found in a group of patients with a familial form of transverse myelitis (TM). To understand how this gene is involved in this immune process, they generated a mouse model with this mutation.
3. The immunopathogenesis of MOG antibody disease: This may depend on a subset of T cells called gamma/delta T cells. These specialize T cells react to MOG in mouse models and attack the central nervous system. In addition to understanding why and how these T cells are involved in MOG antibody disease, they are developing a treatment to target these cells.
4. Biomarker assays for other autoimmune diseases of the central nervous system: They are developing assays that detect autoreactive T cells in NMO and MOG antibody disease. In parallel, they are screening for novel antibodies to glial cells in related disorders such as encephalitis and optic neuritis.