MGFA funds research projects aimed at understanding MG biology

The Myasthenia Gravis Foundation of America (MGFA) awarded four grants, each valued at $110,000, to research projects aimed at better understanding the biology of myasthenia gravis (MG) and improving its diagnosis and treatment.

“MGFA is helping to fuel a sea change in myasthenia gravis diagnosis and care,” Samantha Masterson, MGFA’s president and CEO, said in an emailed statement to Myasthenia Gravis News. “Through our grant program, we invest in science that deepens our understanding of the mechanisms and impacts of disease, with the goal to make life better for everyone living with this rare disease.”

MG is a rare autoimmune disorder marked by self-reactive antibodies that attack proteins at the neuromuscular junction (where nerve and muscle cells communicate), resulting in MG symptoms such as muscle weakness and fatigue. The most common MG-driving antibodies target either the acetylcholine receptor (AChR) or the muscle-specific kinase (MuSK).

Recommended Reading

March 30, 2026 Columns by Shawna Barnes

Finding a balance between symptom tracking and living life

Understanding antibodies

One of the newly funded projects aims to better understand why some anti-MuSK antibodies block MuSK activity, leading to MG, while others activate it, improving muscle function. Researchers will analyze the structures of different anti-MuSK antibody types in detail to better understand what drives these differences.

Maartje G. Huijbers, PhD, and Dana Vergoossen, PhD, at Leiden University Medical Center in the Netherlands, will lead the work.

“We know MuSK antibodies can either damage or support muscle function, but we’ve never been able to see what makes them different,” Vergoossen and Huijbers said in an email to Myasthenia Gravis News. “By mapping how these antibodies bind MuSK, we can unlock insights that could guide more targeted and effective treatments for [MuSK-related] MG patients.”

Another project, led by Vijay G. Sankaran, MD, PhD, of Boston Children’s Hospital and Harvard Medical School, aims to better understand which and how MG genetic risk factors associate with dysfunction of dendritic cells, a type of immune cell involved in MG.

The ultimate goal is to identify molecular pathways that could inform the development of dendritic cell-focused prevention strategies and treatments. Such therapeutic approaches could help reduce reliance on treatments that lead to generalized suppression of the immune system, which can increase the risk of infections.

“There has been significant progress on defining inherited genetic variants that predispose individuals to developing MG,” Sankaran told Myasthenia Gravis News. “However, we have a limited understanding of how these inherited factors contribute to MG development. “Through this work, we hope to be able to intervene in those at risk of developing MG early and potentially prevent the disease in the future.

Valentina Damato, MD, PhD, associate professor of neurology at the University of Florence and Careggi University Hospital in Florence, Italy, will lead a project aiming to better understand why some people with cancer in the thymus, a well-established risk factor for MG, develop MG but others don’t.

The thymus is a gland involved in immune function, and when MG is associated with thymus cancer, or thymoma, it “is often more aggressive and can be more resistant to standard therapies, making early recognition especially critical,” Damato told Myasthenia Gravis News.

“Our goal is to develop biomarker-based tools that allow clinicians to identify high-risk [thymoma] patients before symptoms appear and tailor follow-up and management accordingly,” Damato said. “In the future, this could enable more personalized surveillance strategies and earlier intervention in patients at highest risk.”

The fourth project, led by Sarah Hoffmann, MD, PhD, associate professor and senior neurologist at Charité – Universitätsmedizin Berlin, aims to develop an atlas of immune activity in people with AChR-related MG. Researchers will specifically look at immune activity in three regions: the thymus, the blood, and the neuromuscular junction.

“Most biomarker research has focused on blood,” Hoffman told Myasthenia Gravis News. “The thymus is a likely site where the autoimmune response is initiated and shaped, and skeletal muscle at the neuromuscular junction is where transmission fails and weakness develops, yet these compartments are rarely studied together in the same patients. Studying the three relevant compartments (thymus, blood, muscle) together with modern technologies is timely and essential if we want a more complete picture of MG biology.”

Hoffmann’s project also aims to compare immune activity in MG patients with anti-AChR antibodies and those who are seronegative (i.e., test negative for these antibodies).

“Even AChR-antibody–positive MG, often considered the prototype, still has important unanswered questions, and these gaps are even larger in seronegative MG,” Hoffmann said. “By linking immune signatures across blood, thymus, and muscle, we hope to identify disease patterns that can be translated into actionable biomarkers. Over time, this could improve diagnosis, enable meaningful patient stratification, and support more targeted, personalized treatment decisions, reducing trial-and-error and shortening the path to the right therapy for people living with MG.”