Researchers often dedicate their lives to solving scientific questions and building foundations for the next generation of researchers.
One such researcher, Dr. Emily Mathey, a Postdoctoral Fellow in Medicine, Central Clinical School, Brain and Mind Center at the University of Sydney, Australia, is this year’s Interlaken Leadership Awards (ILA) winner. The ILA is CSL Behring’s annual global awards program that provides monetary grants and/or product supply for investigational use to support research focusing on the potential role of immunoglobulin (Ig) therapy in the treatment of neurological disorders.
Upon being named the recipient, Dr. Mathey discussed with Vita her motivations, inspirations and how she started on her unique path in support of research to help a very select group of patients.
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What is your specific area of research interest?
I’m interested in immune-mediated disorders of the nervous system, especially the role that autoantibodies play in causing damage to nerves and as biomarkers for treatment response. While working on my PhD and post-doctoral studies, I identified novel autoantibody responses in patients with multiple sclerosis and tested whether these antibodies can cause damage to neurons in models of multiple sclerosis. My research continues to focus on identifying novel autoantibody responses in patients with inflammatory neuropathies.
Who inspired you to choose this particular field of study?
My aunt was diagnosed with multiple sclerosis when I was a teenager. This event sparked my interest in neuroinflammatory diseases. As with many researchers who have a personal connection to the disease that they study, I hope to improve the lives of those affected by the disease by contributing to the understanding of the disease and translating this information into the clinical setting.
How will this research make a difference in the future of treatment?
Finding out how the nerves are damaged in different patients could lead to individualized treatments that target particular disease pathways in these patients. The development of biological markers to predict response to certain therapies, especially if detected early in the clinical course, will lead to better patient outcomes and improve the lives of those affected.
Can you describe your current project? What do you hope to accomplish?
My research will examine the effectiveness of intravenous immunoglobulin (IVIg) therapy in a group of patients identified as having anti-NF155 lgG mediated CIDP.Chronic inflammatory demyelinating polyneuropathy (CIDP) is a paralysing disorder of the peripheral nervous system (PNS) in which the immune system mistakenly attacks the peripheral nerve. During this process the immune system strips the myelin away from the axon leaving it uninsulated and unable to conduct nerve impulses efficiently. We have been studying the immune response in patients with CIDP and have found that the target of the response in some patients is also directed at and around the node of Ranvier. The node of Ranvier is a gap in the myelin covering of the nerve fibre which seems to be particularly vulnerable to autoimmune attack. Over recent years, strong evidence for antibody mediated mechanisms involving autoantibodies targeting nodal and paranodal molecules, such as neurofascin and contactin, and have been shown in about 15% of cases of CIDP and are associated with response to certain treatments. IVIg is the major therapy for CIDP although the pathogenesis in most cases remains uncertain.
We propose to study how human anti-neurofascin antibodies obtained from CIDP patients contribute to nerve dysfunction and examine whether IVIg can inhibit their activity. This study will determine the role of these antibodies in the disease process in some patients.
How will the Interlaken Leadership award help your work?
This award will enable me to do some experiments that are essential for demonstrating how human antibodies react in these CIDP patients to see if IVIg treatment can ameliorate the effects of the antibody in these particular models. I hope that my work on early models will provide better insight into the role of pathogenic autoantibodies in the response rate of IVIg therapy. And ultimately might help determine more effective treatment options for these patients.
