Expanding Research: Building on Your Investment
On Oct. 5, 2010, three of the six research teams funded by the CFIDS Association shared preliminary data from their projects, as well as other outcomes of Association support via our 15th webinar of the 2010 Webinar Series. Participants were excited to hear about data sharing that’s “connecting the dots,” new funding awards and clues to targeted treatment. You can watch the webinar recording and view the slides. We’ve also recapped some of what they discussed here.
Gordon Broderick, PhD
Associate Professor, Division of Pulmonary Medicine
Department of Medicine
University of Alberta
Kathleen Light, PhD and Alan Light, PhD
Research Professor, Department of Anesthesiology
University of Utah Health Services Center
Dikoma Shungu, PhD
Physics Professor & Research Scientist, Weill Medical College
Moderated by Suzanne Vernon, PhD
Scientific Director, The CFIDS Association of America
When the CFIDS Association of America launched the Campaign to Accelerate CFS Research, a year-long, $1-million initiative to expand its research program in 2008, a committee of board members and other scientific experts recommended five distinct and specific evaluation criteria for proposals received from researchers. Among those five criteria was this question: "How likely is it that the proposed research will be fostered and will succeed in securing greater funding from larger funding sources (like NIH)?"
This important question underscores how the Association views its research program: the grants we make, made possible through your generous gifts, are investments in the future of CFS science. We don't expect your bucks to stop here – we expect them to grow and spread throughout the research community until, one day, CFS is widely understood, diagnosable, curable and preventable. And the six projects selected for Association are already demonstrating success.
"We had previously shown in a small sample that following 25 minutes of moderate exercise, patients with CFS have increases in expression of several genes beginning as soon as 30 minutes later and lasting for 48 hours that correlate with worsening fatigue and pain," says the University of Utah Health Services Center's Dr. Kathleen Light. "The goal of our study was to test 30 additional patients with CFS (including those who did and did not meet diagnostic criteria for fibromyalgia as well) and 30 healthy controls, to reconfirm our original findings and to see if our post-exercise gene expression markers can differentiate CFS patients with and without fibromyalgia pain. Our original findings were reconfirmed with support from a major pharmaceutical company, we will extend this research to see if treatment with an FDA-approved pain medication helps to normalize these abnormal gene expression patterns in CFS patients who also have fibromyalgia. We are also seeking support from NIH to verify that CFS patients can be differentiated from patients with clinical depression using this same post-exercise gene expression profile."
Gordon Broderick, PhD, of the University of Alberta, directed a cross-disciplinary team from four institutions to study adolescents who became ill with CFS after contracting infectious mononucleosis. Using a very specific and well-defined group of patients, he investigated the immune and endocrine responses of the study subjects from initial infection through the first 24 months of illness. Put very simply, their immune cells were not "communicating" the way that healthy people's cells do. Dr. Broderick parlayed these results into three additional grants awards, totaling more than $4.5 million, from the National Institutes of Health and the Department of Defense. He and colleagues will focus on the neuroendocrine and immune systems, using molecular profiling and examining the systems' dynamics to explore ways to "re-set" them to normal functioning.
Cornell University's Dr. Dikoma Shungu extended his initial Association funding into an additional grant to expand his research into brain lactate levels. He explains, "Following our first CFIDS Association-sponsored brain imaging study that found significant elevations of ventricular cerebrospinal fluid (CSF) lactate in CFS compared to matched patients with anxiety disorder and to healthy control subjects, we received additional support from the Association to try to understand the cause(s) of this increase of CSF lactate in CFS. Our overall hypothesis is that the increased lactate is the result of a secondary brain energy production problem due to mitochondrial dysfunction that arises from accumulation of toxic chemicals known as free radicals. Increased levels of free radicals lead to a condition known as oxidative stress that can damage the mitochondria, leading to a brain energy production problem and associated increases of CSF lactate." He continues, "A decrease in brain blood flow can also lead to increased lactate. To test this overall model, we're using a number of advanced brain imaging methods to replicate our finding of increased lactate in new CFS patients, document decreased brain energy production to establish mitochondrial dysfunction, measure brain blood flow and document the presence of increased oxidative stress. If successfully completed, this research could significantly advance our understanding of some of the causes of CFS."
All three teams of researchers reported on publications added to the peer-reviewed literature and presentations made at professional meetings around the world that have helped raise awareness and deepen understanding of CFS among their scientific colleagues. We look forward to bringing you more exciting news about the discoveries made possible by your support of the CFIDS Association and its research program.
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