“ME/CFS In a Petri Dish”
PI: Assistant Professor Malav Trivedi, PhD
Nova Southeastern University
Dr. Malav Trivedi will lead a study on the use of reprogrammed neurons in ME/CFS. Generated neurons have the potential to not only further our understanding the pathobiology (neuro-metabolic and molecular changes) of ME/CFS, but can also be utilized for targeted drug discovery. The use of this methodology is novel to the field of ME/CFS. The project is in collaboration with Geeta Ravindran, PhD, who has deep knowledge of stem cell research and previously worked to develop neuronal stem cells and transform them into neuronal cell lines at Karolinska Institutet in Sweden.
Major Ramsay goals fulfilled:
✓ Keeping researchers engaged in the field. Dr. Trivedi is co-Investigator on Dr. Lubov Nathanson’s Ramsay 2017 project to characterize the role of epigenetics in ME/CFS and he is now leading his own Ramsay study.
“I am thrilled to deepen my engagement in the ME/CFS field after working as a co-Investigator on Lubov Nathanson’s 2017 Ramsay-supported project on epigenetic regulation in immune cells. With this Ramsay funding, I will be leading my own pilot project that will explore the use of reprogrammed neurons in ME/CFS – a methodology new to the field. During my research career, I’ve had the opportunity to gain expansive experience in different areas of stem cell research. I look forward to applying my knowledge and advancing this research on behalf of people with ME/CFS.”
Read the research team’s study abstract below:
Statistical studies estimate the prevalence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) at 0.23 to 0.41 percent of the general population and it costs up to $24 billion in health care expenditures to United States economy In recent years, researchers have provided some insight into the underlying mechanisms of ME/CFS disease activity, including disease onset and progression. However, there has been limited convergence on biomarkers to provide improvements in diagnosis and/or management.
Current brain imaging studies point towards deleterious neuroinflammation in ME/CFS patients, along with decreased antioxidant levels and a shift towards anaerobic metabolism with elevated lactate levels. However, there is no mechanistic explanation or any underlying molecular pathobiology for such metabolic dysfunction. Separately, neuroanatomy investigations report reductions in gray and white matter in ME/CFS patients, yet there is no specific cell death mechanism identified. However, to test any neuronal hypothesis, we need to characterize CNS of ME/CFS patients; but there is a lack of available post mortem brain tissue of ME/CFS patients, and imaging technologies do not identify molecular changes at cellular level.
To address such gaps for undertaking mechanistic neuronal studies in ME/CFS; (i) we will establish reprogrammed neurons of ME/CFS patients and matched healthy controls (HCs) and (ii) measure any morphological and structural changes in the neurons from ME/CFS patients as compared to HCs.
Reprogrammed neuronal and iPSC models have already supported novel therapeutic development in several neurological and neuropsychiatric diseases, and provides a patient specific tool. This will significantly empower researchers, advance the ME/CFS field in the long-term and benefit patients. It will establish a resource for high through put screening of drugs as well as support future studies to understand neurological issues in ME/CFS by providing a “Disease in a dish model for ME/CFS”