The study expands on a previously-awarded proposal to thoroughly explore the underlying pathophysiology of post exertional malaise (PEM), the hallmark symptom of ME/CFS.
OMF secured a $1 million grant to launch the first year of an international, multi-year study across the six OMF supported Collaborative Research Centers (CRC). The aim of this study is to examine Long COVID transitioning to ME/CFS.
This study seeks to understand the biological mechanisms driving the symptomatology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) using metabolomic and lipidomic high-throughput analysis and high-frequency blood sampling over a 6.5 to 7.5 hour period conducted at two separate sites (Melbourne and Uppsala).
To investigate the metabolite signatures of ME/CFS patient stool, urine and blood samples and the impact that co-morbidities (IBS and Fibromyalgia) have on these signatures.
This project aims to look at metabolic traps in central carbon metabolism that lead to observed altered energy production pathways in ME/CFS.
This project will develop a software tool to rapidly look for metabolism anomalies in an individual which might be explained by their genes. It will also look for potentially damaging genes in individuals and it will attempt to group ME/CFS patients based on their genetic and metabolic profiles.
This project aims to test the nitrogen hypothesis, which is that damaging, nitrogen-containing by-products of energy metabolism accumulate more readily in the cells of ME/CFS patients.
The overarching goal of RASPBERRY-ME project is the characterization of the biomolecular signature of Myalgic Encephalomyelitis using Label-free Raman Spectroscopy (RS) and machine learning models.
The purpose of this study is to capture a post-COVID-19 infected population willing to participate in phenotyping studies early in the post-COVID-19 illness progression, with an aim of providing targeted effective therapies and preventing the onset and progression of ME/CFS.
The primary goal of this project is to complete our comprehensive analysis of the genome, methylome, miRnome, and their interactions in order to fill the gaps in our understanding of ME/CFS pathophysiology and to identify clinically useful biomarkers.