OMF StudyME Registry: Empowering Research Through Global Participation
The OMF StudyME Registry has reached a pivotal achievement in our mission to empower medical research by having over 8,300 participants sign up since its launch in 2023.
OMF StudyME is a participant registry for researchers to connect with people who want to participate in research studies of ME/CFS, Long COVID, and related post-infection illnesses. Learn here more about OMF StudyME
OMF StudyME Highlights
Cleverest Idea: The potential of OMF StudyME has been recognized by Cort Johnson at HealthRising, who highlighted our registry as the ‘Cleverest Idea’ for its ingenious solution to a complex challenge.
Proven Track Record: We are helping to recruit participants for research studies at prestigious institutions such as Stanford, Harvard, Scripps, Mt.Sinai, and universities in Australia.
Easy Sign-up, Lasting Impact: Joining OMF StudyME is a simple, five-minute process that can have a profound and enduring impact on medical research. Participation is open to individuals worldwide.
New Publication from Christopher Armstrong, PhD & Colleagues
We are excited to share the publication of a groundbreaking study conducted by the OMF Supported Melbourne ME/CFS Collaboration, led by Christopher Armstrong, Ph.D. The study titled “In vitro B cell experiments explore the role of CD24, CD38 and energy metabolism in ME/CFS” offers valuable insights into the pathophysiology of ME/CFS.
Research Summary from Dr. Armstrong
In this paper, we explored how the behavior of B cells (a type of immune cell in the blood) differs between individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and healthy controls. Previous research had shown that B cells from ME/CFS patients had higher levels of a protein on the cell surface called CD24. We wanted to understand the connection between CD24, B cell energy metabolism, and mitochondrial mass.
We conducted experiments using purified B cells from both ME/CFS patients and healthy controls, stimulating the cells in a lab setting to observe changes. Each set of experiments on one patient’s cells took a week. It was quite intensive. This is why the population number is small, and we would call this a “preliminary” or “pilot study.”
Even with a small sample size, the detailed characterization of the B cells was able to identify a few interesting details.
- B cells from ME/CFS patients exhibited lower mitochondrial mass.
- ME/CFS B cells took longer to lose CD24 protein from the surface when stimulated compared to those from healthy controls.
- CD38 protein was found to be significantly increased in frequency and expression on ME/CFS B cells. CD38 protein is well known in the aging world as it dictates the reduction of NAD+, a critical molecule for mitochondrial energy production.
- Metabolomic analysis showed that ME/CFS B cells consumed more essential amino acids during proliferation, suggesting an increased need for these substrates to support cell growth and survival. This aligns with previous findings of reduced amino acids in biological fluids from ME/CFS patients.
Overall, this study provides a detailed characterization of B cell behavior in ME/CFS, highlighting abnormalities in CD24 and CD38 expression, mitochondrial mass, and metabolic pathways.
The findings suggest disruptions in normal energy production pathways in ME/CFS patients, emphasizing the need for further research with larger sample sizes to validate these results and explore potential therapeutic implications.
To learn more about OMF supported publications and research, click here.
Submitted by Karolina Kutilek
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