We’re excited to share a new publication from OMF’s Collaborative Center at Montreal titled: “SMPDL3B a novel biomarker and therapeutic target in myalgic encephalomyelitis.”
The Heart of the Matter
- The team at OMF’s Collaborative Center at Montreal published a paper that talks about their study of a molecule called SMPDL3B, which works differently in some people with ME/CFS than healthy controls.
- In healthy people, SMPDL3B helps control the immune system while sitting on the surface of a cell. In people with ME/CFS, another molecule pulls it off the cell so it is floating in the blood and can no longer help control the immune system.
- As part of this study, the team looked at a group of drugs that can help SMPDL3B stay on the surface of the cell. So far, this has only been done in petri dish experiments, but the hope is that clinical testing of these drugs would reduce ME/CFS symptom burden.
- This paper is part of a larger project called MEDUSA, which will remain in the “Data Analysis” stage of the research process while the team is working to identify multiple therapeutic targets for precision medicine approaches to treating ME/CFS.
SMPDL3B a novel biomarker and therapeutic target
in myalgic encephalomyelitis
OMF’s Collaborative Center at Montreal, directed by Dr. Alain Moreau, recently published a paper on their study looking at sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B) as a biomarker and potential therapeutic target in a subset of people with ME/CFS. This study initially evaluated 249 people with ME/CFS and 63 controls, quantifying both membrane-bound and plasma SMPDL3B levels.
SMPDL3B, when it’s bound to the cell membrane, regulates immune signaling through toll-like receptor 3 and 4 modulation. In people with ME/CFS, SMPDL3B is cleaved from the membrane via PI-PLC, which leads to elevated plasma levels of the molecule and immune dysregulation. In this study, the team found that elevated plasma SMPDL3B correlates to symptom severity and that females show higher levels of it than males—a result that is influenced by estrogen.
Initial in vitro (think petri dish) experiments show that drugs inhibiting PI-PLC can restore membrane-bound levels of SMPDL3B. Therefore, SMPDL3B may be a good therapeutic target for people with ME/CFS. These drugs need to be tested in clinical studies to understand if they translate to reduced symptom burden.
Disclaimer: these are preliminary results only and should not be considered medical advice. Clinical studies are needed to understand these drugs’ therapeutic potential.
Read the full publication in the Journal of Translational Medicine.
This paper is part of a larger project: ME/CFS Adaptive Therapeutic Solution Platform (MEDUSA). Phase 1 of the MEDUSA project—identifying promising treatment targets for specific subgroups of people with ME/CFS—is in the “Data Analysis” stage of the research process.
As phase 1 of MEDUSA involves identifying multiple potential therapeutic targets (of which SMPDL3B is one), it will stay in this stage of the research process until all of the planned advanced analysis is done and the project moves on to phase 2.
