Montreal researchers say they’ve made a breakthrough discovery in understanding a poorly understood illness – chronic fatigue syndrome – which has significant ties to post-COVID symptoms.
Université de Montréal professor Dr. Alain Moreau and his team believe they have made a breakthrough by identifying a therapeutic target and potential new biomarker; which is a way of understanding what is happening in a cell for Myalgic encephalomyelitis (ME) – also known as chronic fatigue syndrome – which is linked to long COVID.
“There’s suddenly over 100,000 Quebecers with ME now and this is a very conservative assessment,” said Dr. Moreau. “This is the hope that I want to share with Montrealers, that we are advancing much faster than maybe the last decade.”
Dr. Moreau explained that ME is a very complex disorder impacting thousands in Quebec and the causes are still unknown, saying it can impact a person’s nervous, muscular and immune system.
“The hallmark symptoms is what we call post-exertional malaise (PEM), which means that any minimum physical activity or even a cognitive mental activity minimum will further amplify your symptoms for hours, days and sometimes even weeks,” said Dr. Moreau.
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The research team utilized and investigated the role of a protein called SMPDL3B as a therapeutic target.
“We have also have a paper in preparation that we address also SMPDL3B the attribute issues in long COVID,” said Dr. Moreau. “And I can tell you that we have the same issues. Especially those having long COVID with ME symptoms. We have more or less the same story. I want to make sure that everyone understands that SMPDL3B attribute is not a magic bullet. It’s not a single protein that if we target the protein, we will resolve all these symptoms and issues with ME.”
Dr. Moreau clarifies that they cannot say at this stage that SMPDL3B is the main therapeutic target underlying ME pathophysiology. He explaines that though it is an important one, given the complexity and clinical heterogeneity of ME, it is most likely that other targets/mechanisms are involved.
The study noted that people with ME have higher levels of the soluble form of the protein SMPDL3B in their plasma – meaning the higher the levels, the more severe their symptoms become.
Dr. Moreau says these high levels could be caused by the PI-PLC, which detaches the protein from the cell membrane. He adds that there are known diabetes drugs that inhibit PI-PLC activity.
“When we start to treat the cell, we saw a diminution of the cell reforming and increase of the membrane bound,” said Dr. Moreau. “And this is exactly what we wish for the patients to increase the membrane bound to have to be more effective in the way that the cells now can defend themselves and us against the virus.”
“PI-PLC activity and its higher levels in ME are the main drivers leading to the production of soluble SMPDL3B through the shedding (proteolytic cleavage) of membrane-bound SMPDL3B. Therefore, the pharmacological inhibition of PI-PLC by Saxagliptin or Vildagliptin represents new therapeutic options to treat a subset of ME patients.”
The team is hopeful their study provides a clear pathway for the pharmaceutical industry to seek interest in this but that could still be years away.
“We hope that this paper will not only generate more hope for the patients and physicians, but also will attract attention on venture capital or pharma industry players that would like to team up with us to load the very first randomized clinical trial, especially Quebec.”
