Today, we’re excited to share an interview with Dr. Jonas Bergquist and Dr. Alain Moreau. In this discussion, both OMF Directors draw connections between their research and share their main ideas about ME/CFS.
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An Interview with Jonas Bergquist, MD, PhD, and Alain Moreau, PhD: From Genes to Proteins to Neuroinflammation
The Heart of the Matter
In an interview with Dr. Jonas Bergquist and Dr. Alain Moreau, two of OMF’s Directors, they talk about their main ideas behind ME/CFS, including an immune system that is too active in the brain and spinal cord, inherited factors, and how genes are expressed.
They then discuss connections between their research:
- Moreau’s work found that a protein called SMPDL3B is different in people with ME/CFS. That protein can change cell membrane fluidity and influence a signaling pathway. These changes help contribute to the inflammation markers that Dr. Bergquist has found.
- Dr. Bergquist measures the activity of a type of immune cell called microglia to identify inflammation in the nervous system. Microglia activity can be influenced by the protein haptoglobin and the hormone FGF-21. Dr. Moreau has found that these two molecules play a role in ME/CFS.
An Interview with Jonas Bergquist, MD, PhD, and Alain Moreau, PhD: From Genes to Proteins to Neuroinflammation
Dr. Jonas Bergquist, the Director of OMF’s Collaborative Center at Uppsala, brings expertise in the nervous system, brain, and cognitive dysfunction to his research on ME/CFS. In this interview, he describes his overarching hypothesis of ME/CFS as an over-active immune system in the central nervous system (CNS)—normally a site where you don’t expect to have dramatic inflammation or immune activity—that leads to degradation of cellular function, loss of energy and ability to restore energy and autoimmune reactions.
Dr. Alain Moreau, the Director of OMF’s Collaborative Center at Montreal, brings expertise in precision medicine and molecular genetics of complex diseases to his research on ME/CFS. In this interview, he acknowledges a genetic predisposition for ME/CFS and highlights the importance of the epigenome, as well as bringing together multi-omics to understand all those changes and what they mean for the disease as a whole.
In drawing connections between their research, Drs. Bergquist and Moreau talked about a couple areas:
- SMPDL3B and neuroinflammation: SMPDL3B is a protein that can influence sphingolipid metabolism and toll-like receptor (TLR) signaling. Sphingolipids are structural components of cell membranes, so when SMPDL3B is cleaved from the cell membrane—like it is in ME/CFS—it makes the cell membrane more fluid and incites inflammation. In addition, dysregulated TLR signaling yields more inflammation signals. These findings match Dr. Bergquist’s results in cerebrospinal fluid and the peripheral nervous system, which include markers for low-grade inflammation.
- Haptoglobin, FGF-21 and microglia: Trauma to the brain (e.g., infection) activates microglia, letting them migrate around the CNS, work as an immune cell, and attract peripheral immune cells to the CNS. Haptoglobin and FGF-21 both play a role in that process since they can modulate microglia. Dr. Moreau’s work has shown differences in haptoglobin and FGF-21 in people with ME/CFS, and Dr. Bergquist measures microglia activation with positron emission tomography (PET) and magnetic resonance imaging (MRI) techniques.
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