1) The most interesting presentation during the 2025 Stanford symposium was on PET scans of the entire body.
Dr. Michelle James explained that they found a striking pattern with more TSPO signal in various muscle groups of ME/CFS patients, such as the thigh and shoulders.
2) PET scans work by injecting a radioactive molecule into the veins. The scan records annihilation events where a positron leaves the cell and collides with an electron, creating two photons. That signal tells us where in the body the radioactive molecule is binding.
3) Ideally, you want a radioactive tracer that is highly specific to a certain cell type or process so that you know exactly what the signal means.
In this ME/CFS study, they used the popular TSPO tracer, which binds to microglia, astrocytes, myeloid cells, etc.
4) In particular, they used the molecule [11C]DPA-713. It’s used as a marker of inflammation but also signals mitochondrial function and cellular bioenergetics. It has a half-life of only 20 minutes (meaning the signal is gone after around 3 hours).
5) Participants in the study had a 60-minute brain PET scan, followed by a 20-30 min whole body scan.
ME/CFS patients had significantly more signal in muscle groups such as the upper and lower thigh and the glute minimus (see results in screenshot below).
6) There was also a notable pattern around the shoulders which looked like coathanger syndrome. The signals correlated with measures of fatigue (MFI) or pain (BPI).
7) Dr. James said they are working on more specific tracers that target GPR84 and TREM1 on pro-inflammatory myeloid cells. These could be used in ME/CFS studies in the near future and may provide further insights.
8 ) The full presentation by Dr. Michelle James about the PET-scan study can be viewed here:
• • •
Missing some Tweet in this thread? You can try to
force a refresh
1) We’ve just published our second instalment on the DecodeME results, this timing zooming in on the genes associated with ME/CFS.
2) In our view, the clearest signals point to genes such as CA10, SHISA6, SOX6, LRRC7, and DCC, which are involved in neuronal development and communication in the brain.
3) There are also gene candidates that implicate the immune system such as OLFM4, RABGAP1L, BTN2A2, and TAOK3. These point to e.g. the innate immune system and regulation of T-cells.
Unfortunately, they lie in regions stacked with genes and are therefore more uncertain.
1) We’ve written an article about the DecodeME results: what the study measured, what the results show, and why its findings are important.
2) DecodeME is by far the biggest study on ME/CFS ever done. It may not have caused a big breakthrough, but it adds an important piece to understanding the puzzle of ME/CFS.
3) We therefore think it’s worth digging deeper into the DecodeME summary data (which is publicly available) to understand what it means for ME/CFS research.
Our blog tries to explain the methodology in simple terms so that readers with no genetic background can follow along.
1) This lecture by Prof dr Vivienne Matthies-Boon is a good introduction to the problems with the biopsychosocial (BPS) model and the harms it has caused in the ME/CFS community.
2) In brief: BPS proponents think there is no objectionable pathology in ME/CFS, so they see the disorder as mainly caused by the belief one is ill and the inappropriate resting behavior that follows (sleeping too much, exercising too little, focusing on symptoms, etc.).
3) Everything that reinforces this belief that one is ill, is therefore bad: biomedical research, disability payments, patient organisations, care from family members: these can all be seen as perpetuating factors according to the model.
1) During his presentation at the 2025 Fatigatio conference, Prof. Bhupesh Prusty argued that physiologically, ME/CFS patients look similar to healthy individuals until they are put under stress.
2) He thinks there is something in ME/CFS patients that keeps the sickness response alive. And to study the illness and make it visible, one has to put the cells under different types of stress.
3 ) His group is working on a technique called 'Single-Cell SLAM-seq' that will be able to do this in a fast and efficient way (The screenshot below provides an overview).
1) Prof. Carmen Scheibenbogen's talk at the 2025 Fatigatio conference was mostly about off-label therapies in Germany.
But at the end she also talked about new treatment trials they have planned to pursue the hypothesis that ME/CFS is caused by antibodies.
2) She claimed that immunoadsorption led to an improvement in about 75% of treated ME/CFS patients but that this improvement is unfortunately not sustained. It's not a curative treatment.
Therefore, they are looking at a more targeted treatment.
3) They initially focused on patients with elevated β2 adrenergic autoantibodies but now have a clearer profile of subgroups using modern omics that allow them to test 50 different markers on B-cells.
Different Immune cell signatures had different treatment responses.
1) A new genome-wide association meta-analysis of hEDS found two significant hits:
- one on chromosome 2 that points to the gene ACKR3
- one on chromosome 8 that is less clear but might point to the gene KCNV1.
2) This study had much less participants than DecodeME: only 1815 cases and 5008 controls that came from 3 different cohorts and were added together using a meta-analysis approach.
3) The fact that they found significant hits with such a low sample, indicates that these were much larger effects than seen in DecodeME. Indeed the odds ratios were 1.29 (for chr. 2) and 1.66 (for chr. 6).