1) Dr. Vanessa Velasco gave preliminary results on OMF's new neutrophil study.

She found that neutrophils of ME/CFS patients died quicker and more often than those of healthy controls, under inflammatory conditions. 2) Neutrophils are immune cells that form the first line of defence when there is an infection. The researchers were able to isolate the neutrophils from whole blood, without changing them, and then mimic inflammatory conditions in the lab.

1) Impressive study from Johns Hopkins researchers.

They infected mice with SARS-CoV-2, found that female mice had a stronger immune response and more cognitive problems after 84 days than males, and that this was due to over-expression of genes such as Tlr7 on the X chromosome. 2) The study tries to answer the paradox of why males are more likely to be severely ill during infection, while females are more likely to develop Long Covid.

They confirmed this in mice: males had more severe acute illness while females had more lingering cognitive problems.

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.

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.

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.

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.).

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.

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.

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.

1) A new paper by the Scheibenbogen group reports that ME/CFS and Long Covid patients have more antibodies that target proteins with arginine-rich (poly-R) sequences.

Examples are:

- the neuronal antigen SRRM3
- the ion channel SLC24A3
- the TGF-b signalling regulator TSPLY2 2) Some background: in a previous study these researchers found that ME/CFS patients hade more antibody binding to multiple pieces of protein derived from the Epstein-Barr Virus.

This was particularly the case for arginine-rich (poly-R) motifs in the EBNA6 and EBNA4 proteins.

1) The Australian team of Christopher Armstrong wrote a paper on how Metformin might be useful as a treatment for ME/CFS and Long Covid.

They focus on the multiple pathways it impacts such as mTOR signalling. 2) Metformin is mostly known as a drug for type 2 diabetes as it lowers sugar levels in the blood.

In the 1950s, however, it was also used to treat Influenza because of its assumed anti-inflammatory properties.

1) Interesting interview of Prof. Ian Lipkin by David Tuller (@davidtuller1).

They not only talk about Lipkin's recent study showing heightened innate immunity in ME/CFS but also about past and future studies.

A brief summary 🧵 @davidtuller1 2) Lipkin explained that in the 1990s, his team looked at whether Bornavirus might be the cause of ME/CFS. They found no evidence of that, but they did see immune activation (nonspecific polyclonal B-cell activation) in a majority of patients.

1) ME Research UK and the ME Association are funding more research on the electrical abnormalities found in blood cells of ME/CFS patients.

This builds on the work on the nanoneedle by Ron Davis and his team in 2019. 2) Funding goes to Dr Fatima Labeed (United Arab Emirates University), who authored the initial research, and Dr Jacqueline Cliff, who will host the work in her laboratory at Brunel University of London.

1) 🇳🇴 A new Norwegian study reports that ME/CFS patients have different DNA variants of killer cell immunoglobulin-like receptors (KIR) compared to controls.

According to the authors, this points to the involvement of natural killer cells in ME/CFS. 2) Natural Killer (NK) cells are a type of immune cell and have been implicated in ME/CFS for more than 30 years. The most consistent finding is reduced cytotoxicity of NK cells; their ability to destroy other cells.

Here's a recent review about this:
frontiersin.org/journals/immun…

1) A research team from Arizona university used Invasive cardiopulmonary exercise testing (iCPET) in ME/CFS and Long Covid patients.

They found that muscle oxygen diffusion was the most impaired parameter. 2) The authors used O2 pathway analysis, which breaks down oxygen transport into independent parameters. In ME/CFS and Long Covid patients, the problem seems to lie in the DM parameter, which stands for muscle diffusion capacity (moving oxygen from blood to muscle cells).

1) 🇨🇦 In a new ME/CFS study, the research team of Alain Moreau reports that haptoglobin (Hp) might be a potential biomarker of PEM severity and cognitive impairment.

Its main function is to bind free hemoglobin that is released after the breakdown of red blood cells. 2) To trigger post-exertional malaise (PEM), the authors didn't use an exercise test but an inflatable cuff that gives pulsatile compressions to the patient's forearm.

(we have some doubts if this really triggers PEM).

1) 🇦🇺 The Australian research group of Christopher Armstrong just published a review on cerebral blood flow (CBF) in ME/CFS and orthostatic intolerance.

About half of the ME/CFS studies reported a significant CBF decrease. 2) There were a lot more ME/CFS studies that measured CBF than we expected: 26 on ME/CFS alone and 11 in both ME/CFS and OI.

Unfortunately, the sample sizes were quite small.

1) Suppose this isn't a coincidence:

- Olfactomedin 4 (OLFM4) Is a Biomarker for the severity of infectious diseases.

- OLFM4 is also one of the few DecodeME hits for patients with an infectious onset. 2) OLFM4 is expressed in gut epithelial cells and is stored in the granules of neutrophils, the most common type of white blood cells.

These granules are like storage spaces that contain enzymes, and antimicrobial molecules that neutrophils release during infection.

1) Very preliminary data but Dutch researchers report that antibodies of Long Covid patients caused more cultured muscles cells to die. 2) This comes from the research group of Jeroen Den Dunnen, whose preprint showed that transfer of antibodies (IgG) from Long COVID patients induces symptoms in mice.

Similar findings were reported by the group of Iwasaki and a Belgian team from Namur.

1) Interesting presentation by Anouk Slaghekke at the 2025 Berlin conference.

This Dutch team found that small blood vessels of patients with ME/CFS and Long Covid are clocked up with Collagen IV. 2) They zoomed in on the muscle capillaries, the tiny blood vessels that are so small that red blood cells need to move through them one by one.

1) 🩸 New paper by the team of Ronald Davis.

They found that red blood cells from ME/CFS patients are slower and less responsive to low oxygen levels in a lab device that mimics small blood vessels. 2) Previous studies suggested that red blood cells change their shape more easily when oxygen is low. That allows them to move faster through small blood vessels (capillaries) and deliver oxygen where it is needed.