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Sounds interesting. Only a bit worried that the text doesn't mention controls that don't have ME/CFS or Long Covid. If I understand this NULISA technique correctly it requires two matching antibodies to bind to the target protein. One uses a magnetic bead, the other a DNA tag. The antibodies...

There are newer models like FLAMES that likely give slightly better predictions to which DecodeME genes are involved to ME/CFS. I suspect this is something that could be solved with AI and machine learning in the near future, similar to what AlphaFold did for protein folding.

No problem. Just wanted to clarify because without context it could perhaps be misunderstood as if I started with the neural hypothesis to look for genes that fit the hypothesis, etc. One issue is that there are a lot of other genes nearby the DecodeME signal, making it less certain which genes...

To clarify: I didn't highlight NEGR1 much in my blog article because the gene was quite far from the DecodeME hit. I didn't assume ME/CFS is a nervous system disease and tried looking at potential genes from that angle. Instead, I focused on the protein-coding genes closest to DecodeME signals...

The supplementary table gives the scores for each of the items

Don't think this was one has been increased much in ME/CFS? IL-10 was in some but not many. TGF-beta has been the most consistent one but even there many inconsistent results. For comparison to ME/CFS, just made this brief summary of the cytokine literature on social media 1) Been looking at...

Thanks

This is a literature review. Was wondering if there's some consistency in cytokine responses in Long Covid. There were some big studies that pointed to inflammatory cytokines such as IL-6 being increased such as this one: https://www.nature.com/articles/s41590-025-02353-x Does anyone have...

Abstract Post-acute sequelae of Covid-19 (PASC) refer to persistent symptoms lasting weeks to months after acute SARS-CoV-2 infection. However, identifying biological mechanisms, potential therapeutic targets, and modifiable environmental risk factors remains necessary. Here, we analyzed...

An article about this: https://fortune.com/article/demis-hassabis-deepmind-artificial-intelligence-google-alphabet-drug-discovery-isomorphic/

This is from the same/similar team that published AlphaFold, an AI model that predicts how proteins fold and won them a nobel prize. A couple of days they also published AlphaGenome that helps to understand the effect of genetic mutations, discussed here: Advancing regulatory variant effect...

Today, we are excited to share an update on our progress towards a new frontier of drug design. We have unlocked a new paradigm of predictive accuracy in understanding our biomolecular world, allowing us to rationally design new medicines on a computer with unprecedented understanding and...

Would be great if someone could publish something about this.

BTN3A2 has also been associated with schizophrenia in this study that concluded: "Findings We identified BTN3A2 as a potential risk gene for schizophrenia. The mRNA expression and methylation data showed that BTN3A2 expression in human brain is highest post-natally. Further electrophysiological...

The LDSC genetic correlation with depression was 0.9, which seems very high. Apart from NEGR1 and the BTN hits, most seem quite different from those found in DecodeME. Here's the Manhattan plot:

I think James Baraniuk, Jonas Bergquist, Bjorn Bragee, Mady Hornig have all published studies on cerebrospinal fluid in ME/CFS patients in recent years but couldn't easily find cortisol being mentioned in their papers. If it's important, however, perhaps they could be contacted to ask if they...

This is the slide that went with the statement about gene expression, around minute 8.20 in the video.

The authors gave a presentation about their findings on the NMCB meeting a couple of days ago. I've made a brief summary of the talk on social media: 1) Dr. Felipe Correa da Silva shared more info about the first 10 brain autopsies from the Netherlands. In this new thread, we made a brief...

Nice find. People in the experimental group were given the following info: Their catastrophizing score increased but their pain rating and time in the cold water didn't. They tried to induce negative affect in the control group but that didn't work. As a potential explanation they argue...

Also found this Stanford website with info on enhancers and what has been found in other GWAS: https://e2g-portal.stanford.edu/variant/20_48935095_C_CTCTTTTTT Think this is the preprint that introduced it: https://www.biorxiv.org/content/10.1101/2023.11.09.563812v1