Has it been ruled out that ME could be an antibody mediated disorder? Sorry I’m out of the loop thought novel autoantibodies are difficult to discover without already having some idea of what you are looking for ahead of time.
From my understanding GWAS findings by themselves aren’t causal only correlative. You need to perform additional analyses to do casual inference. See for example an explanation here https://pmc.ncbi.nlm.nih.gov/articles/PMC7614231/
Right but the underlying goal of a genetic study like this is to gain some mechanistic insights as to what triggers or continues to drive the illness, and if the genetic component/influence is very low then these gene variants more likely than not do not play a major role in the pathomechanism...
Right and if true a very high predominance of non-genetic influence, whether stochastic or epigenetic, would further suggest that it’s potentially quite limited what mechanistic insights we might glean from additional genetic studies.
Does anyone know what is the genetic vs environmental influence they’ve estimated for ME given these new GWAS results? I swear I read somewhere that it’s estimated to be only a ~10% genetic contribution? Can’t find the source again
And if it’s predominantly environment that influences ME...
Golden hamsters are a commonly used animal model to study COVID. You will find them used as a robust preclinical model in a lot of studies https://www.pnas.org/doi/10.1073/pnas.2009799117
Maybe there’s some kind of CD38 targeting CAR-NK or CAR-T cell therapy that can better target and deplete CD38 plasmablasts while sparing CD38high NK cells and retaining sufficient ADCC cytotoxicity. Would really help test their theory and see if better responses can be produced in the lower NK...
@Jonathan Edwards you’ve stated repeatedly that RituxME trial results showed that B-cell depletion doesn’t work for ME. Fluge and Mella (and I in previous responses to your comments) disagree they said in their presentation that indeed for a subset it does work. What are your thoughts on this?
I agree, but also this study and possibly others found probable white matter track damage in these brain areas as well via fractional anisotropy DTI measurements.
These kind of studies and hypotheses are intriguing to me because this could also possibly explain why CCI/AAI surgery produces remission in some and possibly why LDA ie partial dopamine agonists significantly help others since the cerebellar peduncles play a very important role in the brain’s...
https://www.medrxiv.org/content/10.1101/2025.04.08.25325108
Abstract
Post-COVID Syndrome (PCS), also known as Long COVID, is characterized by persistent and often debilitating neurological sequelae, including fatigue, cognitive dysfunction, motor deficits, and autonomic dysregulation (Dani et...
https://www.nature.com/articles/s41467-025-57905-4
Abstract
The COVID-19 pandemic caused by the coronavirus SARS-CoV-2 has highlighted the vulnerability of a globally connected population to zoonotic viruses. The FDA-approved coronavirus antiviral Paxlovid targets the essential SARS-CoV-2 main...
I think it goes without saying that everyone here in favor of doing treatment trials without already having an established mechanism are not in favor of just trying things randomly or based on a hunch with little evidence. For sure we would want to have preliminary evidence pointing in a...
I think the lists that were provided were meant to highlight some examples to get us thinking not some kind of comprehensive work.
Also I don’t think jay meant abandoning mechanistic work in favor of trialing treatments, just that treatment trials even without an established mechanism...
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