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In regards to dystrophic microglia in isolation, the absence of a classical cytokine signal in chronic ME/CFS does not mean there was no inflammation. It may simply mean we are looking too late, after an earlier inflammatory phase has already faded. Personally, I find this extremely likely. In...

I can't read the whole text, but just judging from the thread, I am sure it's great and it must have been a lot of work. Thank you! I just wanted to say that, 1. to assume that there must be a detectable and ongoing immune signal in chronic patients under current stratification and 2. to not...

There are some early indications that myelin acts as an energy supply for glia in times of reduced glucose uptake/stress. I went down that rabbit hole a few years ago and it struck me as interesting. What we (might) see here could be downstream of epigenetically reprogrammed metabolism...

One of those studies that will need replication by multiple teams. It would be great to see that sooner rather than later. As far as I understand, this technique is also not fully established/standardized yet. I was involved in funding a more “standard DTI” MRI study in the past, but I am...

What’s relevant here, imo, is that I have these petechiae, and many other patients do too, and we are not in the ICU. So either your microembolism model is incorrect or it does not apply to this subpopulation. In either case, the probable (I cant be sure of the 40%, I can only be sure of my many...

I have many thousands of these 'petechiae', that's 100% not within a normal distribution, there are many patients like me, I ran an informal poll on another platform, 40% reported petechiae. They also are persistent and increase in number with big crashes.

That’s essentially what has already happened with the subgrouping of “hEDS” vs “hypermobility.” My impression is that many 'sceptics' simply haven’t actually read the hEDS diagnostic criteria. They often confuse the formal criteria with what some people describe as “comorbidities” in hEDS...

I'd say it's definitely getting increasingly difficult for 'hEDS' sceptics to maintain their position. No one ever claimed there will be easy answers. Clustering them 'somehow' is important and necessary for non-monogenetic diseases to come up with a 'polygenetic score'. This can then...

I haven't read the study, but I really don't like the elevated heme metabolism bit. Also, once again, without understanding the acute phase of ME/CFS we might go absolutely nowhere.

I haven't read the paper - if it is methodologically sound it's yet another hint that trying to figure out ME/CFS without taking into account the acute phase, by only starting to investigate at the 6 months mark, is ridiculous. Biobanks more or less ignoring the temporal dimension of this...

Sure. Securing this funding is a huge success, but please consider the implications: if this 7.5 million multiomics study fails to yield real results, obtaining future funding for similar omics investigations will be exceptionally difficult. There is a real risk that the underlying sampling and...

I am not saying the study has no worth (apart from the metabolomics maybe), but I'd say it's clear that improving biobanking first would have been sensible. PS: I have read the original biobanking papers and criteria a few years ago, I was not impressed. If you can check them out.

It’s worrying for several reasons. You can’t obtain meaningful data readouts if the samples are not properly pre-stratified. Patients may be at completely different stages of PEM, have blood drawn at different times of day, different stages of disease, are on diets and so on, all of which makes...

Overall, this is of course fantastic news, as the disease needs to be recognized as worthy of funding on this kind of scale. If you look at it from that angle alone, it's already very welcome news. What is slightly worrying, however, is that the data they are collecting likely (?) comes from...

Would certainly be worth a replication study.

I believe, the symptom signal runs full strength more likely because neurological (network) changes have occurred, a different equilibrium with different setpoints has emerged, and not necessarily because of some messenger gone awry chronically.

Absolutely, it would be a huge mistake to not include the spinal cord - I am not sure whether that's feasible within the brain bank framework. @Grigor do you have any knowledge of this and/or had prior contact with them and uncomplicated ways to ask them about it?

Yes, it's probably also worth mentioning that a standard post mortem is very different from what a brain bank does/can do. There seems to be some confusion about this - the idea that ME/CFS is not 'a classic neurological disease' because post mortems have been largely unremarkable has always...

A very common mistake, in my view: “If ME/CFS cannot include multiple mechanisms, then cases with other (underreported, as of yet unidentified) mechanisms are misdiagnosed. Since those cases are misdiagnosed, ME/CFS cannot include multiple mechanisms." That's circular reasoning, I believe. If...

So, that points toward 'regulatory energetic failure' potentially? 'Regulatory energetic failure' of some sorts suppresses cAMP/TORC-CREB signaling because energy-sensing stress kinases actively shut down transcriptional coactivators to conserve energy, leading to functional depletion without...