A massive thank you to the whole DecodeME team! I'm very grateful to everyone who made tonight possible. Lets hope its the start of an interesting and fruitful journey!
So if the gene inhibits the proliferation of CD4+CD8 t cells activated by IFNG does that provide evidence for or againsts JE et als hypothesis?
Inhibition would suggest against to me but I know little about these things.
Any statement by researchers which contributes to the phenomena of patients confidently stating unproven hypotheses as fact, further delegitmising them in the eyes of medics, is deeply irresponsible imo.
My definite (as opposed to possible prodromal) onset was after a dual strep and impetigo infection. Interestingly not the strain of strep that causes impetigo so two different infections.
Point is bacterial infections definitely seem to be a trigger.
The question is have they created PEM in a dish or found the factor that causes ME/CFS exercise intolerance and muscle weakness/fatiguability? As opposed to delayed PEM.
Precicely i feel like they are talking about something that isnt neuroinflammation. These new drugs they are talking about are intriguing but I don't find it particularly compelling as a hypothesis.
I don't feel like the authors provide any evidence that neuroinflammation is the cause. And also is the definition that its 'immune activation within the brain' accurate?
But the idea of targeting the sickness behavior itself rather than the cause of it is kind of intriguing. I guess time will...
Does the idea that its caused by neuroinflammation and will need new anti-inflammatory drugs to treat carry weight with anyone round here? It sort of seems like a shrug type response to me...
What are the implications if this study replicates? If the factor in the serum causing these responses can be identified and removed, will cells and muscles return to normal? The paper calls these effects transient, so one would hope so...
And would this finding gel or clash with the...
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