The oral presentation itself was concise (this is usual in medical conferences) & has possibly saved significant novel findigs until their upcoming article is published.
This may explain why the breakdown on possible biomarkers and treatment options has been so succinct
(...)
However, this won't be an impediment to try to expand (and speculate a bit) on potential biomarker avenues exposed in Bhupesh's talk.
✅First of all, (I know this is an accepted hypothesis but bear with me) their results show strong evidence that #MECFS has an autoimmune basis:
In fact, that ME/CFS patients have overlapping autoantibodies for SLE and MS*
Probably, certain autoantibodies might fulfill criteria for a good biomarker, in the future:
However, autoantibodies aren't the only biomarkers in Bhupesh's talk:
✅Herpesviridae-derived dUDPase (from HSV-1, HHV-6 and EBV) is a potentially valid marker, ready for validation studies and clinical use in the short-term.
Both HV positivity and reactivation seem relevant.
Herpesvirus-derived dUDPase seems to induce mitochondrial dysfunction due to cytoskeletal interference
HVs hijack the cytoskeleton for their own functional needs, while causing mitochondrial damage in the process.
Another candidate named was Fibronectin:
- a multifunctional, adhesive glycoprotein that plays an important role in tissue repair, in regulating cell attachment and motility
In layman terms, it works as a glue and is related to injury response.
Central apnea occurs in many situations, and cranio-cervical instability is definitely the most common
Why does apnea happen?
Because the diaphragm (an essential muscle for breathing) doesn't activate
The breathing impulse gets carried from the brainstem respiratory centers, via brainstem and spine, until it reaches about the 4th cervical/neck vertebra (C4)
Then it exits the spine down to the diaphragm
Anything that compresses the medulla at C4 or above, affects its function