Quickly touching on the Acetylchlone receptor antibody findings in CFS and POTS research recently and in the past...this looks interesting talking about normal prion protein (PrPC):
Using several truncated PrP variants and specific tight-binding
AChE inhibitors (AChEis), we then demonstrate that the PrP-AChE interaction requires two mutually exclusive sub-sites in PrP N-terminal domain and an aromatic-rich region at the entrance of AChE active center gorge. We show that
AChEis that target this site impair PrP-AChE complex formation and also
limit the accumulation of pathological prion protein (PrPSc) in prion-infected cell cultures
&
AChE levels were altered in prion infected cells and tissues, suggesting that
AChE might be directly associated with abnormal PrP.
Source: Interaction of prion protein with acetylcholinesterase: potential pathobiological
implications in prion diseasesTorrent et al. Acta Neuropathologica Communications (2015) 3:18
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383067/
PrPC is on neuron surfaces in the brain. So I wonder if
blood acetylcholine levels correlate with
brain levels? Presumably not.
Either way, out of interest it would be interesting to know if PWME who have low experimental PrPC (REDLABS test) also run a low blood Acetylcholine too. Also then find out what exactly are 'AChE inhibitors (AChEis)' in humans and can we test for them?
If we had two more pieces of evidence alongside low blood PrPc (Naturally this isn't brain it's blood), but anyway, if we had this, it would be rather interesting to see if this then correlates with an infection we all share. Because...
As lymphoproliferative disorders include viruses, autoimmune disorders and forms of cancer, I doubt it's not too wild a guess to propose a shared pathogen could be linked to cause lots of horrible diseases, including ME. (ME just being one genetic outcome of that infection). Others may lead to Leukemia etc.
Theoretically the ensuing immune suppression of 'pathogen X' then makes Lyme (or another infection found in PWME) become chronic - hence we never share the same infections universally as the pathogenesis of ME. If it was a retrovirus, it might not provoke a full immune response in the human host (no antibodies) so it is thus 'stealth'. We could the develop 'ME' after a seemingly innocuous glandular fever/viral event but never get better, the EBV not being the cause, but the trigger (same for Lyme).
Have you noticed this?
PWME generally report an end of high temperatures, diarrhoea and vomiting
once they get sick. Many initially report they 'never get anything any more' despite being housebound or bedridden feeling infected 24/7. Throwing up and shaking with a fever is a
correct immune response to an infection BTW. We tend not to do that any-more once we get ill. (We can still get infections and this happens, but I mean not chronically, despite us saying we feel chronically infected with a virus feeling that never fully goes away and ramps up with exertion).
A defective cancer retrovirus (that leads to autoimmunity) could do that, it might explain why we get episodes of T cell, B Cell, NK cell elevation (lymphocytosis of multiple cell types), but this then turns off without chemo. Like elements of an intermittent, self aborting CLL almost.