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Interesting new science on CFS/ME

Posted , 6 users are following.

Ravenwood
Ravenwood

Brain Behav Immun. 2015 Sep 20. pii: S0889-1591(15)30020-9. doi: 10.1016/j.bbi.2015.09.013. [Epub ahead of print]Antibodies to ß adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome.Loebel M1, Grabowski P2, Heidecke H3, Bauer S2, Hanitsch LG2, Wittke K2, Meisel C4, Reinke P5, Volk HD6, Fluge Ø7, Mella O8, Scheibenbogen C6.Author information

Abstract

Infection-triggered disease onset, chronic immune activation and autonomic dysregulation in CFS point to an autoimmune disease directed against neurotransmitter receptors. Autoantibodies against G-protein coupled receptors were shown to play a pathogenic role in several autoimmune diseases. Here, serum samples from a patient cohort from Berlin (n= 268) and from Bergen with pre- and post-treatment samples from 25 patients treated within the KTS-2 rituximab trial were analysed for IgG against human α and ß adrenergic, muscarinic (M) 1-5 acetylcholine, dopamine, serotonin, angiotensin, and endothelin receptors by ELISA and compared to a healthy control cohort (n=108). Antibodies against ß2, M3 and M4 receptors were significantly elevated in CFS patients compared to controls. In contrast, levels of antibodies against α adrenergic, dopamine, serotonin, angiotensin, and endothelin receptors were not different between patients and controls. A high correlation was found between levels of autoantibodies and elevated IgG1-3 subclasses, but not with IgG4. Further patients with high ß2 antibodies had significantly more frequently activated HLA-DR+ T cells and more frequently thyreoperoxidase and anti-nuclear antibodies. In patients receiving rituximab maintenance treatment achieving prolonged B-cell depletion, elevated ß2 and M4 receptor autoantibodies significantly declined in clinical responder, but not in non-responder. We provide evidence that 29.5% of patients with CFS had elevated antibodies against one or more M acetylcholine and ß adrenergic receptors which are potential biomarkers for response to B-cell depleting therapy. The association of autoantibodies with immune markers suggests that they activate B and T cells expressing ß adrenergic and M acetylcholine receptors. Dysregulation of acetylcholine and adrenergic signalling could also explain various clinical symptoms of CFS.

Copyright © 2015. Published by Elsevier Inc.

PMID:

 

26399744

 

[PubMed - as supplied by publisher]

 

1 like, 9 replies

9 Replies

  • jcnps
    jcnps Ravenwood

    Posted

    HI,

    Just think how useful we are - if we weren't ill so much progess wouldn't be being made in the science of the brain!

    May not help us directly but hopefully the ones coming after us - my father died of a disease that is now treatable - thats progress and I'm sure the same will happen with this disease.

    kind regards

    • Ravenwood
      Ravenwood jcnps

      Posted

      I agree. This might not help us, but maybe future generations will get a cure out of this. That would be wonderful.
  • Sassylass
    Sassylass Ravenwood

    Posted

    Hello!!

    Why don't you think this info wouldn't be of help to us soon? I'm not certain but out seems like this research could open up three treatment of CFS with a some types of drugs not previously used for CFS sufferers. If I'm understanding what I read somewhat correctly that is. I think this could be big news NOW.

    • Ravenwood
      Ravenwood Sassylass

      Posted

      Well, these are my assumptions based on the normal path science takes. I could of course be wrong. First, the two studies are not enough to warrant the label of 'proof' that cfs/me is an autoimmune disease of the neurotransmitters. More conclusive studies would have to be done. Second, rituximab is quite a dangerous drug and very expensive. So, at least in the US human studies would have to be conducted before the FDA would approve it's use for our condition and insurance could then pay for its use. Depending on funding, all of this could take 10 to 25 years to complete. Of course, some of us that live in big cities with research hospitals, might be able to get into one of the studies and try it out.

      I would like to believe that everything will go quickly, and we will get a cure soon. But, over time, I have lost my optimism. I try to be realistic without resorting to out and out pessimism. I hope that you are right and a cure will be right around the corner. I just don't want to get my hopes up and get them dashed once again. I hope you can understand that. Best wishes. Raven.

    • Sassylass
      Sassylass Ravenwood

      Posted

      Hello again! I didn't intend criticism with my comment. CFS sufferers have very good reason to be very pessimistic. Honestly, I don't understand most of that article, but was focused on adrenergic, dopamine, serotonin , etc. because at this point I'm looking at treating the fatigue rather than figuring out the cause of it. And I have reason to believe that some drugs which influence these chemicals and systems will help that, whilst further research is done.
    • Ravenwood
      Ravenwood Sassylass

      Posted

      Cool.  What the article said, was that the researchers found that there seemed to an autoimmune response to adrenergic and acetylcholine neurotransmitters, but not to the seratonin, dopamine, etc. neurotransmitters.  The medication they used to try to treat it is ruximtab, which is a really strong medication used to treat serious cases of autoimmune disease (since one of its side effects is death).  I doubt you could get anyone to administer this drug to you at this time.  More research needs to be done, and the drug is as risky as hell.

      However, the research does suggest that scientists might be on the right path (finally), and may come up with what is wrong with us.  And hopefully, come up with a treatment that doesn't include an IV and possible death.

      Take care,

      Raven

    • caitlin39841
      caitlin39841 Ravenwood

      Posted

      hi Ravenwood.  thank u for that. the closing line gave me a good ''belly'' laugh - an IV death - just in case we hadn't suffered enough lol?

      C

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