Huntington's Disease and CFIDS connection??

Discussion in 'Fibromyalgia Main Forum' started by beckster, Aug 7, 2003.

  1. beckster

    beckster New Member

    where did it go??????I went back to my Prohealth email as I wanted to re-read this article (or, actually a summary of the article). All of the links on that page work EXCEPT the one on Hungtington's and CFIDS. Talk about paranoia. (I tried this 5 times.) So then I check Prohealth's articles and abstracts; could not find it. What do you make of this and how can we access that article???? Beckster
    [This Message was Edited on 08/07/2003]
    [This Message was Edited on 08/07/2003]
    [This Message was Edited on 08/10/2003]
  2. Mikie

    Mikie Moderator

    Shirl and I have nothing to do with website content. I am sorry I cannot help you with this.

    Love, Mikie
  3. mycatprint

    mycatprint New Member

    Is this the one you are talking about?

    Do a google search for "gene profiling and CFS" look for the title

    hugs from Cat
    _________________________________

    NCF Report: Breakthrough "Hidden" Finding in the CDC's Gene Profiling Study
    by Alan Cocchetto Copyright ® 2003

    The Centers for Disease Control recently published the results of their study of CFS patients in work titled "Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome" [1]. One of the authors, Dr. William Reeves, heads up the CFS program at the CDC.

    Vitally important results, neither reported to the public by the CDC nor reported upon by other CFIDS advocacy groups, surfaced several weeks ago when the NCF finally received the publication from the medical journal Disease Markers. "It took several months to get a copy of the journal article because college libraries had difficulty in obtaining it for some reason!" exclaimed Gail Kansky, president of the NCF.

    In an interview in Smithsonian Magazine, Dr. Suzanne Vernon, head of the CDC's gene expression program for CFS and lead author for the study, stated that using gene expression profiling technology, the differences between CFS patients and controls could be seen. Furthermore, she predicted that its utilization would make it a diagnostic tool for CFS.

    However, the NCF's own medical advisors and scientific consultants felt that the CDC failed to adequately inform CFS patients, the public, and the news media about its most significant finding to date!

    Bluntly stated, the CDC ignored their own truths discovered by their own research team! When the CDC examined age matched controls with all CFS cases, the top gene being overexpressed was the Huntington's Disease protein, also known as the HD protein. Since this protein was not expressed in controls but was highly expressed in all CFS patients and this protein proved to have the greatest statistical significance, why then has the CDC ignored this scientific finding? Why hasn't the CDC raised the red flag? Why
    hasn't the CFS patient community or CFS researchers been told? Why hasn't Dr. William Reeves commented on this?

    Perhaps this is because of the following. The Huntington's Disease gene is used in the identification of Huntington's disease [2]. This gene and its identification with Huntington's Disease was first identified in 1993. Now, if CFS patients are expressing this gene in a statistically significant way, then these two diseases are linked together in some significant manner! This truth cannot be ignored nor can it be diluted no matter how hard you try! Furthermore, no "spin" on this will change these basic facts!

    Huntington's Disease (HD) is a devastating, degenerative brain disorder for which there is, at present, no effective treatment or cure. HD slowly diminishes the affected individual's ability to walk, think, talk and reason. Eventually, the person with HD becomes totally dependent upon others for his or her care. Huntington's Disease profoundly affects the lives of entire families, emotionally, socially and economically [3].

    Early symptoms of Huntington's Disease may affect cognitive ability or mobility and include depression, mood swings, orgetfulness, clumsiness, involuntary twitching and lack of coordination. As the disease progresses, concentration and short-term memory diminish and involuntary movements of the head, trunk and limbs increase. Walking, speaking and swallowing abilities deteriorate. Eventually the person is unable to care for him or herself [3].

    While Huntington's Disease is a genetically based disorder responsible for neurodegeneration, it is a disease associated with polyglutamine expansion. Huntington's Disease is one of approximately ten diseases identified thus far with a polyglutamine expansion component.

    The NCF believes that the CDC has purposefully downplayed this key scientific finding due to the fact that CFS patients may have a "new" disease associated with a polyglutamine expansion component that is responsible for neurologic as well as cognitive impairment that has already been identified with these types of disorders. Furthermore, the major implication here is that CFS patients would potentially have an "acquired" Huntington's disease-like process occurring that is no doubt due to a yet unidentified infectious agent.

    The NCF staffers and the scientists who we have contacted are excited by this very important finding because it fits the evolving CFS disease model that we have developed. We firmly believe this work is directly tied to the ciguatera epitope finding and that other work in-progress, via the NCF's Research Grant Program, should yield some major dividends in the near future. All of our research efforts are aimed at scientifically clarifying what we have put together and expediting appropriate medical treatments. The NCF is very committed in this regard and we will be reporting upon our other research efforts in the months ahead. Look for the CDC's article on our website at [[url removed]]

    References:
    1. Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome; SD Vernon, ER Unger, IM Dimulescu, M Rajeevan, WC Reeves; Disease Markers 18 (2002): 193-199

    2. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group; Cell 1993 Mar 26; 72(6): 971-983

    [[url removed]]
  4. beckster

    beckster New Member

    I was hoping and thinking there would be more discussion of this, but if it is no longer accessed here not that many will be reading it. But with your post, they can!

    Anyway, what did YOU make of the article. Love to hear your opinion. Beckster
  5. Mikie

    Mikie Moderator

    This is an amazing article. This would not be the first time the CDC has downplayed research on CFIDS. This is very important, and frankly, scary, info. I hope, though, that it will lead to more knowledge and even a cure.

    It always seems to come back to infectious agents. Perhaps the fact that mycoplasmas play a significan role in our illnesses is one reason the CDC does not seem to want research into CFIDS. At least one strain of mycoplasmas has been bioengineered for germ warfare. I still believe there is a massive coverup by our own govt. on this.

    Thanks for posting this.

    Love, Mikie
  6. mycatprint

    mycatprint New Member

    Beckster,

    I have so many of the huntington's disease symptoms which have started small and grown over the years that the article really frightened me. I tried to talk it over with my dr who is normally a very good doctor. She gave me a referral to a rheumy (which I had asked for) and told me to ask the rheumy. ????? I think huntington's is an endocrinologists thing, isn't it -- or a neurologost thing? Anyway, the new rheumy appt is on the 20th, she is supposed to be a fibro specialist. More on that after the appt.

    The artical is scary! and I think that's why the CDC supressed it.

    hugs from Cat
  7. adageek

    adageek New Member

    Vernon SD, Unger ER, Dimulescu IM, Rajeevan M, Reeves WC.
    Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome.
    Disease Markers 18: 193-199, 2002.

    Summary
    Gene expression profiling examines the activity (transcription) of genes by analyzing cell’s messenger RNA (mRNA). Gene expression is altered by many factors including cell differentiation, metabolic state, and disease status. By comparing expression of many genes simultaneously, gene expression profiles can be compared between persons (and populations) with and without disease and characteristic differences (or associations) can be identified. These differences, known as differential gene expression, can point to markers for diagnosis or altered physiologic pathways. Gene expression analysis is particularly suited to studying CFS because it examines RNA transcripts from thousands of genes at the same time, covering all from immune system proteins, neuroendocrine pathways, stress response proteins, metabolism, apoptosis, cell adhesion receptors, cell cycles and such data is essential for understanding biological pathways and processes. Most gene expression studies have focused on samples derived from cells or tissues with a known lesion, but CFS has no known to sample. We have hypothesized that peripheral blood mononuclear cells (PBMCs) reflect the systemic state, thus allowing for evaluation of multiple pathophysiological pathways. Some of these pathways should be affected by CFS.

    This paper is the first use of gene expression profiling as a biomarker to distinguish persons with CFS from healthy controls and for identifying genes that could serve as CFS biomarkers. The manuscript is intended as a “proof of concept” for use of gene expression profiling for an illness without a known lesion. This study measured gene expression profiles in peripheral blood cells from five persons with CFS and 17 non-fatigued controls identified during physician surveillance in Atlanta. Various other publications (Studies of Causes of CFS) also used these subjects. Both cluster analysis and multidimensional scaling analysis grouped and separated CFS from controls. The materials and methods section provides considerable detail as to the assays that CDC uses for measuring gene expression profiles. The materials and methods also provides detail as to analysis strategies.

    Abstract
    Chronic fatigue syndrome (CFS) is a debilitating illness lacking consistent anatomic lesions and eluding conventional laboratory diagnosis. Demonstration of the utility of the blood for gene expression profiling and biomarker discovery would have implications into the pathophysiology of CFS. The objective of this study was to determine if gene expression profiles of peripheral blood mononuclear cells (PBMCs) could distinguish between subjects with CFS and healthy controls. Total RNA from PBMCs of five CFS cases and seventeen controls was labeled and hybridized to 1764 genes on filter arrays. Gene intensity values were analyzed by various classification algorithms and nonparametric statistical methods. The classification algorithms grouped the majority of the CFS cases together, and distinguished them from the healthy controls. Eight genes were differentially expressed in both an age-matched case-control analysis and when comparing all CFS cases to all controls. Several of the differentially expressed genes are associated with immunologic functions (e.g., CMRF35 antigen, IL-8, HD protein) and implicate immune dysfunction in the pathophysiology of CFS. These results successfully demonstrate the utility of the blood for gene expression profiling to distinguish subjects with CFS from healthy controls and for identifying genes that could serve as CFS biomarkers.




  8. beckster

    beckster New Member

    bump, for weekenders
  9. JaciBart

    JaciBart Member

    I read that a few times and then studied up on Huntington's, I do see similarities of course in the spasms, I have a terrible problem with that, I throw my cup of coffee across the room about twice a week, luckily I haven't done that (yet) with a bowl of fresh blueberries which are my staple these days, that could be awfully hard to clean up. I just do not see a whole lot of other similarities though. I do not see the progressive nature in cfs persons, I know it lasts pretty much forever and is for the most part progressive but Huntington's persons end up way worse off than us in a much shorter period of time. They do not have the unrelenting fatigue. It just seems to me like we have the worst symptom in common but not much else. I could be wrong of course, has happened.

    I tend to think that what we actually get is a bit of all the autoimmune disorders as well as central nervous system diseases, neurological disorders, rheumatological diseases, etc. We are like the Heinz 57 variety of the Merck Manual. I can see myself 100% in MS, Lupus, Myasthenia, Parkinson's, RA, Shojrens, (sp?) and just about every other major illness out there but not too much Huntington's. I would be curious if they did the same testing on genes as the other diseases if we would have the same indications. I just think we have it all.

    Jaci
  10. mycatprint

    mycatprint New Member

    I have beed exhibiting memory loss symptoms -- like driving and forgetting (for about a minute) how to get home. What a panicky feeling! Also other short term and long term memory problems. I have always had exhaustion, but lately it has been very pronounced. I have just begun exploring it with my doctor. I don't even think she knows what huntington's disease is.

    I think I am going to ask for a test for huntington'd disease.

    scaredycat hugs from Cat
  11. beckster

    beckster New Member

    Thoughts???????????
  12. MtnDews

    MtnDews New Member

    YES, lots of thoughts on this. I agree, we are heinz 57. What about family medical histories? Tons of cancer in our family and some Myasthenia Gravis (<- have a sibling with that), all my sibs have been diagnosed with Fibro. I've been diagnosed with that and Ehler's Danlos. I guess we just don't fit a mold very well. I also wonder about the Rh factor.
    H