Charcot Project

The Charcot Project is an initiative to promote research and the dissemination of information around the hypothesis that multiple sclerosis is caused by a virus. It is being generously funded by anonymous donors and AIMS2CURE. 



The Charcot Project is currently developing a clinical trial protocol to test a specific anti-viral therapy that is active against EBV, a herpes virus that is strongly associated with MS. 


The activities of The Charcot Project will be overseen by a steering committee. 

See the Update on the 2013 Presented by Prof Gold

Blog Posts
Charcot Project-Towards a cure for MS

83 comments:

  1. Best wishes with this work.

    What effect will the study be looking at - reduction in ARR or MRI activity?

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  2. Re: "What effect will the study be looking at - reduction in ARR or MRI activity?"

    MRI at first; we won't have the finance to do a study powered on a clinical outcome.

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  3. Can you say how long the trial is expected to last, and how long before the results become available?

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  4. Re: "Can you say how long the trial is expected to last, and how long before the results become available?"

    This will a phase 2a study and take ~6 months to set-up, 6 months to recruit, 6 months to complete and 6 months to analyse the data. First we need to apply for money to do the study.

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  5. Devil's advocate question:

    Why the long timescale? Why not squeeze set-up and recruitment to six months and data analysis to 3 months (plenty of bright interns would help?).

    I get all hopeful when I see these projects, then realise it will be 10 years before a treatment will be available. MS - AHHH!

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  6. Re: "Why the long timescale?"

    The million dollar question. We have been working on the EBV trial for 2 years already and have yet to get funding in place. Unfortunately, science is like any other field; you need to convince the target audience of the need and then raise money for research. Unless of course some wealthy philanthropist decides to help; this is not uncommon in the US. The downside of the latter is you don't receive the wisdom of peer-review.

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  7. Re funding (asking purely out of curiosity): how much money does it need?

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  8. I do not know, the Profs will have to answer this but I believe that there is more than one study planned in the vision and it depends on how the grant applications and other things do .....more from Prof G no doubt.

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  9. Re: "Re funding (asking purely out of curiosity): how much money does it need?"

    A cross-over trial will cost about £500K (phase 2a) and a parallel design close to £2.5M (phase 2b).

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  10. A cross-over trial will cost about £500,000 (phase 2a) and a parallel design close to £2,500,000 (phase 2b).

    Translated means

    Parallel Design = Placebo and drug being run at the same time in two different groups

    Cross over = Start on one side of the trial (e.g. placebo) and then switch to the drug

    After the completion of phase 1 trials (drug exposure in healthy individuals), then you do first set of exposure-response trials
    in patients (Phase 2a) before beginning phase 2B (i.e., patient dose-ranging trial) and phase 3 clinical efficacy-safety trials.

    http://en.wikipedia.org/wiki/Clinical_trial

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  11. Prof G,

    Why not pick 10 of your patients (5 RRMS and 5 SPMS), give them an MRI, give them the anti-viral, and give them and MRI at 6 months and 12 months?

    The current structure for undertaking studies takes too long and costs to much. If you saw someone drowning, you'd jump in the river to save them. There must be scope to use these approach for MS victims, rather than get sucked into the over-bureaucratic approach required by academic.

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  12. Have you considered crowdfunding a la kickstarter? I doubt you'd ever get £2,500,000, but perhaps you could get enough to strengthen your case with a funding agency.

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  13. Re: "Have you considered crowdfunding a la kickstarter? I doubt you'd ever get £2,500,000, but perhaps you could get enough to strengthen your case with a funding agency."

    I have only read about crowd-funding and have never been involved with it before.

    If we went this route it would have to be done by someone else on our behalf. The etiquette of MS Research funding in the UK is complex and this would certainly be off limits, because of potential or at least perceived conflicts of interest.

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  14. Re: "Why not pick 10 of your patients (5 RRMS and 5 SPMS), give them an MRI, give them the anti-viral, and give them and MRI at 6 months and 12 months?"

    We are going to do something like this. However, there is a science and regulatory framework for doing research.

    Firstly, we need to power studies to get a definitive answer. 10 patients is too few. In addition, we can't simply prescribe a drug to patients. We need to get regulatory permission (MHRA) and ethical permission to do the study. MS'ers then have to volunteer and give informed consent. In addition to this we need to get permission from our hospital to do the study. The latter involves insurance to protect study participants etc. Also the NHS won't pay for research; we need to get money to pay for the drug, clinic visits, blood tests, MRI, etc.

    Doing clinical studies is a complex process. A lot has been discussed about this on the blog. I will ask Mouse Doctor to re-post his series about drug development.

    This is all very frustrating and the reason why things take so long to move.

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  15. Oh what I would give to be part of this project! I've spent the past 12 years refusing DMDs and begging for (and being refused) anti virals.

    This project gives me great hope that someone is finally looking down the right avenue.

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  16. Prof G,

    If the trial results were positive, I'd like to get on the treatment ASAP. If this anti-viral tablet is already licenced, could I get a sympathetic GP to prescribe? Otherwise, it will be a decade before it's licensed for MS. I would happily sign any waiver.

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  17. How can I become a part of the Charcot Project from across the pond, Prof G? Do you know of any researchers looking into the virus hypothesis in the US?

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  18. Re: "I would happily sign any waiver."

    We need evidence before make any recommendations. This is why we are applying for funding to do clinical trials to test the hypothesis.

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  19. Re: "How can I become a part of the Charcot Project from across the pond, Prof G? Do you know of any researchers looking into the virus hypothesis in the US?"

    No not at present; but if the initial proof-of-concept studies are positive the next set of studies will need to be international.

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  20. Good news, we have just submitted a grant application to the MRC to fund a phase 2a MS trial of a drug that targets EBV. Please keep your fingers crossed.

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  21. Professor Prineas, (winner of the 2009 Charcot awared) has said:
    "MS may be a disease in which myelin breakdown is a bystander effect of injury to an astrocyte or some other structure related to blood vessels, in other words that it is not primarily a disease of oligodendroyctes or myelin" http://www.msif.org/en/research/msif_research_awards/2009_charcot.html

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  22. If you want to get to the bottom of EBV, you have to look at its root which is being hidden from public knowledge. It was created in a lab clear back in the 60's when they began messing around with Monkey Viruses for polio vaccines, using kidney cells. EBV, a mutation of the SV-40 cancer causing virus that was also being manipulated to cause cancer in Castro and other enemies of the State. Unfortunately, they kept it secret for years, allowing millions to be vaccinated, and poor kids like me were given the old vaccines until early 1990. They found ways around working with the monkey kidney cells anyway, for profit!! Don't believe me, start your own research...good luck!

    Our own govrnment and the powers that be have been making us sick for decades and still won't own up to the erros made in the 60's. Many have died because of this secret and now millions of Americans with auto immune diseases because of their F up!

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    1. What about the insanity virus

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  23. If you want to get to the bottom of EBV,.....................

    Always nice to get a post from IG11!!
    The disease was first described in 1889 and was referred to as "Drüsenfieber," or glandular fever. The term infectious mononucleosis was first used in 1920 when an increased number of lymphocytes were found in the blood of a group of college students who had fever and symptoms of the condition.
    Still, never let the facts get in the way of a good conspiracy story eh?

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  24. It's a very seductive argument. But why do you think valacyclovir, an anti viral well known for its ability to treat EBV, has no significant impact on MS outcomes? http://msj.sagepub.com/content/11/3/286.short

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  25. Re: "valacyclovir"

    This is a prodrug of acyclovir. It has a very short half-life inside cells and has poor activity against EBV, our main target. There is a large literature on this topic.

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  26. So can you say what drug you are most hopeful for, and what your main viral target is (HHV6?) please?

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  27. The Charcot project is moving on more than one front sucess in some parts not so successful..yet.in others. It is not just one drug. and not just one viral target.

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  28. I think on so many levels you are onto the right thing, so it would be very interesting to hear your response to this study:

    http://www.ncbi.nlm.nih.gov/pubmed?term=20220124

    It alluded to an absence of Epstein-Barr virus in the brain and CSF of patients with multiple sclerosis.

    Is this because you are not looking for EBV in particular - but something that EBV triggers (like HHV6?)

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  29. Is this area of interest in the Charcot project? The connections between EVB, Vitamin D and Viral IL-10?

    http://www.medical-hypotheses.com/article/S0306-9877(08)00061-3/abstract

    If so - is there anything that can be done to down-regulate VIL-10?

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  30. The charcot project aims to get rid of viruses that may cause/trigger MS

    Get rid of the viruses and the ViL-10 is not an issue.

    P.S. Great to see you are comming up with these ideas

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  31. This is interesting:

    P171
    Regulation of MSRV (Multiple Sclerosis- associated retrovirus) and syncytin-1 by HIV-1 Tat in PBMC and U-87 MG
    Caterina Serra,1 Alessandra Mei,1 Giuseppe Mameli,1 Luciana Poddighe,1 Elena Uleri,1 Roberto Manetti,2 Bassel E. Sawaya,3 Kamel Khalili,4 and
    Antonina Dolei1
    1Department of Biomedical Sciences and Center of Excellence for Biotechnology Development and Biodiversity Research; University of Sassari, Sassari, Italy; 2Institute of Internal Medicine, University of Sassari, Sassari, Italy; 3Department of Neurology, Temple University, Philadelphia; and 4Department of Neuroscience, Temple University, Philadelphia
    Human immunodeficiency virus type 1 (HIV-1) affects the central nervous system of a majority of AIDS patients, by the mechanisms are not identified completely. MSRVenv and syncytin-1 are the env proteins of two retro-elements of the HERV-W fam- ily, that have potentially neutopathogenic properties, and thus have been proposed as co-factors triggering the immunopathogenesis of multiple sclerosis. Since ~10% of healthy humans are MSRV-viremic, we studied in PBMC and U-87 MG astrocytes the pos- sible regulation of the above HERV-W retroelements by HIV and by HIV-induced proteins, by using real time RT-PCR assays that selectively identify either MSRV-env or ERVWE1-syncytin transcripts. The results highlighted that the expression of both ele- ments is modified by HIV infection and by recom- binant Tat treatment. Surprisingly we detected an opposite regulation of MSRVenv and syncytin-1, since MSRVenv transcription was up-regulated, whilst that of syncytin-1 was down-regulated. Syn- cytin-1 down-regulation is due at least in part to the HIV tat regulatory protein, this result was also con- firmed by Intracellular flow cytometry of U87-MG astrocytes treated with HIV-Tat for 24h and stained by anti-HER-Wenv mAb. It is observed also in astro- cytes transiently transfected with a syncytin-1 pro- moter-Luc reporter plasmid (URE-LTR, ��436/+310)

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  32. I wonder if you are also looking at the issue of Syncytin-1?

    As far as I can establish, retroviral envelopes are pathogenic glycoproteins which - in MS - cause neuroinflammation, neurodegeneration, and endoplasmic reticulum stress responses.

    We know that the human endogenous retrovirus (HERV-W) envelope protein, Syncytin-1, is highly expressed in CNS glia of individuals with multiple sclerosis (MS). And we know that this can result in an increased in Nitric Oxide expression.

    See: “antioxidants ameliorate syncytin-1's neuropathogenic effects raising the possibility of using these agents as therapeutics for neuroinflammatory diseases.”

    (http://www.researchgate.net/publication/45582699_Human_endogenous_retroviruses_and_multiple_sclerosis_innocent_bystanders_or_disease_determinants)

    In light of this, this quote is interesting:

    "Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. Thus, syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention".

    (http://www.researchgate.net/publication/8261929_Human_endogenous_retrovirus_glycoprotein-mediated_induction_of_redox_reactants_causes_oligodendrocyte_death_and_demyelination)

    Ferulic acid is similar to curcumin in chemical structure. Ferulic acid is a ubiquitous plant constituent found in plant cell walls, leaves and seeds (which might explain the eat-more-leaves-theory of MS).

    It has been shown to have strong ant-oxidant potential and it has a possibility of inhibiting lipid peroxidation http://www.ncbi.nlm.nih.gov/pubmed/1398220

    So - are you going to be looking at how to downregulate Syncuytin-1? And will anti-oxidants be one way of so doing this? Or NO antagonists?

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  33. Re: "So can you say what drug you are most hopeful for, and what your main viral target is (HHV6?) please?"

    We can't tell you what drugs we plan to use as this may affect the ability of the Pharma companies involved to patent the idea. We are targeting HHV6, EBV and HERVs.

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  34. "We can't tell you what drugs we plan to use as this may affect the ability of the Pharma companies involved to patent the idea. We are targeting HHV6, EBV and HERVs."

    Can you at least tell us the side effects of these drugs?

    Before testing any substance on humans don't you think there should be convincing evidence that:
    a. HHV6, EBV or HERVs are harmful to animals in an ms-like way.
    b. The drugs you are planning to use do help animals recover from the relevant infections.

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  35. Re: "Can you at least tell us the side effects of these drugs?"

    These are drugs that have been into humans before so we know their side effect profile. Criterion 9 of Bradford-Hill is experimental proof; treating MSers with anti-virals is part of the proof. Proving it before anti-virals is almost impossible.

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  36. "These are drugs that have been into humans before so we know their side effect profile."

    I know you do, but we don't. Don't you think the side effect profile should be disclosed?

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  37. VV if and when the drugs go into MS trials the names will be disclosed and with that the side effect profiles will be known. They will be publicised while recruiting trial participants.
    Why 'should' they be 'disclosed' now? The only people who may find the information useful are those who are about to start taking the drugs, and that is not possible because we dont know which drugs

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  38. Anon 2.55 is correct
    When it is time to disclose they will be disclosed. We have no desire to instigate a stampede of off licence drug-use over the internet.

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  39. "We have no desire to instigate a stampede of off licence drug-use over the internet."

    This makes sense and suggests that the drugs come in affordable price.

    "this may affect the ability of the Pharma companies involved to patent the idea."

    To the contrary, the above is a completely different explanation, suggesting not a precaution measure, but rather a financial obstacle against information availability.

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  40. As we have repeatedly said, studies get done if pharma have the knowledge that they can benefit from their investment.

    If a new patent can be obtained this helps. Universities want us to do this and this would form part of our performance management so that they can benefit from our ideas. We would be foolish not to think about this. This aspect may also impact how the study is performed.

    Kohler and Milstein asked about whether they should patent monoclonal antibody technology.

    A guy from the medical research council, probably buried in a ditch, said it was not a worthwhile idea. This would have funded British Science for years had it done so and the British Government (Medical Research Council)would have got a slice of the action of tysabri, alemtuzumab etc.etc,etc, and think about all the diagnositic tests using antibodies

    Anyway back to the comment. The plans are not finalised when they are you will know.

    I personally would not have even mentioned the Charcot project until something concrete is ready as one is setting ones self up for a fall, if things do not come off.
    But Prof G down under wanted to do it this way.

    I'll give you another reson why they do not want to disclose our precise plans. MSers are not the only people who read the blog and some of these people are pharma and others are researchers. Why do we want to tell others what we are up to until every thing is finalised and we get the head start.

    We give the idea away for free and someone else can do it or maybe stick a spanner in the works. It has happened we talk to someone and next thing we know they have applied to do the same thing.

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  41. Hi Mouse Dr,
    Interesting your point, "MSers are not the only people who read the blog and some of these people are pharma and others are researchers. Why do we want to tell others what we are up to until every thing is finalised and we get the head start".

    Doesn't that say volumes about how the pharma industry works, I guess in my little naive world everyone would pull together for the greater good.I suppose the Dollar speaks the loudest and whoever pays the bills.

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  42. All these sound very reasonable but imply something very disturbing: the world of (MS) research has become so complex that can be motivated by everything but the patients' needs. What was once the tool (funding) has become the goal in an ever growing struggle of research to perpetuate itself, like a living organism leaping into self-awareness.

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  43. VV you believe the MS puzzle is already solved and you are as good as cured (which I hope you are). So why the interest in this particular bit of information? What use is it to you?

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  44. Dear Andy C

    If this was Utopia we would do one thing but we have deal and live with the Real World, stabbing in the back, stealing idea, pipped to the post, redundancy is not unheard of and if you don't have the goal you don't try to get the tool

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  45. PS you think we are joking. We talked with someone about an idea for a study. They where party to our discussions got our idea in writing and and then they proceeded to try get funding for the same idea without us. Justise was done and it bit them in the Ass (Amercian) or Arse

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  46. There are few anti-viral clinical trials done in MS (at least one in US and one in Scandinavia). None of them to my knowledge have met the primary endpoints, though there have been some improvement in patients with highest MRI activity. Any comments on why those have failed and why yours could success?

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  47. Wrong drug, wrong viral target, wrong trial design?

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  48. Re: "Any comments on why those have failed and why yours could success?"

    None of them had much activity against EBV or HERVs. EBV and the HERV (human endogenous retrovirus family) are the most likely culprits.

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  49. I know this is starting to sound like a game of 20 questions ("is the drug bigger than a breadbox?), but I'm curious about how an effective anti-viral would likely be administered to an MS patient.

    Would we simply get a shot and be done with it? Or is it likely to be part of a more drawn out process?

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  50. "I'm curious about how an effective anti-viral would likely to be administered".

    Via the mouth if its a pill, and maybe a needle if its a vaccine :-)

    I remember getting the polio vaccine in a sugar lump.

    The form of delivery depends on the drug.

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  51. Okay, thanks. So it really is that simple. I was thinking about how some treatments require us to "reboot" the immune system in some nasty way or other or come back time and again for boosters. Just wondering if there were any surprises with this approach :)

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  52. No surprises in the approach I think. Sorry for being vague

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  53. are you aware of this trial?

    http://clinicaltrials.gov/ct2/show/NCT01103583

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    1. Reported side-effects are: drowsiness, nausea, vomiting and diarrhea, constipation, mucositis, anorexia, stomatitis, bone marrow toxicity (dose-limiting toxicity; may take 7–21 days to recover after the drug has been discontinued), alopecia (hair loss), skin changes, abnormal liver enzymes, creatinine and blood urea nitrogen.

      Nice.

      Where can I get some????

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    2. I think the issue of 'side-effects' with any drug is complex. Companies are obligated to record any adverse effect while someone is taking their medication, even if it is unclear if the effect is caused by the drug or not. Most drugs have 100s of listed side effects. That is why asking a doctor who has treated many 100s of patients with the drug about their experience. In this case, I can assure you that I have never seen even one of these side-effects.

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  54. Any update on getting funding? Have you reapplied for any grants?

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  55. Re: "Any update on getting funding? Have you reapplied for any grants?"

    Will make an announcement soon! We are almost there with one of the proposed trials.

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  56. Outstanding blog. I am finding answers here I have not found in the past 14 years. I have been trying to get my doctors to pay more attention to my very high antibody levels to EBV. I contracted mononucleosis at age 10 and during or just after that illness, I lost vision in one eye. The vision came back within 24 hours. No one ever knew what that was-probably optic neuritis. More complications have followed-fatigue and depression in early teens and on and off in adult years. First spinal cord lesion and attack appeared in 1998. After reading "Chronic Fatigue Syndrome" by Dr. Jesse Stoff and Charles Pelligrino, I realized Epstein Barr was probably at the heart of all this neurological symptomatology. I was officially dx with MS in 2005 after several attacks and seven years of seeking help and treatment. I have been looking for a way to blast this Epstein Barr sucker into oblivion. So good to know Dr. G is working in this line of research. I will gladly donate to this research and try to recruit other donors if you let us know how to go about donating.

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  57. In case Charcot Project fails to demonstrate something meaningful, will this be attributed to an erroneous viral hypothesis or to partial efficacy of antiviral drugs? Will you be able to make that distinction?

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  58. hi, have you had any human indication that this treatment will work in someone with MS? By this, I mean has anyone with MS been noted as taking this drug for another condition, and found that their MS symptoms were positively affected?

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  59. It all seems to have gone very quiet. The trial is still not recruiting despite having a projected study start date of February 2013. Have I missed something, is it yet another false dawn for a potential cure?

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    1. The trial is active; we have recruited 2 MSers so far.

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  60. Is the idea that if you can neutralise the viral element in the disease, then you can control it, as a vital element in its pathogenesis is removed. Therefore you wouldn't need anti inflammatories or neuroprotectants for RRMSers, or even remyelinating agents, and it might halt progression.

    Or is this running before you can walk?

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    1. This is exactly the theory we are working on. If you can stop the underlying cause of MS then other treatments may not be necessary, or at least not required as often. We don't know if this will be the case for all types of MS. We're just learning how to walk at this stage, but 170 years after Charcot first described MS, it's about time we made some real progress!

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  61. How is recruitment into the raltegravir trial going?

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    1. We have 8 people enrolled, so it's going slowly, but we are optimistic. This is a crucial clinical trial, so we are constantly hopeful people will become interested and want to find out if they are eligible

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    2. Profs G and G,

      It is interesting that your trial was described as the next CCSVI at ECTRIMS. Why are you conducting a trial without a placebo control group? At least the CCSVI study had that. It seems you are trying to 'fudge' a favourable result by picking patients with active disease who will get better anyway regardless of treatment. In this respect Zamboni is a better scientist than you are.

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    3. The next CCSVI...well the worry would be if you think that catching HIV is the way to get the treatments....This is not a sensible approach please do not do it!!!!!!!!

      The trial by the profs G is a proof of concept trial. If (lets be upbeat when) it is active there will need to be proper blinded controlled trials. As to the trial design there is a risk of regression to the mean that is the people on the study are active and this will become less active. I asked PrfG that very question yesterday. The trial design was generated by one of the worlds leading MS statisticians.

      Zamboni is a better......sticks and stones.....

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    4. The trial was not described as the next CCSVI; Alex Pratt simply warned that the community should not allow it to become the next CCSVI. In other word all the quacks out there should not start prescribing raltegravir to people with MS until there is good evidence of it being effective. I doubt it will be the next CCSVI, it is a drug so anybody prescribing it will simply filling Merck's coffers rather than their own back pockets. The main driver of CCSVI was unscrupulous operators wanting to cash in on vulnerable MSers before CCSVI was an established entity that was responsive to treatment.

      I don't like being compared to Zamboni; a lot in the field think his original findings implausible and he didn't declare his conflicts of interest. We have yet to report our findings and we have declared our conflicts.

      Before commenting further I suggest you wait for us to report our results (late 2014); there is a high chance that the INSPIRE study will be negative; unfortunately, that's the nature of science.

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    5. You guys build us up to knock us down! Just once can i come home from work, turn on the computer and read something positive on this blog. Charcot project was supposed to be the black swan. Now you're telling me that there's a high chance of the trial failing! Failure isn't an option in my job - I'd be sacked. Another reason why i'm going to be an msologist in my next life. The pays not bad, plenty of foreign jollies, and you don't have to succeed in anything you do (just put it down to the nature of science). If i send you my cv can see if there are any opportunities at Team G.

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    6. I think Prof G is just trying to play down any unrealistic expectations. We all hope he's wrong but if you don't look you'll never know.
      As for failure, it's a sadly very common feature of science in general and the route to new drugs/treatments is littered with failures along the way so I suspect you would be temperamentally unsuited for a career in MS.
      As Samuel Beckett put it " Ever tried. Ever failed. No matter. Try again. Fail again. Fail better"

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    7. Bit off putting for people with MS who are thinking of joining the trial though. Whilst I wouldn't be thinking of it as a definite cure, I would tend to think 'what's the point', if it is expected to fail. Maybe the professor could choose his words a bit more carefully. That said however, speaking as someone fairly newly diagnosed, this blog gives me hope just because it proves there are people working constantly to identify cause and treat MS. That alone heartens me.

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    8. From a CCSVI standpoint (sorry) I'm excited about the Charcot project. EBV has an affinity for collagen and jugular valves are made of collagen. The virus may be damaging the valves and the endothelium or the capillaries of the blood-brain barrier.

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    9. We have recently been accused of promoting the Charcot Project like Zamboni did with CCSVI, which is clearly inaccurate (see comments above). Therefore to manage expectations I am simply stating that facts; most phase 2 clinical trial programmes turn out to be negative. Although there is anecdotal evidence that anti-HIV drugs may work in MS we have to do this trial to test the hypothesis. We can't make any claims about efficacy until this trial is completed and we have analysed the results.

      You also need to remember that there is scientific evidence that HERVs and EBV play a role in MS. Unless we do clinical trials we will never know if the role they play is causal or simply a bystander effect of the MS process.

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    10. Prof G the evidence that EBV is associated with clinical disease activity is weak, and for HERVs non existent. You don't mention that your study about EBV and MRI was NOT replicated. Please stop spinning the data, be honest. Otherwise people will joke about you like they did at ECTRIMS.

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    11. I agree with Prof G that we can't be too optimistic, but also the comparison with CSVI is insulting. We have designed this early study with the best advice possible and with the small budget we have. There is no other motive than seeing if it works. If not we will keep researching as I strongly believe that there is a viral trigger or cause for MS and we will find it. So I come home from work, not thinking of failure, only think of options.

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  62. Fingers crossed for the Charcot Project. I suppose after 60 years of research with all the big questions still to be answered, MS researchers are always going to be a little downbeat. Perhaps the real black swan will be a maverick MS researcher who drives through their idea without regard to all the bureacracy which claims to be about safety but actually prevents patients (who are ill and at high risk of getting disabled) from getting treatments. The drug you are testing already has a safety record in sick patients. If a small trial showed dramatic effect then those with MS should be given an option to have it. If it was a treatment for bunions i'd understand the need for safety trials. But when someone has a life-shortening / disabling disease the focus on safety, when the drug is already in use, is a mockery. The current dogma around trials / licensing etc is e real reason why progress has been so slow.

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  63. I'm sure if you were able to publicise the trial more widely people would volunteer to participate - I know I would if I fit the criteria, which unfortunately I don't.

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  64. Hi, I got HIV through drug use and then got MS. If I got HIV through sex are you saying o wouldn't have got MS?

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  65. How is the trial going? Have you finished recruiting? When will the results be available? How are things looking?

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