Tuesday, 12 June 2018

NIH Charcot Lecture 2018

I delivered my Charcot lecture at the Washington Press Club, to approximately 125 people, last night. My main message was that there are compelling reasons to do MS prevention studies and if we don't start them ASAP we will be letting down the next generation of people who will develop MS. I view this as a ticking time bomb. The continual increase in the incidence of MS across the world, particularly in places like Scotland and central Canada, indicates that we have an epidemic on our hands. Don't you think we need to do something about it?

Thank you for completing the MS prevention survey; I included the results in my talk and one very touching and poignant quote.

As promised I have uploaded my slides onto SlideShare. I hope you can follow the thread.



  1. SLE and RA seems to deteriorate with HAART while MS seems to improve. Interesting, isn't it?

  2. "Innate immune activation is a hallmark of the active ms lessions"

    Rituximab is very good at clearing "active ms lessions"

    So Rituximab works on the innate immune system?


  3. "Typically, the onset of clinical disease was acute and progressed rapidly with the median time between presentation of disease to humane euthanasia being 6 days (range, 0 days-121 days)."


    This is the macaque disease. No clinical resemblance to MS. Therefore, biological resemblance and reasoning by analogy of Bradford Hill criteria should be NO.

  4. "Innate immune activation is a hallmark of the active ms lessions"

    In multiple sclerosis lesions, we found a dominance of CD8+ T cells and a
    prominent contribution of CD20 + B cells in all disease courses and lesion stages, including acute multiple sclerosis cases with
    very short disease duration, while CD4+ T cells were sparse.

    Our data underline the potential importance of CD8 +
    T lymphocytes and B cells in the inflammatory response in established multiple sclerosis lesions. Tissue-resident T and B cells may
    represent guardians of previous inflammatory brain disease, which can be reactivated and sustain the inflammatory response, when
    they are re-exposed to their specific antigen.

    The compartmentalized inflammatory
    response in the multiple sclerosis brain is
    composed of tissue-resident CD8+
    T lymphocytes and B cells




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