Why haven’t we cured MS yet?

What would an MS cure look like? #MSBlog #MSResearch

“The following is my talk from the 5th UCLP MS Research Day. I was asked to answer why we haven’t cured MS yet. As you can see from the slides the experiment is currently running and is a 15-25 year experiment. Are MSers who are rendered with NEDA by induction therapies (bone marrow transplantation, alemtuzumab, cladribine) cured? It is also important to manage expectations and explain that someone who already has MS, but has acquired disability, is cured they may be left with some disability. A cure will simply stop you getting worse; it is not neuro-restoration. The other point I make is that our current definition of NEDA is too restrictive and we need to include markers that address the part of the iceberg we can’t see. I also conclude the talk with the “black swan” and the fact that the autoimmune hypothesis does not explain everything about the epidemiology of MS and that MS  could still be due to a virus.”

“For more defining a cure, please read my previous post; NEDA: defining a cure.”

CoI: multiple

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.


  • Prof G,

    After another commenter mentioned Prof Ebers' theories in a recent comment, I had a read and was wondering if you feel your and his views on MS line up at all? I may be reading this the wrong way, but he seems to believe that any of the current DMTs, no matter how effective against relapses will not affect the overall outcome in MS.

    I thought that even the interferons were able to reduce mortality, which would be considered a pretty hard endpoint. Are your theories completely at odds with his?


    • Re: "….wondering if you feel your and his views on MS line up at all?"

      Not really; Prof. Ebers doesn't think relapses and MRI activity count; I do. Prof Ebers wants the onset of SPMS to be the primary outcome in clinical trials. I agree with him that this would be ideal; but have not idea how we would operationalise it. Prof. Ebers does not support the viral hypothesis of MS. Prof Ebers is also concerned about early effective (aggressive) treatment in MS. Saying this I have heard him being supportive the the bone marrow transplantation in MS experiment.

      Although we agree to disagree on things we did talk a lot at meetings and via email. This is how science works.

      Let's hope he comes out of retirement soon; he is one of the most original and provocative thinkers in the field.

  • The reason why MS isn't cured yet is because too many people are making money from it. The disease is a full-fledged industry with many snouts in the troth. The cash is plentiful and executives are creating pharmacological dynasties out of it. The MS sufferers are largely desperate and stupid people: aching to shift from one promisingly expensive fad to the next. There is huge disarray and derisory foul play in action.

    There is no cure for MS. We're pathetic to think otherwise. No-one even knows why the blasted disease even happens in the first place. Please don't insult our intelligence by making out that these new DMTs are a cure, Prof G.

    • I think you are being cynical and missing the point. If the progression of MS can be contained then a cure has been found I've got SPMS and would be ecstatic if I knew it was not going to get any worse.

      Too many people think that a cure means eliminating MS from the body and repairing the damage. One day that might happen. Meanwhile be thankful that people diagnosed with RRMS now have a chance. When RRMS is diagnosed it is possible to contain multiple sclerosis, stop it getting any worse. Maybe something similar for people with PPMS and SPMS might be on the horizon.

    • Please don't insult our intelligence by making out that these new DMTs are a cure, Prof G.

      Which DMTs?

    • I never said any DMT cures MS; all I said is that the experiment is running and I defined what I think is a reasonable starting point to look if some of our treatment strategies cure the disease. Please don't misquote me.

  • I'm grateful for you sharing the presentation. I could make the research day. I find it strange that the experiment as to whether we have got a cure (from highly effective dmts) will take 2o plus years. In cancer research they seek to understand the disease and then identify treatments. MS research seems to focus on giving patients treatments and then use this to draw some conclusions about the disease. Given this, why do MS researchers both with pathology studies? If MS is due to a virus, why can't it be found in the brain? Will your presentation change in 3, 5, 10 years, or will we still be waiting on the long term follow up of the highl effective dmts?

    • It took almost 50 years to realise that most cases of Hodgkins Lymphoma are triggered by the Epstein Barr virus, and all that time it was already known that Epstein Barr caused other cancers of the lymphatic system. These viruses have the ability to hide from the body and the scientist even though they have become incorporated into the cells. You are also assuming the virus has to be in the brain to have an effect, it could modify something else like the behaviour of the immune cells it infects, and these cells then affect other cells. This is seen in lymphomas.

    • It doesn't take 20 years to evaluate this "experiment". Wiser researchers already know the answer.


      "Effective suppression of inflammation in the face of ongoing atrophy was also observed in the Campath 1H study (Coles et al., 2005). When multiple sclerosis patients were treated with an anti-leucocyte monoclonal antibody (CD 52, Campath-1H), the number of new gadolinium-enhancing lesions was effectively suppressed.

      However, patients with SPMS showed sustained accumulation of disability due to uncontrolled progression marked by ongoing cerebral atrophy. In contrast, patients with RRMS had a reduction in disability 6 months after Campath-1H infusion. This study suggests that once the cascade of events leading to irreversible tissue injury is established, suppression of inflammation does little to slow or prevent ongoing brain atrophy and clinical progression (Coles et al., 2005)."

      MS can be stopped if you are in the relapsing stage. The 20 year experiment won't help anyone in a progressive state. There is no mystery here. The focus should be on a fool proof test for MS to keep people from progressing ASAP as well as neuropotective therapies.

    • Readers may dissociate the potential difference between early verses late (the subject matter of the reports mentioned above that we are well aware of) treatment.

      if relapsing disease conditions progressive disease which it does in animal models of ms then it is a valid argument.

  • Dear all,

    I hope today went well (i coudn't attend). Would be interested if anyone who attended could post a sort para on the main highlight of the day i.e something promising which we hadn't aleady heard of. Thanks.

    • That's all we need a God who has it in for people because they live further from the Equator. Makes the Greek gods look sane.

    • I am atheist, there is no evidence that God exists. Unfortunately, there is plenty of evidence that MS exists.

  • seriously, the video is up already, and I've only just made it home (7pm)!

    A great day, I thought, learned some stuff, got to annoy some people, which is always a bonus, and came away feeling a lot more positive about it all. And all geared up for the imminent hopefully not too bloody battles with my neuro about getting regular MRIs, and more treatment options.

    And a special thank you to Samantha, who said she 'only' did admin for your team, there as a volunteer, kind and funny, and I had a lovely chat with her when I skipped out in the afternoon for a break.

  • Prof G,

    How would you describe the sort of work being undertaken by Prof Franklin and colleagues in Edinburgh – is this work about neurorestoration? My definition of a cure involes getting something back e.g . Walking faster, being able to play tennis again. I wish th researchers could get a sense of the losses this disease causes, maybe then they would aim a bit higher than just stopping the disease getting worse or slowing down progression.

    • If you dont stop the process, repair is a plaster or logs on a fire. It is part of a multipronged approach.

      repair to myelin is one aim and the repair to nerves is another aim this much harder as the body has designed a system to stop this happening

  • Profs,

    Grateful for all your work. I suppose what I and I'm guessing everyone else with this disease wants is to get better. I can think of lots of diseases where this is the case. I don't really see this aim as being part of the current research. It all seems a bit tippy-toeing around the issue. Using David Cameron's phrase relating to a different issue – we should become more muscular about the issue. MS research is taking too long (the 25 year experiment wit h highly effective DMTs is a classic example). Given that one research paper said that th average life expectancy after diagnosis is 30 years, the 25 year experiment will be of little value to those with the disease today. I'd like to see some drive to make a real difference to Current MSers. Not just from ateam G but from CAmbridge and Edinburgh. There seems to be a lack of real collaboration (academic egos?) and a tendency to drive up deadends (simvastin a good example).

    • I think the UK is one of the most collaborative places on the planet, in terms of its MS medical machinery.

      Driving up deadends is part of research.

      The simvastatin is another issue and this relates with the capacity to deliver treatments after trials….

    • Is it really fair to call the Simvastatin trial a dead end? If its results are real, it has to be one of the biggest advances in secondary progressive MS yet discovered.

      I'd love to know if there's enough money around for a number of MS charities (from wherever in the world) to collaborate to pay for the phase 3 trials required – do these charities ever collaborate?

  • Somebody complemented, or criticised, me for getting a designer to make my slides. Unless, I am presenting commercial trial data I tend to make all my own slides. I also borrow slides from other people and adapt them. If I do the latter I usually acknowledge them. It takes me hours to prepare my presentations.

By Prof G



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