Dr. Alasdair Coles: Guest Spot. Long-term follow up of CAMPATHers

You asked “Regarding a Cure; The earliest MSers to be treated with alemtuzumab were in the 90’s. Even if there were only a handful, have any of them progressed yet?”

Prof G said “At some stage we will have to ask Alastair Coles to post on this issue”.

So why not now, so we have passed on the question of one of the A’s from Cambridge and wrote “I was wondering if you are able to make any comment for the blog on your experiences on the long-term follow-up of CAMPATHers”.

Revd Dr Alasdair Coles, yes a neuro ordained in 2009, wrote

An excellent question. We are in the business of trying to get just such an analysis together for a paper……Should have news in a couple of months

Without the persistance of Alasdair Coles and Alastair Compston, I doubt that CAMPATH-1H, (the worlds first humanised monoclonal antibody)/Alemtuzumab/Lemtrada would be on the MS agenda. This drug has told us a great deal about the disease already and has more to offer.

However as you know, if Dr. C has the answer in a few months it will take about 6 months to a year to hit the newstands. However as Neuros often present at meetings before the paper we may get to hear more. We will keep you posted.

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  • Mouse,

    I've heard that campath is good at reducing relapse. You say it has told us things about MS. Can I ask what sort of things.

  • Yes it is very good at reducing relapses.

    "Can I ask what sort of things".

    (a) Relapses are caused by the action of the immune response

    (b) You can make much greater impact on relapse than the intial first line therapies

    (c) Removing large parts of the immune system can have consequences

    (d) MSers have an altered immune system, so when it reboots after treatment it gives a different response to say people getting campath for cancer.

    (e) Progression is not caused by the same action of the immune response that inhibits relapse. Therefore we need a different strategy for progressive MSers

    (f) There are things in immune cells that block nerve impulse transmission.

    (g) If you stop relapses early enough it allows repair mechanisms to kick in an reverse deficit (With the proviso that this could be a direct Alemtumab effect)

    (h) Injection of proteins can lead to anti-protein response.

    (i) Drug companies see MS as a cash cow….although they could prove me wrong with sensible pricing structure.

    (j) University generated ideas can make it and make cash for the inventors.


  • Mouse,

    Thanks for the detailed reply. You shouldn't be working so late. Hope you took Mrs Mouse to the local Indian and bought her a single rose.

    Hope Prof G is feeling better. I'm betting he enjoys the Jeremy Kyle show when he's stuck at home.

  • Re "Relapses are caused by the action of the immune response"

    The fact that immune response suppression leads to fewer relapses does not necessarily mean that relapses are the direct manifestation of the damage itself. It only means that they are the manifestation of the immune response, a secondary sign of the damage.

    So, reducing relapses could be just a futile attempt to silence the signs of the damage, but not the cause of damage. Proof for this:
    1.The weak correlation between number of relapses and long term disability in the natural history of MS.
    2.The inability of DMDs to halt progression in the long run.

  • If you think the immune response is irrelevant then you have the option not to take immunosuppressive DMD..I would not do that.

    DMD do not appear to halt progression when started late in MS and animals, we do not know what happens when this is treated early in MS. Based on the phase II data with alemtuzumab then there is physical improvement. Time (about 15-20 years) will tell about the rate of progression or not.

    In animal autoimmunity it is clear.

    Treat late and progression continues despite no relpases, treat early and the diseability is stabilised and it will take along time or more like never that they accumulate the deficit that is accumulated due to relapsing attacks.

    However some nerve damage will occurr even from the earliest
    phases. Therefore we need early treatment to deal with inflammation and neurodegeneration

    Although development of disability may not correlate with the number of relapses at the population level, disability is correlated with the degree of relapses in early disease activity in MS

    In animals.

    Do the number of relapses have to correlate with the degree of disability…NO. One strain of animal can accumulate as much damage after one or two attacks that takes another strain four attacks. However are the relapses associated with accumulated disability. Absolutely yes. So is stopping relapses important?.

    Well I think yes. I met one of our Mser teachers recently and that person had wanted to go on alemtuzumab and missed out. That person had a few relapses before eventually getting on alemtuzumab and having no relapses subsequently. Try telling this person that the permanent disability that was accumulated whilst waiting to get on alemtuzumab is not caused by the relapses.

  • We have agreed before that mice don't get MS, so any paradigm from the lab is simply irrelevant to human MS.

    Betaseron has been proved inefficient in the long term. Testing alemtuzumab in early MS proves nothing since early relapses usually leave no trace.

    You keep connecting inflammation with neurodegeneration when so such connection has been proven in MS. I doubt exactly this: Inflammation accompanies the cause of the damage in a purely natural way. But it is that unidentified cause that leads to deurodegeneration, so however early or effectively you suppress inflammation you will not get away with neurodegeneration. Unless you can prove that such a cause is non-existent you are wrong in targeting the immune system.

  • VV
    Whatever we say and no matter how much we explain things, you have a blinkered mind. No-one is saying that inflammation is the only story but it IS a major player. Just to say people are wrong is insulting.

  • Re "You must have missed this post:"

    I believe you are referring to this:

    That's a press release. I couldn't find the published study. Nevertheless, i think many things were different during those 21 years, apart from receiving or not betaferon. Moreover, could you explain the difference between "mortality" and "risk of mortality"?
    And then, what about the following post?


  • Dear Andy

    Please check out our post, when we discussed the paper in February


    As you may realise this study was geared to recreate the John Prineas lesions in MS and show oligodendrocyte loss and then see if that is the cause or trigger of autoimmuntiy it was not.

    Is this the end of the autoimmune hypothesis…maybe not, because a negative could mean they missed something. They should perhaps have done it on a NOD mouse background which at least has the genetics to get spontaneous autoimmune disease.

    However we know the authour of the paper is reading the blog so I wont say anything about it.,..you can make your own mind up..which you may done already.

    Many people, including Prof G and may I add the people who have reviewed and binned my idea for a grant application, think the autoimmune hypothesis is mushroom food.

    A shame as the study was the closest thing I have done towards developing a cure (no joke).
    …if my ideas were right.

    Now you can see why progress is slow. Loads more time down the toilet.

    Oh well tomorrow is another day.

  • This 62 year old Grandma is totally overwhelmed by all this info (attention span of a gnat ) but would like to know if age 62 is too old to be diagnosed with MS? MRI shows 2 lesions on my brain and my drs are telling me nothing.

    • Not too old at 62. Just more unusual. I guess if I was being generous, your neuros might be taking the wait and see approach before committing themselves.

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