Wednesday, 21 December 2011

Guest Post: John Prineas

In relation to a heated Thread on Pathology

You wrote: "I wonder how your Prof Prineas wouls react to the manner in which you are using his work"

So as you want posts from Guest Experts I decided to ask "How Prof Prineas would react to the manner in which his work was being used"

so I wrote

"Dear Professor Prineas
I hope that you don't mind this intrusion but the reason I am writing to you is that I ( a basic
scientist. We met in Cambridge once) contribute to a research BLOG for MS patients and their families. One of the things that often occurs in comments about postings is that your previous research on the findings that early lesions of MS appear to have oligodendrocytes damage and few immune cells, is often used as support for the concept of CCSVI or a (structural) vascular deficit. I was wondering if you have a few moments to write a few (lay words) words in support of or against the above thought. I am know that our readers would really appreciate your views on this topical matter.

Hoping to Hear from You".

John Prineas is one of the World's Most Respected MS Pathologists and Sends his comments from Australia

John Prineas wrote
"I apologise for not replying sooner to your email re path studies of MS that have been used by some to support CCSVI and the possibility of a vascular structural defect in MS.

If oligodendrocyte injury with few inflammatory cells present was the only or main feature characterizing the MS lesion, perhaps such a possibility might be worth discussing.

However there is absolutely nothing else about the very complex pathology of the evolving MS lesion that even remotely could be considered to support the sort of vascular pathology that has been proposed.

The vascular pathology in MS is quite typical of inflammation as it occurs in any solid organ i.e. with respect to structural changes and upregulation of all of the mediators expected in an immune mediated disease. Also there is no experimental or naturally occurring type of vascular lesion known that can cause the extraordinarily selective and permanent loss of myelin typical of some inflammatory demyelinating diseases.

Also important is the fact that veins of all sizes in and around MS lesions look absolutely normal, or show changes only of a type seen as mentioned above in any inflammatory disease.

I must say that instead of supporting the idea that there is a structural change in veins anywhere that could contribute to lesion genesis in MS, the pathology of MS argues very strongly against such an idea.

Again , sorry for not replying sooner.

John Prineas


  1. Vasilis Vasilopoulos, I was worried that you might feel obliged to retort on this subject. It's been so nice and quite on this blog for the last few weeks and that is mainly because you've not been starting fights with the folk who run the site.

    No Vasilis Vasilopoulos, you 'may not' take us down this path again. You do it all the bleeding time and I am sick of it. Your rantings leave me and most othe readers confused. You're taking attention away from serious matters in order to shine the light on your meaningless CCSVI crusade.

    We're not interested. If you want to hark on about the virtues of CCSVI then start your own blog. Dont to it here.

  2. Awesome! Thank you MouseDoctor and Dr. Prineas! Last year, I had printed out an article that he had authored, "Relapsing and Remitting MS: Pathology of the Newly Forming Lesion". I didn't understand it when I first read it but I'm hoping that what I learned in Immunology this year will enable me to understand it this time.

    And I want to second Carol's comments. I too, noticed that the blog has been a more pleasant site to visit since VV was gone, but I was afraid to say anything for fear my comments might provoke a response. Unless you have the same medical expertise as MouseDoctor or Dr. Prineas, I'm not interested in reading any woefully misinformed CCSVI rantings. And no, having MS does not make you a MS expert, just an expert in YOUR MS.

  3. VV, I agree with what you said once that it's sad MS'ers are so divided. I wrote 'wonder what Prof Prineas would think...' because your comments were extremely irritating (never thought it would lead to this!) There's no reason to doubt the intelligence of the experts or their commitment to fighting MS and I'm not at all surprised by Prof Prineas's reply.

    Prof B is the right person to reply to 'May I?' My guess is you'll say that Prof Prineas's findings are useful but his conclusions from them as regards CCSVI are wrong.
    I think amateurs fishing around for anything that supports something they want to believe are much more likely to be wrong.

  4. Now we have a cliff hanger, it looks like Prof B has gone too,

    Can VV wait until 2012 for an answer?

  5. Now that the dust has settled, i should have a word:
    Prof Prineas work was never referenced as supportive of any vascular theory of MS, but as a proof against the autoimmune hypothesis. Too bad this point was not reflected in the message sent to him, too bad he didn't comment on it.

  6. The message sent was a direct response to points/questions made by bloggers. These were unrelated to autoimmunity, so it is not surprising he was not asked about this and it is not surprising therefore that he did not comment on autoimmunity, just as he did not comment on the EBV hypothesis or what I had for breakfast etc.

    If you post cryptic comments/questions you get cryptic answers. A case for autoimmunity for could accommodate the lesions seen by Prineas but that will need to wait until Dr Love goes back to Pathology in MS.

    Anyone who read the BLOG can see that alternatives to the autoimmune hypothesis exist.

  7. VV you expect too much if you want Team G to read between the lines and get what you are trying to say.
    Prof Prineas is very much in the neurology mainstream. His views on autoimmunity are most unlikely to match yours

  8. "Too read between the lines" does not sound very scientific to me. I appreciate this being a science blog.

  9. Prof Prineas was specifically asked to comment about an alleged connection of his results with a vascular pathology. Not me, not anyone else implied that his work supports that kind of pathology. It was your initiative to put the question that way.

  10. VV
    I think you forget what you imply and what you don't, buts it's funny that for you everything is either rubbish because it doesn't support CCSVI or it obviously does support CCSVI in ways too obscure to go into.
    Now lets move on.

  11. prof prineas is the sort of person who will answer the question directly and not twist or confuse the issue.

  12. Anonymous Case Lawyer said...


    Then Link DELETED (MAybe post was well meant but this is how you get virues on your computer)


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