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
"






Labels: