Elswhere in this forum there is an article from Australia that is getting alot of reading, and which is VERY interesting in light of CCSVI. http://www.thisisms.com/article63.html It says essentially that MS may not be an auto-immune disease after all, but is a result of oligodendrocytes dying for some other reason and the immune response is what has been inturpreted as autoimmunity. Could the "other reson" be poor cirrculation, i.e. CCSVI?
What is it with thes Aussies thinking outside the box so well? Maybe because they have to look at the world upside down.
Convergence of new thinking about MS!!
- fogdweller
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Re: Convergence of new thinking about MS!!
That kind of ties in with Marc's meeting with the Myelin Repair Foundation people and some of their comments concerning this:fogdweller wrote:Elswhere in this forum there is an article from Australia that is getting alot of reading, and which is VERY interesting in light of CCSVI. http://www.thisisms.com/article63.html It says essentially that MS may not be an auto-immune disease after all, but is a result of oligodendrocytes dying for some other reason and the immune response is what has been inturpreted as autoimmunity. Could the "other reson" be poor cirrculation, i.e. CCSVI?
What is it with thes Aussies thinking outside the box so well? Maybe because they have to look at the world upside down.
http://www.thisisms.com/ftopicp-78354-.html#78354
Of course that's just one of the possibilities when speaking of oligo death, the other being reflux+tight junctions separating+iron deposition=oligo death, followed by immune system cleanup which then takes out the myelin, and that is open to correction and oversimplified....
Or like Marc's post, do the oligo's die first THEN release their iron content, or does the iron get in there and kill the oligos? Ouch my brain hurts.
It's going to be an intriguing couple of years up ahead...
Mark.
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap
- Ruthless67
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Hi fogdweller and CureIous,
Isn't this all so facinating! I'm enjoying learning and investigating all this stuff. And when we can start connecting the dots, it's amazing!!
Here's another article along the same lines of thinking.
http://www.mult-sclerosis.org/howms.html
Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become. In some ways, it is fair to say that multiple sclerosis is a disease of oligodendrocytes.
Recent research has looked at the brains of people who have died in the very early stages of MS lesion development and found that oligodendrocyte death actually precedes inflammation [Prineas et al, 2004]. It must be emphasised that these are the results of a very small study which have not yet been reproduced. Although few would deny that the inflammation contributes to MS damage, this work has the potential to turn the world of MS research upside-down. It suggests that looking for an autoimmune cause for MS may be misguided. It also challenges the current anti-inflammatory focus of most MS therapies. Are we, by analogy, treating a broken pipe by sticking a bucket under it rather than fixing the leak? That's not to say that these therapies don't produce results, just that tackling inflammation may not be the optimal stategy. For people with MS, this is a space to watch eagery.
Lora
ps: I wonder if they are speaking of the same young lady? The year is right; 2004.
Isn't this all so facinating! I'm enjoying learning and investigating all this stuff. And when we can start connecting the dots, it's amazing!!
Here's another article along the same lines of thinking.
http://www.mult-sclerosis.org/howms.html
Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become. In some ways, it is fair to say that multiple sclerosis is a disease of oligodendrocytes.
Recent research has looked at the brains of people who have died in the very early stages of MS lesion development and found that oligodendrocyte death actually precedes inflammation [Prineas et al, 2004]. It must be emphasised that these are the results of a very small study which have not yet been reproduced. Although few would deny that the inflammation contributes to MS damage, this work has the potential to turn the world of MS research upside-down. It suggests that looking for an autoimmune cause for MS may be misguided. It also challenges the current anti-inflammatory focus of most MS therapies. Are we, by analogy, treating a broken pipe by sticking a bucket under it rather than fixing the leak? That's not to say that these therapies don't produce results, just that tackling inflammation may not be the optimal stategy. For people with MS, this is a space to watch eagery.
Lora
ps: I wonder if they are speaking of the same young lady? The year is right; 2004.
Oh I'm sure they are, and of course we are just resurrecting some oft-talked about topics and examples in here, along with our fearless leader's astute research, so not trying to act like there's a big aha here BUT, it deserves as much talk as we can give it too... Thanks a bunch for the read, there's always much to learn and this is a printout to be sure!Ruthless67 wrote:Hi fogdweller and CureIous,
Isn't this all so facinating! I'm enjoying learning and investigating all this stuff. And when we can start connecting the dots, it's amazing!!
Here's another article along the same lines of thinking.
http://www.mult-sclerosis.org/howms.html
Lora
ps: I wonder if they are speaking of the same young lady? The year is right; 2004.
Here's a very good thread with all our resident brainiacs on board from when I first started:
http://www.thisisms.com/ftopicp-63222-o ... html#63222
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap
The paper you reference "Pathology of a newly forming lesion" by Barnett and Prineas came out in '04 . It is important work for us and has been referenced several times because it does show that the AI model is probably not as sure as they seem to. It is one of my favorite papers and I own a copy.
You may find as I did that your neuro never heard of it.......... depressing.
It takes knowledge of these types of papers to be open to the CCSVI model. Without awareness of this kind of literature you might think that the AI model is pretty certain.
It is a good paper and thanks for bringing it up.~!
You may find as I did that your neuro never heard of it.......... depressing.
It takes knowledge of these types of papers to be open to the CCSVI model. Without awareness of this kind of literature you might think that the AI model is pretty certain.
It is a good paper and thanks for bringing it up.~!

I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
If anybody wants to see more of Prineas et al's latest work, Prineas did the "Charcot Award Lecture" at this year's ECTRIMS conference, the content of which is described a bit at the thread below (his focus has shifted a bit from oligodendrocytes to astocytes based on some NMO findings): http://www.thisisms.com/ftopicp-68302.html
Also, there is a webcast of the lecture if you're interested: http://www.sessions2view.com/ectrims09c1/
Last but not least, there is a lot of good discussion about this and related topics here (sorry, I always bring up this thread, but it's a classic): http://www.thisisms.com/ftopict-3707.html
Also, there is a webcast of the lecture if you're interested: http://www.sessions2view.com/ectrims09c1/
Last but not least, there is a lot of good discussion about this and related topics here (sorry, I always bring up this thread, but it's a classic): http://www.thisisms.com/ftopict-3707.html
Hey there's some good Lyon quotes in that last one! ;) Thanks for the links will toss em in the to-do pile...dignan wrote:If anybody wants to see more of Prineas et al's latest work, Prineas did the "Charcot Award Lecture" at this year's ECTRIMS conference, the content of which is described a bit at the thread below (his focus has shifted a bit from oligodendrocytes to astocytes based on some NMO findings): http://www.thisisms.com/ftopicp-68302.html
Also, there is a webcast of the lecture if you're interested: http://www.sessions2view.com/ectrims09c1/
Last but not least, there is a lot of good discussion about this and related topics here (sorry, I always bring up this thread, but it's a classic): http://www.thisisms.com/ftopict-3707.html
Mark.
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap