This Is MS Multiple Sclerosis Community: Knowledge & Support

In the hopes that someone will replicate Putnam, I looked into if anyone has done a mouse model for chronic venous insufficiency, the condition most similar to chronic cerebrospinal venous insufficiency.

Yes, they have.

http://www.jvascsurg.org/article/S0741- ... 9/abstract

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"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition

Wow. It seems that the model did not involve the brain, but the relationship with "inflammatory cascades" and treatment with "free radicals scavenging" is really impressive.

By the way, the link is not clickable. Try to add http:// at the beginning

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You can get a worldwide list of available sites for CCSVI at http://www.ccsviclinic.info

Link is still broken! I tried.

Would the inflammatory cascades and free radicals scavenging happens in the same way in CCSVI? This is inflammation within the veins.

One of the differences between CVI and CCSVI (besides proximity to delicate brain and spine tissue!) is the effects of gravity on a condition at the bottom of the body, where blood needs to be pumped up a good distance, and at the top of the body, where gravity is working with us. (We would all be in even worse shape if our brains were in our feet. ) Not sure how this affects any comparisons.

This article also talked about in CVI how one blockage causes blocked up blood which causes a further-up valve to blowout...I raised this question in DrS's thread and he did not think much of this was going on in CCSVI, that the valve issues in question are predominantly valvular malformations not secondary blowouts.

The main thing I took away from this article is that making a mouse model is easy enough for CVI. They can occlude the veins or ligate them or whatever the third way was. I don't see doing this in a brain-draining vein as being that different. The difficulty would be in creating the right degree of occlusion, so that a longer-term effect can be seen; MS takes on average 30 years to show up. The other concern might be the structure of the neck and if that affects brain drainage in a mouse as compared to a human. I will look and see if there are mouse models for cerebral thrombosis or that sort of thing can tell us anything.

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"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition

I was thinking about the lifespan of mice and found that they average 2 years in the lab.

Not very good for a disease that might take 30 years to show itself... how would we speed up the disease progression in mice?

Is this why Putnam used dogs?

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If you can't explain it simply, you don't understand it well enough. - Al Einstein

Well. Keep us informed if you find something!!
About the link, try to remove the URL tags. It should work anyway, but just in case.
If not, the link is here, just to make things easier

http://www.jvascsurg.org/article/PIIS07 ... 9/abstract

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You can get a worldwide list of available sites for CCSVI at http://www.ccsviclinic.info

Putnam's dogs showed lesions in nine months, didn't they?

I suppose it doesn't have to be perfect: EAE is by no means a perfect MS autoimmune mouse model, yet it sufficed.

There's got to be someone working on this, wouldn't you think? Or is it that IRs are the ones taking up the cause and IRs don't do mouse research?

(frodo, thanks for the help with the link.)

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"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition

I though Stanford was looking into this

http://www.thisisms.com/ftopicp-82755.html#82755