MS, CCSVI and Animals

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

MS, CCSVI and Animals

Postby cah » Wed Dec 23, 2009 2:11 pm

Hi,

the mouse model and the fact that animals don't have MS was mentioned time and again in different threads, so I took the liberty to make a new one instead of choosing one of them. Especially the question why there's no animal MS was discussed in the german csvi-ms.net forum some time ago. Here are some statements made there.

There are three main questions concerning MS, CCSVI and animals:

1. Could the CCSVI Paradigm explain why there's no MS among animals?

2. Could there be a animal model for CCSVI?

Of course I cannot come to a definite answer, but there's some common knowlegde which might give a clue. (Translated) from german Wikipedia (I always wonder why the articles are so different in both languages): "The external jugular vein is a vein in the cervical area. It runs directly under the skin, in animals inside of the Sulcus jugularis..."
Seems that there is no Sulcus jugularis (jugular channel) in humans.

And further: "The external jugular vein is significantly bigger as the internal jugular vein in animals. This vein is used in many species for intravenous blood withdrawal. Permanent catheders are placed here as well, whereas the internal jugular vein is used for that in humans."

And another naive yet compelling thought from the german thread: "Animals don't lay down as humans do. They don't sleep on their back. Usually, when animals lie on their back, their dead."
Inclined bed therapy for mice? Ridiculous.

I don't know exactly but what is clear is that the anatomical situation of the cervical veins is completely different in animals and humans. Whereas the immune system is pretty much the same...

I think it's really hard to reproduce the outcome of jugular vein stenosis on animals.

But for the third big question I don't have even the tiniest clue:

3. If diagnosis on humans is quite simple and save and if there are enough volunteers for treatment, why the heck has it to be tested on animals???
"There is only one good, knowledge, and one evil, ignorance." Socrates
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Postby Billmeik » Fri Dec 25, 2009 11:58 pm

in general the animal model for MS is called EAE.
Thats experimental autoimmune encephalomyelitis..

To create it you take some nervous system tissue from a different species and tranfer it to the test animal. So it is a kind of allergic reaction to this. Really it has nothing to with MS.


Now is there animal studies of ccsvi? Hmm Cheerleader suggested these were coming, while Ashton Embry was maybe referring to animal tests that failed?

In Zambonis paper he talks about eae and how useless it is as an animal model.

I have my doubts about animal ccsvi but if a study reported it it would surely help.
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Re: MS, CCSVI and Animals

Postby NHE » Sat Dec 26, 2009 2:46 am

The SJL/J mouse used for EAE research is really screwed up to begin with and has many problems in addition to a susceptibility to acquire EAE, e.g., spontaneous cancers and myopathies.

http://www.thisisms.com/ftopicp-12025.html#12025

To me, this suggests that it's a poor model for MS research. In contrast, I remember reading about a new model that was being developed which also involves B cells which might be a better model (I can't find the thread just now, I'll have to do a little digging).


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Postby ozarkcanoer » Sat Dec 26, 2009 7:37 am

It is my understanding from earlier posts on this board (by cheer maybe?) that someone at Stanford is in the process of trying to develop a mouse model of CCSVI in mice. If the mice get MS lesions then that would be a way to bolster the CCSVI theory and scientists would have a better model for MS !!

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Postby cinder21 » Sat Dec 26, 2009 8:02 am

that would be great!!!
22 yr old male located in the caribbean. Suffering with MS like symptoms from early 2008 with multiple relapses under my belt with optic neuritis. Not dx'd as yet however. Hope is to ultimately be tested for CCSVI
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Animal Models Nerve regeneration History

Postby AndrewKFletcher » Sat Dec 26, 2009 8:24 am

In the early 1940s, a future Nobel laureate, Roger Sperry, then at the University of Chicago, revived the research into chemical guidance of growing and regenerating axons. Sperry would later be called “the rebellious graduate student” because he began these studies while still working on his doctorate and challenged the views of his teachers, among them some of the strongest proponents of the physical guidance idea.7 He devoted more than a decade to nerve regeneration studies in fish, frogs, and salamanders and showed that growing nerve fibers did not follow a fixed mechanical path but appeared to carry chemical labels that enabled them to sort each other out.

In one of his most famous regeneration studies, Sperry showed that even when regenerating fibers are artificially deflected from their course, they adopt tortuous routes and find ways to grow back to their normal targets. In one experiment, he cut the optic nerve of a frog, which, unlike that of mammals, can regenerate and restore normal vision. He then rotated the eye 180 degrees, waited for the nerve to regenerate, and submitted the frog’s vision to a simple test. When presented with a bug, the frog flicks its long tongue to snap its favorite delicacy; if it can see well, it won’t miss. Sperry found that the regenerated optic fibers from the frog’s rotated eye followed a roundabout route to their original targets in the brain. For example, the axons from what had originally been the bottom side of the retina restored connections with the part of the brain normally responsible for receiving signals from the bottom of the retina. As a result, the frog now saw the world upside down and backwards; the floor appeared to be above its head and the ceiling below, and on the vision test the frog acted accordingly: It erroneously flicked its tongue downward to catch the bug above its head and upward to catch the bug below. The preprogrammed wiring had been restored with ruinous consequences for the frog’s ability to feed itself. These results suggested that the axons did not follow a predetermined mechanical path but searched out the appropriate target, apparently guided by chemical cues.
http://www.dana.org/news/cerebrum/detail.aspx?id=2852
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Postby frodo » Sat Dec 26, 2009 8:32 am

Billmeik wrote:in general the animal model for MS is called EAE.
Thats experimental autoimmune encephalomyelitis..

To create it you take some nervous system tissue from a different species and tranfer it to the test animal. So it is a kind of allergic reaction to this. Really it has nothing to with MS.


Not only that. Even after the autoimmune reaction mice do not develop EAE. A special substance called an adjuvant has to be injected to open up the BBB. No immune theory of the the BBB breakdown has ever been presented and nobody has ever cared about this "little" detail.
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Postby cheerleader » Sat Dec 26, 2009 1:53 pm

ozarkcanoer wrote:It is my understanding from earlier posts on this board (by cheer maybe?) that someone at Stanford is in the process of trying to develop a mouse model of CCSVI in mice. If the mice get MS lesions then that would be a way to bolster the CCSVI theory and scientists would have a better model for MS !!

ozarkcanoer


yup....docs at Stanford are trying to give mice CCSVI. They'll let us know when and if they do.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: MS, CCSVI, and Animals

Postby NHE » Sat Dec 26, 2009 2:17 pm

frodo wrote:Even after the autoimmune reaction mice do not develop EAE. A special substance called an adjuvant has to be injected to open up the BBB.


I believe that the normal use of the word adjuvant with respect to vaccinations is...

Webster wrote:a substance (as one added to a vaccine) enhancing the immune response to an antigen


...and not something that specifically opens up the blood brain barrier.

For example, it used to be popular in research to link an antigen of interest to a foreign protein such as keyhole limpet hemocyanin (KLH) in order to enhance the immune response and generate antibodies against the antigen of interest. However, subsequent research has demonstrated that much of antibodies produced can be directed against KLH and not the desired antigen.

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Postby Johnson » Sat Dec 26, 2009 4:45 pm

Andrew K Fletcher & NHE,

Both posts were fascinating to me. I like quirky inspirations. Thanks.
My name is not really Johnson. MSed up since 1993
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