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In neurological research circles it seems you're nothing unless you have a mouse to back you up. So if this pans out, CCSVI vascular doctors will be able to strut their behinds down the corridors of MS neurology departments, like they owned the place.

Really thousands of humans treated for ccsvi mean nothing,but one mouse! If this pans out it totally negates placebo and pretty well proves ccsvi. Putnam didn't keep his dogs alive long enough to get gait issues so all that he proved is encephalomyelitis. I found it disturbing that this paper didn't mention the lesions, at least in the teaser, but if they're there, that's huge! And stanford lesions are better than lesions from say a state university.they're lesion gold!
Still cece is right, expect disappointment. It has been the norm in m.s. research for a couple of hundred years.

Very interesting to discover here that the Murine Model of MS--MMMS dates back to at least the early 1600's.*

I think we can be fairly certain that the origin was Italian. Had it been uncovered by an Anglo-Saxon scientist, it is doubtful that it would have been announced in song. But an Italian scientist of that era? Probably quite likely since it would be the perfect thing to do between a major medical discovery and say painting a chapel in the Vatican.

So let's break this down:

Three blind mice.

Optic neuritis, no doubt. And we can probably safely assume that they were double blind, n=3.

See how they run

Well, we know how they run: Dragging a foot, stumbling, not very fast or far. But why go into these details in announcing your discovery of a Murine Model of MS?

They all ran after the farmer's wife,
Who cut off their tails with a carving knife,

Okay. Looks like a lot of poetic license here. The lab technician, not the farmer's wife, severed their internal jugular veins, not cut off their tails with a carving knife, but anyone who has ever read the results of a pharmaceutical clinical trial will understand that authors take considerable poetic license in reporting their findings. Same here.

Did you ever see such a sight in your life,
As three blind mice?

The answer is not until another Italian scientist applied his mind to the problem some 400 years later.


* Link is just a place-holder for a real report in the future. :>)

Squeekycat,

Shear brilliance! You're definately a mouser! It must be in your blood!

The current mouse model for MS (EAE) has misled researchers for about 50 years so why are folks so excited about a mouse model for CCSVI syndrome ??? I truely hope that vascular researchers do not waste 50 years on a new mouse model.

MS is far more complex than a mouse model could possibly be, in my seldom humble opinion.

Some postings were very funny but please treat any mouse model of MS only as a joke.

MarkW

if it is a joke why is this study to be presented at the ISNVD conference in March?

If they had such a poor record with EAE, that doesn't mean another model is not valuable. Putnam reported lesions similar to 'MS'. If they appear in mice will we disregard 'MS' lesions altogether, because they suddenly are associated with CCSVI?

In fact I think back in the Sixties there was a model named Murine, who was famous for her eye drops. She may have had neuritis caused by too much frequenting with mice, which was not as frowned on as it is today.

MarkW wrote:The current mouse model for MS (EAE) has misled researchers for about 50 years so why are folks so excited about a mouse model for CCSVI syndrome ??? I truely hope that vascular researchers do not waste 50 years on a new mouse model.

MS is far more complex than a mouse model could possibly be, in my seldom humble opinion.

Some postings were very funny but please treat any mouse model of MS only as a joke.

MarkW

Because researchers created autoimmunity in mice when they saw autoimmunity occuring in humans (EAE). Now, we have the opposite: we have discovered venous insufficiency in humans therefore, we can replicate the same conditions in mice (CCSVI) and see what happens.

If you notice, EAE is good thinking but backwards. Also, animal studies are a huge part of medicine, they are so standard, they can't be disregarded.

CuriousRobot wrote:If you notice, EAE is good thinking but backwards. Also, animal studies are a huge part of medicine, they are so standard, they can't be disregarded.

I agree with this. The mouse model is another bit of evidence and good evidence in favor of CCSVI. CCSVI as a whole has compelling clinical findings but not yet much in the medical literature.

This wouldn't be an animal 'model' but this mouse would have real Ms. Lesions plus a symptom. Revolutionary.

All other factors, genetics, vitamin d, would be disproven. MS ican be caused caused by ccsvi alone.

Billmeik wrote:This wouldn't be an animal 'model' but this mouse would have real Ms. Lesions plus a symptom. Revolutionary.

All other factors, genetics, vitamin d, would be disproven. MS ican be caused caused by ccsvi alone.

Bingo, Billmeik. And the labs at Stanford don't spend this many research hours on jokes. Animal models of disease process are essential. We have them cardiovascular disease and stroke, and those are very important for understanding endothelial dysfunction and nitric oxide disruption, as well as treatments for the same.

Here's Dr. Cooke's research site where he refers to murine models (that's mice) in peripheral arterial disease:

The basic research is focused on induced pluripotential stem cells (iPSCs) for vascular regeneration. We are developing cell-permeant proteins and new chemical entities for nuclear reprogramming, and for differentiation of iPSCs into endothelial cells. Human iPSC-derived endothelial cells are currently being tested in our murine model of PAD.

http://med.stanford.edu/profiles/John_Cooke/

And not to toot my own horn too loudly, but I'm rather proud that I got Dr. Zamboni's research into this department's hands in '08. No false modesty from me
cheer

disproven is too strong a word. Unnecessary. The inference is that if you clamped the veins on a human they'd get MS just as simply.
This is elegant and mechanical and straightforward, and leaves pharma out of the equation so will be challenged as heresy.
Hard to disprove though..

MS can be caused by ccsvi. Point proven.

I suggest folks find out about EAE. It does NOT create MS in mice rather it gives mice 'MS like' lesions, not MS. Most of you disagree with me, that's life. I suggest the mouse modellers at Stanford think very carefully about their model and read the critics of EAE before spending too many years creating CCSVI syndrome in mice which looks like MS.

Group think is sometimes dangerous.

MarkW

MarkW wrote:I suggest folks find out about EAE. It does NOT create MS in mice rather it gives mice 'MS like' lesions, not MS. Most of you disagree with me, that's life. I suggest the mouse modellers at Stanford think very carefully about their model and read the critics of EAE before spending too many years creating CCSVI syndrome in mice which looks like MS.

Group think is sometimes dangerous.

MarkW

Mark, I agree with you that EAE is not MS, and that we should be careful about creating a mouse model before we fully understand the role of CCSVI in MS. Evidence suggests that there is more to MS than just CCSVI. Faulty immune and vascular systems, environmental factors, and possibly other unknown factors would have to find themselves into this new model before it would really start looking like MS. I'm afraid that the models I've been reading about may lead researches down a path that provides less answers than EAE.

Here is an article criticizing EAE as a model for MS. In particular, check out the table on page 3. http://www.direct-ms.org/pdf/Immunology ... ritque.pdf

I'm not too worried about the Stanford folks wasting their time on lesions, as I think they know that EAE lesions are perivascular as well as 'MS' lesions, and that there has been difficulty associating lesion load with disability, anyway. If they are working on an animal model, it probably has a good use.

Even if it can be shown that liberation therapy in a mouse can cure or prevent EAE or lesions, wherever they come from, that in itself is a step that has often been a red herring; a better test might be inducible and treatable disability, or associated atrophy. A disease model that is intractable and incurable is a nasty trick to have played on you. It has also been suggested here that mice are not as appropriate as are primates, because of gravity and locomotion, which could be as important as other reasons speculated about. However proving that stenoses cause similar lesions and/or symptoms to EAE or 'MS' might be revealing, as would be the finding of oligodendrocyte death and immune cells in these cases.

At some point consideration for the individual animals used for such experiments should happen as well.

Maybe EAE and 'MS' lesions are both due to stenoses - they are both perivascular. Maybe we know as little about the pathology of EAE as we do about 'MS'.