EAE in mice vs. the new Stanford animal model of CCSVI by Dr. Michael Dake
May 17, 2011 at 7:39pm
Here is part of Dr. Dake's lecture from the Hubbard Foundation conference:
First, Dr. Dake explains how the current model of EAE is created in mice. It is a rather convoluted procedure--
"There's an animal model, but it's not really, unfortunately, like most animal models, it's not really a human model. Basically, you take like a mish of ground up spinal cord and brain from some other species, you mix it with some oily substance, some TB bacilli, and some bordadella pertussis, some whooping cough toxin, and inject into peridium, and what you get is this whopping inflammatory response, and that's good because you get the accelerated disease process, but obviously in humans, it's a much more chronic and progressive thing.
So, what we've done is taken mice and ligated (the jugular veins) and we're going to move now up to marmosets, because that's the next level of the species, and marmosets you can actually partially occlude the veins and keep them open without totally ligating them.
And these mice and their veins, we've got a recipe that we think is right where we want it. We're starting to see not only clinical performance differences between mice that are ligated and mice that aren't ligated, but now there's a way to tomographically, in a little mouse brain, to make these wafer thin micron sections thru the whole brain and we're learning a whole lot. I think it's going to be very interesting as we move up to a larger model to really see....but we think that we're seeing an accentuation of the venous ligation on the disease process."
No words to describe how much I respect this man. He listened to us and was interested, treated my husband's venous malformations, and continues to speak out on CCSVI. Thanks, Dr. Dake.
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