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In humans, active periods of the debilitating disease Multiple Sclerosis (MS) can last for mere minutes or extend to weeks at a time. They're caused by lesions in the brain that develop, partly heal, and then recur.

Research into a cure has been difficult, because to date scientists have not been able to replicate these brain recurring symptoms in laboratory mice. That's frustrating because these lab animals, known as animal "models," are the primary tool for research into the mechanisms and potential treatments for MS.

But now, by using a mouse model for diabetes instead, Dr. Dan Frenkel of Tel Aviv University's Department of Neurobiology, working alongside Prof. Yaniv Assaf and Ph.D. student Hilit Levy, may provide a surprising breakthrough for research into a cure for MS.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1845

mmmm Isn't that what copaxone is??? Its meant to be a myelin copy so how can studies show this diverts the immune system from attacking myelin whereas this study suggests it makes the immune system attack Myelin?? Confused.com

LR1234 wrote:mmmm Isn't that what copaxone is??? Its meant to be a myelin copy so how can studies show this diverts the immune system from attacking myelin whereas this study suggests it makes the immune system attack Myelin?? Confused.com

I think what this article is saying is that these researchers developed a mouse model that mimics MS better than the traditional mouse model, EAE. Mice can only develop EAE if injected with myelin protein that is in an adjuvant. And it was shown that just injecting the mouse with myelin protein, without the adjuvant, would actually protect it from developing EAE. Incidentally this was tried in humans by Jonas Salk, among others, in the 1970's. They tried injecting people with MBP to see if it would cure their MS.

It looks like these researchers found that if they inject only myelin in a mouse that also has type 1 diabetes, it would develop some sort of neurological disease (though it doesn't say why this combination). And, according to the article, it sounds like this mouse disease imitates MS better than EAE, with a relapsing-remitting nature and brain lesions.

By the way, I think more recent research has shown the "myelin imitation" explanation for how Copaxone works might be an over-simplification. I've been told and have read that Copaxone has effects that shift the T-cell response to one that isn't inflammatory (of course this too might be an over-simplification).

Thanks for the explanation Patientx....Sometimes its so hard to decipher these studies and what they actually mean to us MSers x

LR1234 wrote:Thanks for the explanation Patientx....Sometimes its so hard to decipher these studies and what they actually mean to us MSers x

Definitely. Of course, that's my interpretation of the article - I could be way off base. I'm curious to know how these doctors came up with the combination of injecting myelin in diabetic mice.