Quote:
Originally Posted by chrishadms
See I think it will work for this reason alone:
Mice and Human DNA is SOOOOOOO close. Very different but soooooooo close.
In those mice they give the Copaxone to they can't give them MS. As well as in Humans, if they are given Copaxone very very early on in this disease a good deal of these people never go past the one flair up they have. In some of the studies with Copaxone they have actually seen Myelin repair in Mice, and people if it is early on in the disease process.
So with that said now that our immune systems have been set right and it's like it was before we all activated. The hope is all the clinical trials of early Copaxone use and how good they went, along with the success of Copaxone in those mice, with healthy immune systems and the Copaxone as a training tool, we will not reactivate.
The folks who have stayed on Copaxone even after if they were treated were the ones who haven't reactivated yet. This compared with the animal data and existing Copaxone data made it perfect sense.
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Interesting theory, and maybe there is something to that.
We do know that animal studies with MS hardly ever pan out the same way in humans . . . how many times have I said I wish I was a mouse?
. . . but maybe they will learn something more about the disease by trying.
The PreCISE trial, which measured the reduced for developing MS, with the early use of Copaxone for Clinically Isolated Syndrome (CIS), showed there was a reduction from 43% (on Placebo) to 25% (on Copaxone). In absolute numbers, that means a reduction of 18% of conversion to MS (with a 16% drop-out rate) . . . which really isn't all that great. However, perhaps combined with the HiCy, the odds will be better.
http://www.medicalnewstoday.com/articles/104462.php
Cherie
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