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PostPosted: Mon Apr 30, 2012 6:01 am 
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Scientists claim to have discovered that the progress of debilitating disease multiple sclerosis could be slowed or even stopped by blocking a protein which contributes to nerve damage.

An international team has shown that the key role played by the collapsing response mediator protein 2 (CRMP-2)) in the development of multiple sclerosis (MS), the `Brain` journal reported.

In their research, the scientists found that a modified version of CRMP-2 is present in active MS lesions, which indicate damage to the nervous system, in a laboratory model of MS.

The modified CRMP-2 interacts with another protein to cause nerve fibre damage that can result in numbness, blindness, difficulties with speech and motor skills, and cognitive impairments in sufferers.

When either the modified CRMP-2 or the interaction between the two proteins was blocked, using a method already approved in both the US and Australia, the progression of the disease was halted.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... geid/3461/

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PostPosted: Mon Apr 30, 2012 6:16 am 
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In their research, the scientists found that a modified version of CRMP-2 is present in active MS lesions, which indicate damage to the nervous system, in a laboratory model of MS.


If this is the mouse EAE model, then I wouldn't get too excited. Back in the mid 90's my wife took part in a trial for a drug that stopped and reversed MS in the mouse model. The trial was stopped after one year when one patient died after suffering severe heart damage.

Hopefully this is something very different.

Harry


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PostPosted: Mon Apr 30, 2012 6:17 am 
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This research is an example of what I mean if I say they could all go on "playing their own little games in their own little garden"...

See posting top of page general-discussion-f1/topic15188-315.html

The intervention by this future medication (if ever, where did I hear that before ha, ha, ...) is very sclerose-centric ... And that is far too late in the process..

MS is not a neurological disease, that is only where the symptoms show up...

And therefore it should be tackled elsewhere.. Almost every other discipline in medicine comes around the corner to help solve our problem (vascular, interventional radiology, endocrinology, gastroenterology, diabetology..)
But paradoxically enough the neurology is not there.


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PostPosted: Mon Apr 30, 2012 9:43 am 
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I personally find this very interesting. Regardless of what people postulate, the fact is nobody knows what MS truly is (neurological, venous, combination, bacteria, etc). Personally I feel if we can unlock the mystery behind oligodendrocyte apoptosis it will make a lot of other things more clear. We know in other neurological diseases that certain proteins are key contributors (amyloid in Alzheimer's for example), and I would not be shocked if managing these proteins are the key to managing the disease. I know CCSVI is perhaps the biggest thought train, and who's to say, these protein abnormalities may also be related to venous problems.

As a caregiver for someone with PPMS I don't want to see any doors closed, any little hint of something that possibly halt progression needs to be fully investigated. Looking forward to seeing where this new theory leads the researchers.


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