Researchers develop tx for MS mouse model
 

http://www.eurekalert.org/pub_releas...-drt112106.php

Public release date: 21-Nov-2006
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Contact: Ron Najman
ron.najman@downstate.edu
718-270-2696
SUNY Downstate Medical Center


Downstate researchers target multiple sclerosis

Researchers at SUNY Downstate Medical Center have developed a substance that inhibits the progress of multiple sclerosis (MS) in an animal model. The agent, a novel calpain inhibitor, can be administered orally.

Calpains are a family of proteolytic enzymes naturally found in the human body. Inappropriate activation of calpain is associated with a number of neurodegenerative and autoimmune diseases such as MS. It is known to destroy the myelin sheath that coats and protects the nerves.

In a paper published in the Journal of Neuroimmunology, SUNY Downstate and Maimonides Medical Center researchers described the use of the calpain inhibitor for the treatment of a mouse model of MS. Whether administered by injection or by mouth, the inhibitor produced an almost complete cessation of the disease's progress.

Wannabe,

While this may be an interesting discovery I can't get too excited about the fact that it got excellent results on that poor MS mouse. There have been many therapies that have worked on that mouse that never translated into anything for human MS.

About 10 years ago my wife took part in a clinical trial with a drug that stopped and reversed MS in the mouse. About a year into the trial, a patient that was receiving the large dose of the drug died when the drug affected his heart severely. They abruptly stopped the trial.My wife was on the placebo...whew!

Let's hope that this recent discovery proves to go against the odds and something really positive comes of it.

Harry

Thank you for posting this, Wannabe..all research in this area is interesting to me. I'm with Harry on the darn mouse thing again..I wish they would find a better model. :rolleyes:

I'm beginning to hate hearing that the @#$%^#@ mouse has, once again, been cured of EAU. What we don't hear is, that the mouse died a few weeks later from the Cure!!!

It's odd to me, how enzymes that are meant to protect our bodies from harm are the very ones to turn on us.:mad:... I looked up Calpain at Wikipedia.com and found it very interesting.

Anyway, the only way we are going to find a cure for MS, is to keep on doing the research, studies and trials....so on with the fight and thanks again.:)

I don't know, these results of virtually a complete cessation of disease activity, in a pill form, it's peaking my interest. Going to watch this closely and hopefully we'll see some human trials in the works soon..

Researchers target multiple sclerosis
NEW YORK, Nov. 22 (UPI) -- U.S. scientists say they have developed a substance that inhibits the progress of multiple sclerosis in an animal model.

The scientists at the State University of New York's Downstate Medical Center say the agent, a calpain inhibitor, can be administered orally.

Calpains are a family of proteolytic enzymes naturally found in the human body. Inappropriate activation of calpain is associated with a number of neurodegenerative and autoimmune diseases, such as MS. It is known to destroy the myelin sheath that coats and protects the nerves.

The researchers say they used the calpain inhibitor for the treatment of a mouse model of MS. Whether administered by injection or by mouth, the inhibitor was shown to reduce clinical illness signs and prevent demyelination and inflammatory infiltration in a dose- and time-dependant manner, holding promise in treating both the acute and chronic phases of MS.

The scientists say the inhibitor might also be successful in treating other degenerative illnesses, such as Alzheimer's, Huntington's and Parkinson's diseases.

The study appears in the current issue of the Journal of Neuroimmunology.

Copyright 2006 by United Press International. All Rights Reserved.

Harry,

What trial did you wife take part in that was pulled and damaged people's hearts? Not sure if I heard of that one.

I'm with Harry. The mouse model is pretty much a dead dodo. We need to find out how and why MS works in humans, not mice. Until we have that information, all treatments are just shooting from the hip, hoping to hit something in the general spray of bullets. Or at most band-aids, such as we have now. My money would be on the Accelerated Cure Project, which is trying to discover just that. You can't cure something if you don't know what it is.

Even with the treatments we have now, ABCR, steroids, and chemo, the general statistic that 50% of people with RR will pass on to SP hasn't changed. And these drugs don't seem to affect PP or relapsing progressive at all. Of course the latter fact seems to suggest that PP and RP aren't in fact MS at all, but some as yet unknown disease. But that's for another discussion.

Chris

Wannabe,

The drug was called TNF...tumour necrosis factor..( I think it was given some kind of number at the time) and was trialled in 5 other MS centers across Canada back in the mid 90's.

It got amazing results with the poor mouse...stopped and reversed the disease. Marg was the first patient to start the trial here at the MS Clinic in London, Canada. I don't even know who the drug company was that sponsored the trial....back then I wasn't really into all the nitty, gritty details like I am today.

The trial lasted just under a year and was stopped when a male patient at the Calgary MS Clinic died from heart complications. Each patient got an MRI every month and was followed closely. That was the first MRI that Marg ever got and the lesions they saw were old and non-active. Yet her MS at the time was slowly getting worse. The trial was stopped immediately and I never heard anything about the drug again.

Harry

This is the same as my MRI, the lesions are deemed old and (supposedly) inactive. In other words, none of them enhance so that no active inflammation is involved. Yet, it's impossible to argue with the clnical picture; my MS is obviously progressing. To me this means one of two things. Our imaging techniques are at this time unable to show the active inflammation. Or, there is in fact no active inflammation, and some other mechanism is driving my progression. Personally I'm leaning towards the latter, since neither cytoxan nor solumedrol, both of which target inflammation, did anything at all for me.

Chris