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Accidental Find May Help Lou Gehrig's Patients (Parkinson's and Alzheimer's too?) By Sue Vorenberg - <[log in to unmask]> Tribune Reporter June 7, 2004 Patients with Lou Gehrig's disease can't waste much time on hope. The disease, which causes progressive weakness, often kills within three years. The only drug approved to fight it, Riluzole, typically extends that life span by just three months. In other words, it's a quick ride to a death sentence, said Marcus Keep, a University of New Mexico neurosurgeon. "People with Lou Gehrig's disease go from weakness, to a cane, to a walker to a wheelchair to a feeding tube fairly quickly," Keep said. "In the end maybe they can move a few fingers and that's it. It's horrible because their minds stay the same all the way to the end while they watch their body deteriorate." Keep is part of a group of doctors and scientists developing a drug that could potentially double the life spans of Lou Gehrig's disease sufferers - perhaps giving them an extra three years of life. They have formed a company called MAAS Biolab LLC, which is running animal trials and hopes to start the first human clinical trials in Albuquerque in a year, Keep said. "In our testing with mice carrying the disease we got them to live twice as long," he said. "That's encouraging enough that we'd like to try giving the drug to people. We're hoping it has a similar result. Of course, it doesn't keep them in perfect condition until the end - it just slows the progression." The group is using a drug called cyclosporin, an immune system suppressor typically used to stop patients from rejecting organs during transplants, but they're using it to protect neuron cells - something it hasn't been used to do before. They are trying to get Food and Drug Administration approval to do clinical trials but must first complete another round of trials in laboratory rats. The company is also trying to find funding to continue its work, Keep said. "The results are promising," he said. "We're very hopeful that we can really help people with this sort of treatment in the near future." Still, not everyone is convinced it will work. Jeffrey Rothstein, a neurology professor at Johns Hopkins in Baltimore, said results from mice and rats don't typically transfer all that well into humans, and the drug might not be as helpful as Keep thinks. "Everyone agrees that we need drugs to slow the disease down, but no drug will make these people better," Rothstein said. "It's also interesting to note that most mice trials fail in humans. That's not to say they have no value, but it's not a 100 percent predictor of success." The drug might actually have a toxic effect on humans, he added. "In some studies cyclosporin was found to increase toxicity," Rothstein said. "It's a funny drug because it has had mixed results. That makes it hard to understand its value. Still, we're all looking for a better drug. But many drug tests so far have already failed." Keep and Eskil Elmer, a Swedish doctor, stumbled across the new use for cyclosporin by accident, when both were working at Lund University in Sweden. "We were doing some experiments grafting cells into rat brains, and we used cyclosporin to keep them from rejecting the foreign cells," Keep said. "We were trying to give the rats strokes, but none of them had them. The boss said 'You didn't do a good job - they didn't have strokes at all.' He told us to move on." They didn't listen. Instead of moving on, the two decided to find out why the rats didn't have strokes. What they discovered was that if cyclosporin is injected into the brain, it has a completely different function - it protects neuron cells from damage, Keep said. "So we tried the experiment again without the cyclosporin and, sure enough, all the mice had strokes," he said. If the work transfers successfully to humans, the discovery could be important for the roughly 5,000 people a year who are found to have Lou Gehrig's disease - and for several other neurological diseases. Lou Gehrig's, Alzheimer's and Parkinson's diseases are all caused when neuron cells deteriorate in different parts of the brain. Neuron cells send signals from the brain to different parts of the body, telling it what to do. Nobody knows exactly why the cells deteriorate in the various diseases, but when they deteriorate, the signals can no longer travel, causing weakness, shaking or memory loss, depending on the disease, Keep explained. "We think if it works for Lou Gehrig's disease it will also work in Parkinson's and Alzheimer's," Keep said. "We wanted to focus on one disease first, but if it works, we'll try to develop it for other diseases." SOURCE: Albuquerque Tribune, NM http://tinyurl.com/2l8qz * * * ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn