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WEDNESDAY, Nov. 28 (HealthDay News) -- Studies in mice point to a possible treatment for amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.
Scientists injected a protein normally found in human cells into mice that were genetically engineered to develop ALS. The team found that the treatment delayed symptoms and increased the rodents' lifespan.
ALS is a neurodegenerative disease that causes the death of motor neurons, the nerve cells that control muscles.
According to a team from Wake Forest University in Winston-Salem, N.C., treatment with the protein, called recombinant heat shock protein 70 (Hsp70), increased total lifespan of mice with ALS by 10 percent (10 days), compared to one day of increased lifespan achieved with Riluzole, the only ALS treatment approved by the U.S. Food and Drug Administration.
For comparison purposes, Riluzole increases the lifespan of humans affected by ALS by about 60 days, the scientists noted.
Treatment with Hsp70 -- which was given three times a week beginning 50 days after the mice were born -- also delayed symptom onset, preserved motor function and prolonged motor neuron survival.
Heat shock proteins are produced naturally by cells are part of the stress response to protect themselves from injury. But in a number of animal models of ALS, motor neurons do not appear to mount the typical stress response.
The study appears in the Nov. 28 issue of the journal Neuroscience.
While the findings suggest a new treatment approach for ALS, the treatment is not ready for clinical trials in humans, the Wake Forest team noted.
"This is another piece of the puzzle of what causes ALS and how best to treat it. It's possible that one day a treatment based on this finding could be part of a 'cocktail' for attacking the disease from different fronts," study lead author David Gifondorwa, a Ph.D. candidate, said in a prepared statement.
-- Robert Preidt
SOURCE: Wake Forest University, news release, Nov. 27, 2007
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