MONDAY, Oct. 20, 2003 (HealthDayNews) -- New research indicates that molecules called free radicals play a major role in the death of nerve cells in people with amyotrophic lateral sclerosis (ALS).
A study of cell cultures by a team of scientists at the University of California, Irvine offers evidence that free radicals prevent the destruction of glutamate, a potentially toxic molecule. As levels of glutamate increase, cells respond by producing more and more free radicals, further hampering disposal of glutamate.
The findings were presented at this week's annual meeting of the American Neurological Association in San Francisco.
"If this model is borne out, it could explain how a range of initial inciting factors could feed into one disease mechanism," researcher Dr. John H. Weiss says in a prepared statement.
"This is important for potential ALS therapies, because in a complex pathway such as this, multiple interventions targeting different steps in the cycle may be far more effective than single drugs at slowing or preventing disease," Weiss says.
ALS affects motor neurons, the nerve cells that control muscle action. In people with ALS, the motor neurons and their nerve fibers slowly deteriorate. That results in weakness, muscle spasms and tremors, and, eventually, paralysis. Most people who develop ALS die within 10 years, half within three years.
There is no cure. Exercise can help people with ALS maintain muscle strength and drugs can ease muscle spasms or cramps.
Recent research suggests an overabundance of glutamate may contribute to the death of motor neurons in people with ALS.
Glutamate is a signaling molecule that lets neurons communicate with each other. But once released, glutamate needs to be quickly eliminated. That's because too much glutamate can be toxic to neurons.
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