CHICAGO, Nov 28 (Reuters) A human protein generated while the body encounters environmental stress helped delay symptoms of amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease in mice, U.S. researchers said.
Genetically engineered mice with ALS that were injected with this protective protein lived 10 per cent longer than untreated mice.
''When we administered the protein every other day, we saw mice develop symptoms later than untreated mice. They performed better on a behavior test and they lived longer,'' said Carol Milligan, a researcher at Wake Forest University School of Medicine, whose study appears in the Journal of Neuroscience.
ALS progressively kills nerve cells that control muscle movements known as motor neurons.
Milligan, in a telephone interview, said the protein -- known as recombinant heat shock protein 70 -- appears to slow the death of motor neurons near the muscle.
Before a neuron dies, it typically detaches from the muscle, a process called denervation. Milligan said she believes the protein helped delay this process in the ALS mice.
Other studies of ALS in animals have shown the motor neurons do not behave normally when exposed to stress.
Milligan and Wake Forest researcher David Gifondorwa wanted to see if injecting mice with heat shock proteins might have an impact on ALS.
Gifondorwa traced this protective effect to the motor neuron junction, the place where the nerve attaches to the muscle.
''Rather than working in the central nervous system, this protective effect is working at the neuromuscular junction,'' Milligan said yesterday. ''We're keeping the motor neuron functional longer.'' Milligan said she does not think the study will help in research toward a cure for ALS, but it might help forestall its symptoms.
It also may lead to two-pronged treatments that attack the disease at the spinal cord and at the nerve-muscle junction.
About 5,600 people in the United States are diagnosed with ALS each year, according to the ALS Association.
REUTERS ARB KP0847