THURSDAY, Oct. 24, 2002 (HealthDayNews) -- Canadian researchers are encouraged by a new stroke treatment that seems to block brain damage in rats and could translate into hope for human patients.
Rats treated with a manmade protein suffered fewer side effects after strokes when treatment began within an hour after an attack, scientists from several Canadian universities report.
"We believe that this approach is extremely promising for use in people, and -- funding permitting -- could be in clinical trials [in humans] within a couple of years," says study co-author Dr. Michael M. Tymianski, an assistant professor of neuroscience at the University of Toronto.
Despite a number of advances in recent years, stroke remains a top killer. According to the National Stroke Association, about 600,000 Americans will have a stroke this year, and 160,000 of them will die. Only cancer and heart disease are more deadly.
The most dramatic development in stroke treatment has been the increasing use of a drug known as tPA, which can stop a stroke in its tracks if given within three hours after an attack. But tPA is not suitable for some stroke patients, and many victims don't get to a hospital within the required time period. Because of the various challenges, tPA is appropriate for only about 3 percent of stroke patients, Tymianski says.
In the new study, Tymianski and colleagues explored the process that begins when a stroke starts cutting off blood supply to parts of the brain.
Neurons -- also known as nerve cells -- communicate with each other through neurotransmitters. During a stroke, the production of one neurotransmitter known as glutamate is stepped up, overwhelming the doors that provide access to the nerve cells, Tymianski explains.
At that point, the cell doors -- known as receptors -- cannot properly control how many calcium ions get into the cell. "When there is too much calcium, the cells die," Tymianski says.
In their experiment, the researchers designed small pieces of protein to protect brain cells by blocking a molecular process that leads to their deaths during stroke. Their findings appear in tomorrow's issue of Science.
The treatment reduced brain damage in rats that had artificially induced strokes, and the rats performed better on behavioral tests after the attacks.
Unlike some other stroke drugs that have been tested, the protein developed by the researchers doesn't stop neurotransmitters from doing their work in the brain, Tymianski says. "The use of the older drugs is analogous to shutting down the power to your computer in order to treat a computer virus. It will stop the virus, but if that computer is running your body, you'll have serious side effects."
It's not yet clear if the protein has side effects, and other studies are examining whether it is toxic, he says. But for now, researchers are hopeful about the treatment, especially because paramedics may be able to administer it at the scene of a stroke instead of waiting for a doctor at a hospital. "That could exponentially increase the number of patients who could benefit from treatment," he says.
What To Do
For a range of information on strokes, visit the National Stroke Association or the National Institute of Neurological Disorders and Stroke.
