Scientists have found an enzyme is responsible for the death of nerve cells after a stroke and say an experimental drug that reduces brain damage in mice may also offer hope for humans.
Previous attempts to design drugs that can protect the brain from damage after a stroke have had limited
success.
However, Dutch and German researchers say their work shows a potential new approach to treating stroke, which is the most common cardiovascular problem after heart disease and kills about 5.7 million people worldwide annually.
In tests on mice, the scientists found an experimental drug, known as VAS2870 and being developed by the German biotech firm Vasopharm, dramatically reduced brain damage and preserved brain functions, even when given hours after the stroke.
"The indications are strong the same mechanism may apply for human stroke," said Harald Schmidt from Maastricht University in the Netherlands, who led the study with Christoph Kleinschnitz from Wurzburg University in Germany.
Ischaemic stroke is the most common kind of stroke, caused by a clot or other blockage disrupting the flow of blood to the brain. The only available treatment is a clot-busting drug called a t-PA, or tissue plasminogen activator, but it must be given within three hours of a stroke and only about 5 per cent to 10 per cent of stroke victims get it.
Scientists facing a paucity of effective stroke drugs have been investigating whether tissue damage after stroke may be linked to a mechanism called oxidative stress, in which reactive oxygen species (ROS) accumulate within a cell.
Previous experimental drugs designed to "soak up" loose ROS after stroke have failed in late-stage clinical trials. A compound from AstraZeneca called NXY-059 proved to be an expensive flop for the Anglo-Swedish drugmaker in 2006.
But in this study, Schmidt and Kleinschnitz focused on finding and then trying to block the source of ROS.
The enzyme they identified is called NOX4, and by blocking NOX4 with the experimental drug in mice with stroke, they dramatically reduced brain damage.
They also found that eliminating the gene linked to NOX4 in mice did not result in any abnormalities.
