An antibody that could reduce the side effects of a common stroke drug has been developed by scientists.
The traditional treatment for ischaemic stroke, in which a blood clot cuts off the blood supply to brain tissue, is a drug called rtPA, which dissolves the clot.
However, people with haemorrhagic stroke, in which a blood vessel in the brain bursts, should not receive rtPA as it increases the risk of bleeding.
Now a new discovery by Denis Vivien of the University of Caen Basse-Normandie in France has put a different perspective on this relatively simple picture: rtPA is actually released by brain cells, reports New Scientist.
In small quantities, rtPA binds to brain-cell receptors for a chemical called NMDA. This triggers a short-lived influx of calcium, enhancing learning and memory.
But damaged neurons release rtPA in large quantities, and this can cause neighbouring neurons to die. High levels of rtPA can also damage the blood-brain barrier, which may explain why the drug sometimes triggers dangerous bleeding.
Vivien has also developed an antibody that could overcome these problems. It stops rtPA from binding to the NMDA receptors, blocking its negative effects.
When mice were injected with the antibody on its own or in combination with rtPA, the amount of brain damage resulting from a stroke was reduced by up to 70 per cent - both when the antibody was given immediately after the stroke and 6 hours later. Three months later, these mice also showed significantly less disability.
"With the antibody, we completely prevent the deleterious effect of rtPA and we can increase the time window during which it can be given," New Scientist quoted Vivien as saying.
The results were presented at the Forum of European Neuroscience in Amsterdam, the Netherlands.