Stroke is the second leading cause of death and disability worldwide. By blocking blood flow in the brain, it destroys brain cells. Now, new research shows a drug already approved to treat other conditions not only limits stroke damage, but it also promotes repair. In rats, it reduced the number of brain cells killed and spurred birth of new ones.
The study, led by the University of Manchester in the United Kingdom, is published in the journal Brain, Behavior, and Immunity. The researchers believe the findings offer further support for developing the new drug as a treatment for stroke.
A stroke is an event that blocks or interrupts the blood supply to the brain, depriving cells of essential oxygen. Without oxygen, cells die within minutes. There are few effective treatments for stroke and they apply to a low proportion of patients.
A stroke can lead to lasting brain damage, long-term disability, or even death.
The new study concerns
The researchers, led by Stuart Allan, professor of neuroscience at Manchester, investigated the effect of an anti-inflammatory drug, interleukin-1 receptor antagonist (IL-1Ra), on rats after a stroke.
- One American
dies from a strokeevery 4 minutes
- Nearly 1 of 4 strokes are in people who have had a previous stroke
- Stroke costs the United States $34 billion each year.
IL-1Ra is already licensed for the treatment of other conditions – such as rheumatoid arthritis – and several early stage clinical trials for its use as a stroke treatment have already been completed in Manchester.
The researchers found that rats treated with IL-1Ra not only had reduced brain damage in the early stages following a stroke, but several days later, they showed increased numbers of new brain cells (neurogenesis). They found the results were just as promising whether the rats were young, old, lean, or obese.
The authors note that while stroke itself can also trigger a robust repair response following injury, many of the new cells generated fail to survive or integrate into the circuits that are already there.
When they analyzed the effect of IL-1Ra on neurogenesis in the rats’ brains, they found the drug “not only increases stem cell proliferation, but also significantly enhances neuroblast migration and the number of newly born neurons after cerebral ischemia.”
The researchers suggest previous attempts to find a drug to prevent brain damage after stroke have not successfully completed the journey from the lab to the clinic because they fail to deal with the strong inflammatory response that occurs in a stroke.
“The results lend further strong support to the use of IL-1Ra in the treatment of stroke, however further large trials are necessary.”
Prof. Stuart Allan