Scientists have made a new discovery that could eventually lead to new drugs that are able to protect the brain following a stroke.
It has long been known that when a stroke occurs and part of the brain is cut off from blood and oxygen for long enough, that part will die.
Following the cell death, the tissue undergoes a process called liquefactive necrosis in which enzymes and the body's white blood cells turn it from a rubbery substance into a liquid. There is no recovery of the lost tissue and the space it occupied instead fills with liquid and debris.
At the edge of the boundary where the stroke damage occurred and the rest of the brain, tissue called a glial scar forms to section it off from the healthy matter.
As part of the new research, scientists at the University of Arizona College of Medicine wanted to examine the nature of the liquefied brain tissue and its potential effects long after a stroke.
They used a mouse model to extract fluid from the area of liquefaction in a post-stroke brain and then placed it in a petri dish alongside living neurons. After just four hours, more than half of the healthy neurons had died, demonstrating that the fluid is highly toxic.
They also wanted to test the efficacy of the glial scar barrier, which the researchers likened to a fence made of tightly twisted branches. This was done by injecting dye into the liquefied part of a post-stroke brain.
It was found that by seven weeks later, the dye had spread past the glial scar and into the healthy brain region, suggesting that toxic substances with the potential to kill healthy neurons would also have gone with it.
Writing in the journal Neurobiology of Disease, lead study author Dr Kristian Doyle said: "We found that the glial scar is a pretty decent barrier, but it's not perfect. Imagine putting sandbags around your house; they will reduce flood damage, but not control everything."
Since the dead brain fluid remains in the body for a long time, Dr Doyle added that he believes it may be one of the causes of dementia following a stroke if it is able to leak into the parts associated with memory.
Indeed, out of ten million stroke survivors each year, around a third are likely to develop dementia later on for reasons that have been unclear so far.
It is hoped that the discovery could lead to new treatments to prevent dementia following a stroke, potentially including a drug that makes the glial barrier stronger.
"We used to think that the glial scar forms a fool-proof barrier, and had no idea about the toxicity of the liquefied brain materials. Thanks to this research, we now will be able to consider new and different stroke therapies," commented fellow researcher Janko Nikolich-Zugich.
There are around 100,000 strokes in the UK each year and some 1.2 million people are survivors of the condition.