Sep 28 2016
Scientists Discover a Neuroprotective Mechanism in the Brain
Last week we wrote about a study published recently in the journal Scientific Reports that demonstrated how brain damage spreads and how it could be limited with a neuroprotective mechanism.
Following this blog, we decided to talk to the lead author of this study, Andrew Samson, who works in the division of neuroscience at the University of Dundee in Scotland.
First, he explained how brain damage spreads across the brain.
“Following an insult to the brain, either as a result of a stroke or a traumatic brain injury, cells at the insult site die rapidly, spilling out large quantities of toxic chemicals into the surrounding area,” Samson said. “These toxic chemicals spread out, killing more cells, which in turn causes a further release of toxic chemical, and therefore a ‘snowballing’ of toxicity could occur.”
He said that any insult to the brain that kills brain cells should spread and consume the entire brain. But this doesn’t happen. This was how they knew there must be some neuroprotective mechanism at work in the brain.
“We have recently developed a model for this spreading toxicity and this has allowed us to discover the existence of the in-built neuroprotective signal that spreads rapidly as a warning signal when local damage occurs,” Samson said. “In our study, we demonstrated that an artificial non-toxic stimulus could also trigger this response and so prevent spreading damage.”
He said that this provides the scope for a therapeutic block to prevent brain damage.
“If properly harnessed, this innate protective mechanism may provide a fast acting strategy to terminate spreading damage caused by a stroke or traumatic brain injury, just when a rapid response is essential,” he said.
He explained that no current treatment exists for spreading toxicity following stroke or traumatic brain injury, and current therapy is limited to promoting recovery and physical rehabilitation.
“Our research has identified a new opportunity to prevent damage spreading into surrounding networks of the brain, thus limiting brain damage and speeding recovery,” he said. “Our research however is in the very early days, and a significant amount of work now needs to be done in order to fully characterise this protective mechanism and how best to harness this natural protective power in acute, emergency situations.”
As for Samson’s hope for the future, he hopes his team can develop a device that will stimulate the protective power of the brain after an acute injury. His team also plans to investigate whether or not this kind of therapeutic device can help protect against spreading toxicity in chronic diseases, such as Alzheimer’s.
“There is still a long way to go, but we have at least opened the door,” he said.