A study published in the journal Scientific Reports demonstrated how brain injury spreads and how it could potentially be limited with a neuroprotective mechanism. The discovery was made in a collaboration between neuroscientists and engineers at the Universities of Dundee and Strathclyde. The study was published online Sept. 21, 2016.
The researchers, led by Andrew J. Samson, a neuroscientist at the University of Dundee, found a mechanism that uses the neuronal networks to provide protection against secondary damage of traumatic brain injury or strokes.
Neurodegenerative diseases, traumatic brain injuries or strokes tend to have acute secondary damage, where neurotoxicity is spread into uninjured brain areas. One of the researchers, Christopher N. Connolly, said that if the network could be triggered in a clinical setting as soon as possible then secondary damage could be minimized and recovery time shortened.
Network neuroprotection can be stimulated after a brain injury, opening a new window to therapeutic intervention. Current treatments are limited to aiding the recovery process, because only slow-acting network neuroprotection is known, which has little clinical, realistic significance.
The researchers have identified that neuronal networks react to an injury by sending warning signals very rapidly (in minutes) to protect against brain damage. This may be a mechanism that can be used in clinical settings to prevent brain damage. They can recruit the help of surrounding neurons for the neuroprotective help.
They also found that benzodiazepines, anxiety medications, can mimic neuroprotective mechanisms. This is a possible pharmacological treatment for stroke, but must be tested further, Connolly said.
The neuroscientists, Samson and Connolly, teamed up with engineers, including Michele Zagnoni, who said they were able to study the spreading of damage in the brain using microfluidic technology in the lab.
Through this technology, they were able to see how damage is spread in the brain by simulating a brain injury and to identify a “fast-acting neuroprotective signaling mechanism.”
This therapy uses surrounding networks of neurons grown in the lab to protect against secondary damage. This could be stimulated in order to stop the spread of brain damage. This requires more work, but is an interesting, exciting possibility.