A new study from the University of Pennsylvania’s School of Engineering and Applied Science indicates that drug intervention to minimize intercellular signaling between astrocytes after traumatic brain injury can reduce long term damage and cognitive defects.
The study, published in Brain, discovered that astrocytes, star-shaped glial cells in the brain and spinal cord, play a large role in cell death following brain injury. A single injury in the brain can trigger widespread signaling through the astrocyte network, which adversely affects communication among neurons in the network.
“We were initially very surprised that the effect of astrocyte signaling on neuronal communication was so profound after injury,” David F. Meaney, leader of the study, told Medical Xpress.
The team then studied how these changes traveled through the astrocytes in the brain and cell culture, and saw that one unique type of signaling can reduce the response dramatically. They screened several drugs, and found one that could trigger the unique type of signaling, slowing the more damaging signaling and improving cognitive recovery after even a single brain injury.
Up until now, most drug testing for traumatic brain injury focuses on other symptoms of the condition such as headaches, anxiety, and depression, as cognitive problems are often more complicated and closer related to processes that occur immediately after the injury and can cause problems for well after the chemical processes have stopped.
This method attempts to prevent the cognitive defects by treating the signals naturally set off by brain injury, and could be a major change in how traumatic brain injury is handled, especially in the time immediately following the injury. It also shows the importance of being checked for brain injury immediately after any serious head collisions. Symptoms may not be immediate, but the processes that create those symptoms are.