Mark Burns, PhD
Ph.D., 2000, National University of Ireland, Galway, Ireland
New Research Building, Room EG17A
Dr Burns’ lab investigates the link between traumatic brain injury (TBI) and Alzheimer’s disease. Exposure to TBI can quadruple the risk of developing Alzheimer’s disease, and amyloid plaques similar to those seen in Alzheimer’s disease have been found in the brain of TBI fatalities. Dr Burns’ lab recently found that the same pathways that are activated long-term in Alzheimer’s disease are activated short-term after TBI. By blocking the activation of these pathways in mice, the physical disability or memory impairments following brain trauma were completely abolished and the amount of brain damage was reduced by over 70%. This research is providing new insights into how toxic proteins produced in the brain in Alzheimer’s disease and TBI are causing neuronal cell damage and memory loss.
“‘The findings mirror what has been observed about such damage in humans years after a brain injury, especially among athletes,’ Burns says. ‘Studies have shown that almost all people with single concussions spontaneously recover, but athletes who play contact sports are much more susceptible to lasting brain damage. These findings help fill in the picture of how and when concussions and mild head trauma can lead to sustained brain damage.’”
“The researchers focused on how sex alters key neuroinflammatory responses that follow TBI. They specifically looked at microglial cells, which are the resident immune cells of the brain, and movement of macrophages from the blood into the injured brain. Macrophages, which are also immune cells, offer the first line of defense against infection.”
“Burns also says that although the female mice have less of the negative effects of neuroinflammation such as neuron cell death, there are also positive aspects to neuroinflammation that are missing in female mice such as waste removal and wound healing. Understanding how to minimize the negative effects while maximizing the positive effects of inflammation is an important goal in TBI research.”