In short it details the latest information concerning a “switch” that turns “on” and “off” inflammation in the brain after trauma and was performed using a mouse model to study the role of p38a MAPK in trauma-induced injury responses in the microglia resident immune cell of the brain.
Who carried out the research?
Linda Van Eldik, a Director at the University of Kentucky Sanders-Brown Center on Aging (SBCoA) as well as a team of researchers:
Rachel K. Rowe
Which journal does it appear in?
The paper is entitled “The p38a MAPK regulates microglial responsiveness to diffuse traumatic brain injury” and is included in the Journal of Neuroscience.
What do the experts say?
Linda Van Eldik said:
“The p38a MAPK protein is an important switch that drives abnormal inflammatory responses in peripheral tissue inflammatory disorders, including chronic debilitating diseases like rheumatoid arthritis. However, less is known about the potential importance of p38a MAPK in controlling inflammatory responses in the brain.
Our work supports p38a MAPK as a promising clinical target for the treatment of CNS disorders associated with uncontrolled brain inflammation, including trauma, and potentially others like Alzheimer’s disease. We are excited by our findings, and are actively working to develop drugs targeting p38a MAPK designed specifically for diseases of the brain.”
Adam D. Bachstetter, the lead author of the paper said:
“I was surprised when I looked under the microscope at the brain tissue of mice that had a diffuse brain injury. Microglia normally look like a small spider, but after suffering a brain injury the microglia become like angry spiders from a horror movie. In brain-injured mice that lack p38a MAPK there were no angry-looking microglia, only the normal small spider-like cells.
When I started the study I never expected the results to be so clear and striking. I believe that the p38a MAPK is a promising clinical target for the treatment of CNS disorders with dysregulated inflammatory responses, but we are still a long way from development of CNS-active p38 inhibitor drugs.”
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