According to a latest research published by the University of Maryland School of Medicine (UMSOM), overactive immune cells in the brain can be targeted with an experimental drug which could further limit brain cell loss. In addition, it can also reverse cognitive and other motor difficulties caused due to traumatic brain injury (TBI).
The latest research is therefore beneficial for suggesting new treatment for TBI and for other brain injuries.
For the study the team studied a CSF-1r inhibitor for a week to mice, starting one month after TBI. The time is also crucial because it is when animals have brain inflammation and other neurological deficits. Furthermore, the research findings also draw attention to the drug depletion which was more than 95 percent of the brain’s overactive immune cells (microglia) which are also known to cause neurotoxic inflammation.
Reports suggest several weeks after the treatment the cells regenerated and new cells were similar to normal microglia with its less inflammatory features. In addition, the mice recovered better in comparison to control group which did not undergo any treatment. Post treatment there was also less loss of tissue and neuron and improved motor and cognitive performance.
“We were surprised to see that the extent to which such late treatment could reverse the inflammatory state and the cognitive effects of experimental TBI,” explained co-author Rebecca Henry, PhD, Research Associate in Anesthesiology at UMSOM. “This was a proof of concept study that depletion and subsequent repopulation of microglia cells after injury has a strong protective effect, but we clearly need more research to better understand this process before clinical translation.”
Both animal and human brains have specialized immune cells known as microglia, which help to protect against viruses and bacteria that enter the brain. Sources allege researchers will work further on isolating microglia cells and use RNA resequencing techniques in order to understand genes driving inflammation and overactivation.
“These preclinical studies suggest that the consequences of TBI on brain degeneration and related neurological impairment may be modifiable quite long after injury,” commented co-author Alan Faden, MD, the David S. Brown Professor in Trauma at UMSOM. “We can potentially alter these effects by even highly delayed targeting of inflammatory pathways, a finding at odds with widely accepted views about treating head injury.”