Washington D.C. [USA], Mar. 15 : Researchers have identified a new mechanism, by which inflammation can spread throughout the brain after injury and may play a role in other neurodegenerative diseases.
The findings were published in the Journal of Neuroinflammation.
According to researchers from the University of Maryland School of Medicine in the US, this new understanding has the potential to transform, how brain inflammation is understood, and, ultimately, how it is treated.
"These results potentially provide a new conceptual framework for understanding brain inflammation and its relationship to brain cell loss and neurological deficits after head injury and may be relevant for other neurodegenerative disorders such as Alzheimer disease in which neuroinflammation may also play a role," said Dr Alan Faden.
"The idea that brain inflammation can trigger more inflammation at a distance through the release of microparticles may offer novel treatment targets for a number of important brain diseases," Faden added.
The researchers showed that microparticles derived from brain inflammatory cells are markedly increased in both the brain and the blood following experimental traumatic brain injury (TBI).
These microparticles carry pro-inflammatory factors that can activate normal immune cells, making them potentially toxic to brain neurons.
The researchers studied mice and found that in animals who had a traumatic brain injury, levels of microparticles in the blood were much higher because each kind of cell in the body has a distinct fingerprint and could track exactly where the microparticles came from.
In this study, the microparticles released from cells known as microglia, immune cells that are common in the brain. After an injury, these cells often go into overdrive in an attempt to fix the injury.
But this outsized response can change protective inflammatory responses to chronic destructive ones.
The research has found that neuroinflammation often goes on for years after TBI, causing chronic brain damage.
The chronic inflammation has been increasingly implicated in the progressive cell loss and neurological changes that occur after TBI.
These inflammatory microparticles may be a key mechanism for chronic, progressive brain inflammation and may represent a new target for treating brain injury.