A common dormant virus in our brains can be awakened by head trauma and trigger processes that cause conditions such as Alzheimer’s disease, according to new research from Tufts University and the University of Oxford. The findings may explain the long-observed link between head injury and subsequent neurological problems and suggest new prevention strategies.
The study, published in Science Signaling, shows how concussions and other head injuries can lead to neurodegeneration, especially in people who carry herpes simplex virus type 1 (HSV-1), which is present in more than 80% of the population. It reveals how a series of events can be triggered that lead to. .
“We wondered what would happen if we exposed a brain tissue model to a physical disruption similar to a concussion. Would HSV-1 wake up and begin the process of neurodegeneration?” from the Tufts University School of Biomedical Engineering. said Dana Cairns, researcher and lead author of the study.
Using a laboratory model that recreates the brain tissue environment, researchers found that simulated concussion can actually reactivate the dormant HSV-1 virus. This reactivation led to the appearance of markers associated with Alzheimer’s disease, including protein plaques, inflammation, and dying neurons.
Traumatic brain injuries affect approximately 69 million people worldwide annually, with an estimated economic cost of $400 billion, and their impact extends far beyond sports. Athletes in contact sports and military personnel exposed to explosive forces are especially at risk.
“This raises the question of whether antiviral and anti-inflammatory drugs may be useful as early preventive treatments after head trauma to halt HSV-1 activation and reduce the risk of Alzheimer’s disease. Dr Cairns points out.
The study is based on 30 years of research by co-author Ruth Izaki of the University of Oxford. He was the first to identify HSV-1 in a high proportion of the brains of older people and suggested that stress and suppression of the immune system could reactivate HSV-1.
To test their theory, the researchers created a sophisticated brain tissue model using a donut-shaped material containing neural stem cells that develop into mature neurons and supporting cells. Some tissue models contained dormant HSV-1 virus, while others did not contain virus.
When subjected to a shock that mimicked a concussion, only cells containing the virus showed signs of virus reactivation, followed by Alzheimer’s disease-like changes. Multiple impacts produce more severe reactions, consistent with epidemiological observations that repeated head trauma can double or even increase the risk of neurodegenerative diseases.
“Brain tissue models take us to a new level in investigating the connections between injury, infection, and Alzheimer’s disease,” says David Kaplan, professor of engineering at Tufts University. “We can recreate a normal tissue environment similar to the inside of the brain and track viruses, plaques, proteins, gene activity, inflammation, and even measure levels of signaling between neurons.”
The findings suggest that early intervention with antiviral drugs after head trauma may help prevent or reduce the risk of subsequent neurological problems, potentially opening new avenues for preventive treatment strategies. It suggests that.
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