Common viruses lying dormant in our brains might be awakened by head trauma, potentially triggering processes that lead to conditions like Alzheimer’s disease, according to new research from Tufts and Oxford universities. The finding could explain the long-observed connection between head injuries and later neurological problems, while suggesting new preventive strategies.
The study, published in Science Signaling, reveals how concussions and other head trauma might set off a chain of events leading to neurodegeneration, particularly in people carrying herpes simplex virus 1 (HSV-1), which is present in over 80% of the population.
“We thought, what would happen if we subjected the brain tissue model to a physical disruption, something akin to a concussion? Would HSV-1 wake up and start the process of neurodegeneration?” says Dana Cairns, research associate at Tufts University’s Department of Biomedical Engineering and lead author of the study.
Using a laboratory model that recreates brain tissue environment, researchers found that simulated concussions could indeed reactivate dormant HSV-1 virus. This reactivation triggered the appearance of markers associated with Alzheimer’s disease, including protein plaques, inflammation, and dying neurons.
The implications extend far beyond sports, as traumatic brain injury affects about 69 million people worldwide annually, with economic costs estimated at $400 billion. Athletes in contact sports and military personnel exposed to blast forces are particularly at risk.
“This opens the question as to whether antiviral drugs or anti-inflammatory agents might be useful as early preventive treatments after head trauma to stop HSV-1 activation in its tracks, and lower the risk of Alzheimer’s disease,” Cairns notes.
The research builds on three decades of work by co-author Ruth Itzhaki of Oxford University, who first identified HSV-1 in a high proportion of elderly brains and suggested its potential reactivation by stress or immune system suppression.
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 were virus-free.
When subjected to impacts mimicking concussions, only the virus-containing cells showed signs of viral reactivation followed by Alzheimer’s-like changes. Multiple impacts produced even more severe reactions, matching epidemiological observations that repeated head trauma can double or further increase the risk of neurodegenerative conditions.
“The brain tissue model takes us to another level in investigating these connections between injury, infection, and Alzheimer’s disease,” says David Kaplan, professor of engineering at Tufts. “We can re-create normal tissue environments that look like the inside of a brain, track viruses, plaques, proteins, genetic activity, inflammation and even measure the level of signaling between neurons.”
The findings suggest that early intervention with antiviral medications following head trauma might help prevent or reduce the risk of later neurological problems, opening new avenues for preventive treatment strategies.