A groundbreaking study reveals that concussions and repetitive head injuries in sports could trigger latent viruses in the brain, such as HSV-1, leading to Alzheimer’s disease.
Researchers suggest that early use of antiviral drugs might prevent these effects, offering a new perspective on managing long-term brain health risks associated with sports.
Sports-Related Neurological Risks
Concussions and repeated head trauma, common in sports like football and boxing, were once seen as an unfortunate but inevitable part of athletic competition. Today, they are recognized as serious health risks. Research has highlighted links between head injuries and neurodegenerative diseases such as chronic traumatic encephalopathy (CTE), Alzheimer’s disease, and Parkinson’s disease, prompting sports organizations to update protective equipment and modify rules to reduce these dangers.
Unveiling Hidden Dangers: The Role of Latent Viruses
Scientists at Tufts University and Oxford University have discovered mechanisms that may explain how head trauma leads to these diseases. Their findings suggest that concussions could activate dormant viruses present in most brains, triggering inflammation and long-term damage over months or even years. This research opens the door to potential early interventions, such as antiviral treatments, to mitigate the risks. The study was published today (January 7) in Science Signaling.
The Viral Connection in Brain Health
The microbiome—which includes many hundreds of bacterial species that inhabit our bodies—provides aid in digestion, immune system development, and protection against harmful pathogens. But the microbiome also includes dozens of viruses that swarm within our bodies at any given time. Some of these can be potentially harmful, but simply lie dormant within our cells. Herpes simplex virus 1 (HSV-1), found in over 80% of people, and varicella-zoster virus, found in 95% of people, are known to make their way into the brain and sleep within our neurons and glial cells.
Experimental Insights into Concussion and Alzheimer’s Link
Dana Cairns, research associate in the Department of Biomedical Engineering at Tufts University and lead author of the study, had found evidence in earlier studies suggesting that activation of HSV-1 from its dormant state triggers the signature symptoms of Alzheimer’s disease in lab models of brain tissue—amyloid plaques, neuronal loss, inflammations, and diminished neural network functionality.
“In that study, another virus—varicella—created the inflammatory conditions that activated HSV-1,” said Cairns. “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?”
The link between HSV-1 and Alzheimer’s disease was first suggested by co-author Ruth Itzhaki, Visiting Professorial Fellow at Oxford University, who over 30 years ago identified the virus in a high proportion of brains from the elderly population. Her subsequent studies suggested that the virus can be reactivated in the brain from a latent state by events such as stress or immunosuppression, ultimately leading to neuronal damage. In the current study, the researchers used a lab model that reconstructs the environment of the brain to better understand how concussions may set off the first stages of virus reactivation and neurodegeneration.
Simulating Brain Injuries to Study Neurodegeneration
The brain tissue model consists of a 6mm wide donut-shaped sponge-like material made of silk protein and collagen, suffused with neural stem cells, which are then coaxed into mature neurons, growing axons and dendrite extensions and forming a network. Glial cells also emerge from the stem cells to help mimic the brain environment and nurture the neurons. The neurons communicate with each other through their extensions similarly to how they would communicate in a brain. And just like cells in the brain, they can carry within them the DNA of dormant HSV-1 virus.
After enclosing the brain-like tissue in a cylinder and giving it a sudden jolt atop a piston, mimicking a concussion, Cairns examined the tissue under the microscope over time. Some of the tissue models had neurons with HSV-1, and some were virus-free. After the controlled blows, she observed that the infected cells showed re-activation of the virus, and shortly after that the signature markers of Alzheimer’s disease, including amyloid plaques, p-tau (a protein that creates fiber-like “tangles” in the brain), inflammation, dying neurons, and a proliferation of glial cells called gliosis.
Potential Therapeutic Approaches Following Brain Trauma
More strikes with the pistons on the tissue models mimicking repetitive head injuries led to the same reactions, which were even more severe. Meanwhile, the cells without HSV-1 showed some gliosis, but none of the other markers of Alzheimer’s disease.
The results were a strong indicator that athletes suffering concussions could be triggering reactivation of latent infections in the brain that can lead to Alzheimer’s disease. Epidemiological studies have shown that multiple blows to the head can lead to doubling or even greater chances of having a neurodegenerative condition months or years down the line.
“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,” said Cairns.
Broader Implications for Traumatic Brain Injuries
The problem goes far beyond the concerns for athletes. Traumatic brain injury is one of the most common causes of disability and death in adults, affecting about 69 million people worldwide each year, at an economic cost estimated at $400 billion annually.
“The brain tissue model takes us to another level in investigating these connections between injury, infection, and Alzheimer’s disease,” said David Kaplan, Stern Family Endowed 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. There is a lot of epidemiological evidence about environmental and other links to the risk of Alzheimer’s. The tissue model will help us put that information on a mechanistic footing and provide a starting point for testing new drugs.”
Reference: “Repetitive injury induces phenotypes associated with Alzheimer’s disease by reactivating HSV-1 in a human brain tissue model” by Dana M. Cairns, Brooke M. Smiley, Jordan A. Smiley, Yasaman Khorsandian, Marilyn Kelly, Ruth F. Itzhaki and David L. Kaplan, 7 January 2025, Science Signaling.
DOI: 10.1126/scisignal.ado6430
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1 Comment
With a family and personal history of severe head trauma and very, very mild food allergy reactions, with only myself learning of my multiple food allergies causing chronic inflammation (exacerbated with added FDA approved neurotoxic MSG since 1980) in time to avoid/prevent dementia, it appears to me that identifying and avoiding one’s personal food allergy offenders and totally avoiding (e.g., FDA reversal of approval) added MSG would be better ways to address any potential trauma/dementia disorders than to keep wasting time and money on inventing probably toxic new drugs. Also, your findings sound like a good reason to abolish spectator sports in public schools, on the public dime; ‘pay now, pay later;’ double-down-dumb.