“Hidden Dangers: How Head Injuries Could Unleash Dormant Viruses and Trigger Neurodegeneration”

Concussions and repetitive head injuries in sports like football and boxing, which were once seen as unfortunate byproducts of competitive sports, are now acknowledged as significant health risks.

Particularly alarming is the relationship between head trauma and neurodegenerative disorders like chronic traumatic encephalopathy, Alzheimer’s disease, and Parkinson’s disease, prompting sports authorities to modify protective gear and gameplay regulations to reduce these risks.

Investigators from Tufts University and Oxford University have recently identified mechanisms that could link traumatic events to the onset of these diseases, indicating that latent viruses residing in our brains may be triggered by such jolts, resulting in inflammation and cumulative damage that may manifest over subsequent months and years.

The findings propose the potential use of antiviral medications as early preventive measures following head injuries. These results are detailed in a study published in Science Signaling.

The microbiome—which encompasses numerous bacterial species inhabiting our bodies—supports digestion, immune system evolution, and defense against harmful pathogens. Yet, the microbiome also contains dozens of viruses that coexist within us at any time. While some of these can pose risks, many remain dormant within our cells.

Herpes simplex virus 1 (HSV-1), present in over 80% of individuals, and varicella-zoster virus, found in 95% of the population, are known to infiltrate the brain and reside within our neurons and glial cells.

Dana Cairns, a research associate in the Department of Biomedical Engineering at Tufts University and the principal author of the study, found indications in previous research suggesting that reactivation of HSV-1 from its dormant condition may trigger the distinct symptoms associated with Alzheimer’s disease in laboratory models of brain tissue—characterized by amyloid plaques, neuronal loss, inflammation, and compromised neural network functionality.

“In that study, another virus—varicella—induced the inflammatory environment that triggered HSV-1,” stated Cairns. “We wondered, what would occur if we subjected the brain tissue model to a physical disruption, similar to a concussion? Would HSV-1 awaken and initiate neurodegeneration?”

The association between HSV-1 and Alzheimer’s disease was first proposed by co-author Ruth Itzhaki, a Visiting Professorial Fellow at Oxford University, who identified the virus in a significant percentage of brains from the older population over 30 years ago. Her later studies indicated that the virus could be reactivated in the brain from a dormant state due to factors such as stress or immunosuppression, eventually resulting in neuronal damage.

In the current investigation, the researchers employed a laboratory model that simulates the brain environment to enhance understanding of how concussions might activate the initial stages of virus reactivation and neurodegeneration.

This brain tissue model consists of a 6mm-wide donut-shaped, sponge-like material made from silk protein and collagen, infused with neural stem cells, which are subsequently encouraged to develop into mature neurons, growing axon and dendrite projections while establishing a network. Glial cells also develop from the stem cells to help replicate the brain environment and support the neurons.

The neurons engage with one another via their extensions, analogous to how they would interact in an actual brain. Furthermore, like cells in the brain, they can harbor the DNA of dormant HSV-1 virus.

Following the encasement of the brain-like tissue in a cylinder and delivering a sudden jolt atop a piston to imitate a concussion, Cairns scrutinized the tissue under a microscope across time. Some tissue models contained neurons with HSV-1, while others were free of the virus.

After the controlled impacts, she discovered that the infected cells demonstrated reactivation of the virus, and shortly thereafter, the hallmark indicators of Alzheimer’s disease, such as amyloid plaques, p-tau (a protein that creates fiber-like “tangles” in the brain), inflammation, dying neurons, and an increase in gliosis, a proliferation of glial cells.

Repeated strikes with the pistons on the tissue models, simulating repetitive head injuries, resulted in similar responses, which were even more pronounced. Meanwhile, the cells lacking HSV-1 showed some gliosis but none of the other indicators of Alzheimer’s disease.

The findings strongly suggest that athletes experiencing concussions may be triggering the reactivation of latent infections within the brain that could contribute to Alzheimer’s disease. Epidemiological studies have indicated that multiple impacts to the head can significantly increase the likelihood of developing a neurodegenerative disorder months or years later.

“This raises the question of whether antiviral medications or anti-inflammatory substances could be beneficial as early preventive treatments following head trauma to halt HSV-1 activation and reduce the risk of Alzheimer’s disease,” remarked Cairns.

The issue extends far beyond the