Researchers from Oxford’s Institute of Population Ageing, Manchester University, and Tufts University have discovered that repeated head injuries may reawaken a dormant virus in the brain, prompting the onset of Alzheimer’s and dementia. They hope that the findings will lead to the development of new treatments for neurodegenerative disorders.
In recent years, there has been increased worry about the long-term repercussions of repetitive head injuries, particularly in contact sports like American football, rugby, and boxing. These injuries have been associated with an elevated risk of neurodegenerative disorders such as Alzheimer’s and chronic traumatic encephalopathy (CTE).
Studies have also looked into the connection between head trauma and Alzheimer’s disease, indicating that traumatic brain injury (TBI) may be a risk factor for neurodegenerative diseases [1].
Researchers at Tufts University and Oxford University have now discovered mechanisms that may link trauma events to disease development.
According to the new study, repeated head trauma, such as concussions, which are the known Alzheimer’s risk factors, may reawaken a common dormant virus in the brain, raising the risk of the disorder and other neurodegenerative diseases. Researchers discovered that this cascade of events can be set off by even a minor brain trauma, resulting in detrimental alterations linked to memory loss and cognitive decline.
The journal Science Signaling published the research [2].
Viruses in the Brain: Where Do They Come From?
The hundreds of bacterial species that live in our bodies make up the microbiome, which helps with immune system development, digestion, and defense against harmful diseases. However, the microbiome also contains dozens of viruses constantly swarming inside our bodies. Some of these are potentially dangerous yet remain latent within our cells.
Herpes simplex virus 1 (HSV-1), prevalent in more than 80% of individuals, and varicella-zoster virus, found in 95% of people, have been shown to enter the brain and sleep within our neurons and glial cells [3].
Exploring the Connection Between Head Injury, Virus, and Alzheimer’s
For over 30 years, Professor Ruth Itzhaki, who led the research with Drs Cairns and Kaplan at Tufts, has been investigating the possible involvement of HSV-1 in Alzheimer’s. Her team started at the University of Manchester, where they found the HSV-1 DNA in the human brain in a significant percentage of elderly individuals. It was the first microbe to be definitively identified in normal human brains. They later found that the virus increases the likelihood of getting the disease when it is present in the brain combined with a particular genetic component [4].
In earlier research, the researchers showed how common viruses like varicella zoster virus (VZV), which causes shingles and chickenpox, and herpes simplex virus type 1 (HSV-1), also known as the cold sore virus, contribute to the development of Alzheimer’s [5].
HSV-1 can remain dormant in human cells for a lifetime. However, when it re-emerges, it can cause gliosis, neuroinflammation, amyloid plaque-like formations (PLFs), and impaired functionality, similar to the alterations seen in the brains of Alzheimer’s patients.
In the most recent investigation, the researchers tested the impact of physical trauma on brain cells using their tiny, three-dimensional, bioengineered human brain tissue model [2]. Once dormant, the HSV-1 virus became active when repeated “mild blows,” akin to concussions, were applied to the brain tissues. Inflammation, beta-amyloid plaque accumulation, and the production of toxic tau proteins—which can destroy brain cells and impair memory—were all brought on by this reactivation.
Dana Cairns, research associate in the Department of Biomedical Engineering at Tufts University and lead author of the study, stated that Their findings raise the question of whether antiviral medications or anti-inflammatory therapies could be used as early preventive therapy following head trauma to halt HSV-1 activation and reduce the risk of Alzheimer’s disease.
The researchers discovered that suppressing the inflammatory molecule Interleukin-1 beta (IL-1β) reduced negative consequences in lab models, potentially leading to new treatments for individuals at risk.
Significance of the New Research
According to Itzhaki, head injuries and the cumulative effect of common infections are already acknowledged as major risk factors for disorders such as Alzheimer’s and dementia, but this is the first time they were able to show a mechanism for that process.
They observed that in the brain model, these injuries can reawaken a dormant virus, HSV1, causing inflammation that leads to the same alterations seen in Alzheimer’s patients.
She went on to say that understanding both the risk factors for dementia and Alzheimer’s, as well as the process by which they develop, is critical for targeting therapy and prevention at the earliest possible point.
According to David Kaplan, Stern Family Endowed Professor of Engineering at Tufts, the brain tissue model advanced their understanding of the links between injury, infection, and Alzheimer’s disease.
He stated that they could recreate natural tissue settings similar to those seen inside the brain, track viruses, plaques, proteins, genetic activity, and inflammation, and even evaluate the level of transmission between neurons. There is a lot of epidemiological research linking environmental factors to the development of Alzheimer’s. The tissue model could help them put that information on a mechanistic basis and give a starting point for testing new medications.
The researchers believe that their findings will open the way for new treatments to prevent neurodegeneration, particularly for people who are at high risk due to repeated concussions.
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References
- Gottlieb, S., 2000. Head injury doubles the risk of Alzheimer’s disease. BMJ, 321(7269), p.1100.
- Cairns, D.M., Smiley, B.M., Smiley, J.A., Khorsandian, Y., Kelly, M., Itzhaki, R.F. and Kaplan, D.L., 2025. Repetitive injury induces phenotypes associated with Alzheimer’s disease by reactivating HSV-1 in a human brain tissue model. Science Signaling, 18(868), p.eado6430.
- Concussions may trigger Alzheimer’s symptoms through latent viruses. News Medical. https://www.news-medical.net/news/20250107/Concussions-may-trigger-Alzheimers-symptoms-through-latent-viruses.aspx. Published Online: 7th January, 2025. Accessed: 11th February. 2025.
- Viral role in Alzheimer’s Disease discovered. University of Oxford. https://www.ox.ac.uk/news/2022-08-02-viral-role-alzheimers-disease-discovered. Published Online: 2nd August, 2022. Accessed: 11th February, 2025.
- Cairns, D.M., Itzhaki, R.F. and Kaplan, D.L., 2022. Potential involvement of varicella zoster virus in Alzheimer’s disease via reactivation of quiescent herpes simplex virus type 1. Journal of Alzheimer’s Disease, 88(3), pp.1189-1200.
- New study reveals link between head injuries and viruses in Alzheimer’s Disease. University of Oxford. https://www.ox.ac.uk/news/2025-01-08-new-study-reveals-link-between-head-injuries-and-viruses-alzheimers-disease. Published Online: 8th January, 2025. Accessed: 11th February, 2025.
- Concussions ‘reactivate dormant virus in brain’. BBC. https://www.bbc.com/news/articles/cvgn2p2yvvlo. Published Online: 8th January, 2025. Accessed: 11th February, 2025.
- Smith, R. Head Trauma Reactivates Hidden Viruses That Fuel Alzheimer’s Disease. Technology Networks. https://www.technologynetworks.com/cell-science/news/head-trauma-reactivates-hidden-viruses-that-fuel-alzheimers-disease-394833. Published Online: 9th January, 2025. Accessed: 11th February, 2025.
