Prime Highlights:
A new study suggests that herpes simplex virus 1 (HSV-1), the virus behind cold sores, may link concussions to dementia risk.
Brain injuries like concussions can trigger inflammation that reactivates dormant herpes viruses in the brain.
The research used lab-grown miniature brain models to simulate concussions and observe HSV-1 reactivation.
Key Background:
A recent study sheds light on a potential connection between concussions and dementia, suggesting that the herpes simplex virus 1 (HSV-1), the cause of cold sores, may play a critical role in this link. Using lab-grown brain models, researchers discovered that physical injury to the brain, such as a concussion, could reactivate dormant herpes viruses, triggering inflammation that may contribute to dementia-like changes in the brain.
Concussions, a common form of brain injury, have long been associated with an increased risk of neurodegenerative conditions like Alzheimer’s disease and chronic traumatic encephalopathy (CTE). The new research provides insight into the biological processes following brain injury that could lead to these diseases. Previous studies have suggested that herpes viruses, including HSV-1, could potentially contribute to these changes by lying dormant in the brain and reactivating under certain conditions, such as inflammation.
Lead author Dana Cairns, a postdoctoral research fellow at Tufts University, explained that herpes viruses, once dormant, can remain in the body for life and reactivate during times of stress or immune suppression. The new study, published in Science Advances, used miniature brain models made from stem cells to explore this phenomenon. The models were infected with HSV-1 and then subjected to two types of brain injury: severe injury and concussion. Following injury, the researchers found that the HSV-1 virus reactivated in the brain models, triggering inflammation and the accumulation of proteins typically associated with dementia. The results were consistent with the concept that repeated head injuries may exacerbate neurodegenerative conditions.
These findings suggest that targeting inflammation after injury may help prevent viral reactivation and its associated damage. While these experiments were conducted on lab-grown models, further studies in animal models are needed to validate the results and explore potential therapeutic options, such as antiviral or anti-inflammatory treatments, that could mitigate the risks of brain injury leading to dementia.
