Researchers from the University of Oxford, in collaboration with the University of Manchester and Tufts University, have uncovered new insights into the relationship between head injuries and Alzheimer’s disease. A recent study reveals that repeated head trauma, such as concussions, may trigger the reactivation of dormant viruses in the brain, increasing the risk of neurodegenerative diseases, including Alzheimer’s.
The research, led by Professor Ruth Itzhaki from Oxford’s Institute of Population Ageing, along with Drs. Cairns and Kaplan from Tufts University, suggests that even mild brain injuries could set off a chain of events that leads to cognitive decline and memory loss. The study highlights how head trauma could awaken common viruses like the herpes simplex virus type 1 (HSV-1), which is known to lie dormant in brain cells for extended periods.
“We’ve long recognized that head injuries and infections contribute to Alzheimer’s and dementia,” said Professor Itzhaki. “But this is the first time we’ve demonstrated a direct mechanism through which these factors trigger the disease process. The reactivation of HSV-1 leads to brain inflammation, which in turn causes the damage we associate with Alzheimer’s.”
HSV-1, often associated with cold sores, can remain dormant in the human body for life. When reactivated, it causes changes that mimic the neurological damage seen in Alzheimer’s patients, including the buildup of beta-amyloid plaques and harmful tau proteins. These plaques and proteins are hallmarks of Alzheimer’s and other neurodegenerative diseases.
In the study, the team used bioengineered 3D brain tissue models to simulate the effects of repeated mild brain trauma, similar to concussions. When the brain tissue was exposed to physical stress, the dormant HSV-1 virus was reactivated, triggering a cascade of harmful effects in the brain. Inflammation was induced, leading to the formation of beta-amyloid plaques and tau proteins, which are associated with cognitive decline and memory loss.
The researchers also discovered that blocking the inflammatory molecule Interleukin-1 beta in their lab models significantly reduced these harmful effects, presenting a potential avenue for future treatments. This breakthrough could pave the way for earlier interventions for individuals at risk of Alzheimer’s due to head injuries or viral infections.
Professor Itzhaki, who has spent over 30 years researching the role of HSV-1 in Alzheimer’s disease, previously demonstrated that HSV-1 DNA is present in the brains of a high proportion of older individuals. This latest study builds upon that foundation, offering new hope for understanding and potentially mitigating the impact of head injuries on Alzheimer’s and other forms of dementia.
The findings underscore the complex interplay between physical trauma, viral infections, and neurodegenerative diseases, and open new doors for research aimed at early diagnosis and preventative measures.
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