Inflammation in the brain can reawaken dormant viruses, which may lead to the onset of neurodegenerative disease, a new study finds.
New research has shown for the first time that repeated head injuries – a known risk factor for Alzheimer’s disease – may reactivate a common virus that can lie dormant in human cells for a lifetime.
According to Alzheimer’s Research UK, almost half of dementia cases worldwide could be prevented or delayed. Without severe head injuries, there would be three fewer cases of dementia for every 100 people who develop it now.
READ MORE: How to tell if you’ve got ‘real flu’ as top GP names symptoms that wipe people out
READ MORE: New HMPV virus outbreak symptoms and risks explained as it hits China
Published in the journal Science Signaling, the study suggests that the herpes simplex virus 1 (HSV-1), or the so-called cold sore virus, which is found in over 80% of people, may connect the dots between head trauma and brain disease.
“We thought, what would happen if we subjected the brain tissue model to a physical disruption, something akin to a concussion?” asked Dana Cairns, research associate in the Department of Biomedical Engineering at Tufts University and lead author of the study. “Would HSV-1 wake up and start the process of neurodegeneration?”
In earlier studies, Cairns had noted that activation of HSV-1 from its dormant state triggers the signature symptoms of Alzheimer’s disease in lab models of brain tissue.
Almost half of dementia cases worldwide could be prevented or delayed -Credit:PA
Researchers from Oxford’s Institute of Population Ageing and the University of Manchester, and Tufts University then set out to reconstruct the environment of the brain in a lab model to better understand how concussions may set off the first stages of virus reactivation and neurodegeneration.
Under lab conditions, researchers created a brain-like tissue using neural stem cells, enclosed it in a cylinder and gave it a sudden jolt to mimic a concussion, before examining the tissue under a microscope.
They observed that the infected cells showed re-activation of the virus, and shortly after that the signature markers of Alzheimer’s disease.
More strikes to the tissue models mimicking repetitive head injuries led to the same reactions, but even more severe.
Earlier evidence suggests brain injuries raise the risk of dementia, and the more blows someone takes to the head, the higher that risk becomes
“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.
Traumatic brain injury is one of the most common causes of disability and death in adults, affecting about 69 million people worldwide each year.
Last year, a report commissioned by Alzheimer’s Society said the cost of dementia to the UK was forecast to be £42 billion in 2024, rising to £90 billion in 2040.
Professor Itzhaki, Visiting Professorial Fellow at the Oxford Institute of Population Ageing and Emeritus Professor at the University of Manchester, said: ‘Head injuries are already recognised as a major risk factor, as are the cumulative effect of common infections, for conditions such as Alzheimer’s and dementia, but this is the first time we have been able to demonstrate a mechanism for that process.
‘What we’ve discovered is that in the brain model these injuries can reactivate a dormant virus, HSV1, setting off inflammation which, in the brain, would lead to the very changes we see in Alzheimer’s patients.
‘Understanding both the risk factors for dementia and Alzheimer’s, and the mechanism by which they develop, is important in being able to target treatment and prevention at as early a point as possible.