Football, rugby, boxing … The link between neurodegenerative diseases and concussions and head trauma repeated in these sports is well documented today.
A recent study, conducted by researchers from the universities of Oxford and Tuffs and published in the journal Science Signalingsuggests that the dormant viruses of our microbiome could play a role there.
Concretely, scientists have discovered by what mechanisms these traumatic events could lead to the emergence of Alzheimer’s disease: dormant viruses, reactivated by tremors, would lead to inflammation and a chain of lesions and damage similar to those caused by Alzheimer .
Several studies have already highlighted the role played by the Type 1 herpes virus (HSV-1), the Labial herpes virus in the development of Alzheimer’s disease. This virus present in the microbiome of the majority of the population is known, according to a press release from the University of Tufts, to enter the brain and remain inactive in neurons and glial cells.
Previous studies have shown that the HSV-1 could remain sleeping in human cells during a lifetime. But if he woke up, he could then cause chain events similar to the signs observed in the brain of patients with Alzheimer’s disease. This link had been highlighted via brain tissue laboratory models.
How and why does the virus wake up?
The Pre Ruth Itzhaki, which participated in this study, discovered the association between HSV-1 and Alzheimer’s disease over 30 years ago. Other studies had suggested that the virus could be reactivated in the brain by events such as major stress or immunosuppression and train in fine Neuronal lesions.
« We wondered what would happen if we subject our brain fabric model to a physical disruption, something that is a gear. Would HSV-1 wake up and trigger the process of neurodegeneration? », Questions Dana Cairns, main author of the study, researcher at the University of Toft.
The brain fabric model used reconstructs the brain environment with the highest precision. Mature neurons, axons, dendritis extensions, glial cells … everything is there. This exact 3D human brain replica was subjected to repeated light blows.
-Under their effects, the HSV-1 virus, hitherto sleeping in certain fabrics, has become active. And this reaction resulted shortly after, in infected cells, the appearance of markers characteristic of Alzheimer’s disease – amyloid plates, tangling proteins, inflammation, death of neurons and proliferation of glial cells (phenomenon called gliosis ).
Towards a preventive treatment after a head trauma?
“Head injuries are already recognized as a major risk factor, as well as the cumulative effect of current infections, for diseases such as Alzheimer’s disease and dementia, but this is the first time that we have could demonstrate a mechanism for this process, commented the pre Itzaki.
What we have discovered is that in the brain model, these injuries can reactivate a dormant virus, the HSV1, triggering an inflammation which, in the brain, would lead to the same changes that we observe in patients with the disease of the disease ‘Alzheimer’s ”.
“This raises the question of whether antiviral drugs or anti-inflammatory agents could be useful as early preventive treatments after head trauma to stop the activation of HSV-1 and reduce the risk of Alzheimer’s disease”, Jouted Dana Cairns.
Because, in addition to updating the mechanism, researchers also discovered that inhibiting the pro-inflammatory interleukin-1 beta (IL-1β) in the laboratory brain model.
But even beyond the concerns raised by this study for athletes, what about the 69 million people, victims each year in the world of a head trauma?
