Concussions can cause Alzheimer's symptoms via latent virus

Concussions and repetitive head injuries in sports such as football and boxing, once accepted as an unpleasant consequence of intense athletic competition, are now recognized as serious health threats. Of particular concern is the link between head trauma and neurodegenerative diseases such as chronic traumatic encephalopathy, Alzheimer's disease and Parkinson's disease, and sports governing bodies are implementing protective equipment and rules to minimize risks. are being asked to adjust.

Tufts University and Oxford University researchers have uncovered a mechanism that may connect the dots between traumatic events and the emergence of disease, suggesting that most of our brains harbor latent viruses. They point out that it can be activated by shock. inflammation And the damage can accumulate over the following months and years. This result suggests the use of antiviral drugs as a potential early preventive treatment after head injury. This finding is published in the following study: science signaling.

of microbiomeIt contains hundreds of bacterial species that live in our bodies and aid in digestion, immune system development, and protection from harmful pathogens. But the microbiome also contains dozens of viruses that flock to our bodies at any given time. Some of these are potentially harmful, but they just lie dormant inside our cells. Herpes simplex virus 1 (HSV-1), which is found in more than 80% of people, and varicella-zoster virus, which is found in 95% of people, are known to invade the brain and lie dormant within neurons and glial cells. It is being

Dana Cairns, a researcher in Tufts University's School of Biomedical Engineering and lead author of the study, found that in laboratory brain models, activation of HSV-1 from a dormant state causes the characteristic symptoms of Alzheimer's disease. Previous research has found evidence suggesting this. Tissue amyloid plaques, neuronal loss, inflammation, and decreased neural network function.

“In that study, another virus, chickenpox, caused an inflammatory state that activated HSV-1,” Professor Cairns said. “We wondered what would happen if we exposed a brain tissue model to a physical disruption similar to a concussion. Would HSV-1 wake up and begin the process of neurodegeneration?”

The link between HSV-1 and Alzheimer's disease was first suggested by co-author Ruth Izaki, a visiting professor at the University of Oxford, who discovered more than 30 years ago that the virus was found in a high proportion of the brains of older people. Identified. Her subsequent research suggested that the virus can be reactivated from a latent state in the brain by events such as stress or immunosuppression, ultimately causing neurological damage. In the current study, researchers used a laboratory model that re-creates the brain's environment to better understand how concussions trigger viral reactivation and the first stages of neurodegeneration. Used.

The brain tissue model consists of a 6 mm wide donut-shaped sponge-like material made of silk protein and collagen, which is filled with neural stem cells that are guided to become mature neurons and form axons. Dendrites elongate and form a network. Glial cells also emerge from stem cells and help mimic the brain environment to nurture neurons. Neurons communicate with each other through extensions, just as they communicate in the brain. And like brain cells, they can carry dormant HSV-1 viral DNA within them.

Cairns trapped brain-like tissue inside a cylinder, delivered a sudden shock over a piston to mimic a concussion, and then examined the tissue under a microscope over time. Some of the tissue models had neurons containing HSV-1, and some had no virus. After a controlled blow, she found that infected cells showed reactivation of the virus, followed shortly by hallmarks of Alzheimer's disease such as amyloid plaques and p-tau (a protein that creates fibrous “tangles” in the body). We observed that a marker appeared. brain), inflammation, death of neurons, and proliferation of glial cells called gliosis.

Further blows of the piston to the tissue model, mimicking repetitive head trauma, produced the same reaction, but more severe. On the other hand, cells without HSV-1 showed some gliosis but no other markers of Alzheimer's disease.

The results were a strong indicator that concussed athletes may be causing a reactivation of latent infections in their brains that can lead to Alzheimer's disease. Epidemiological studies have shown that multiple blows to the head can double or even increase the likelihood of developing a neurodegenerative disease months or years later.

“This allows us to determine whether antiviral drugs or anti-inflammatory “These drugs could serve as early preventive treatments after head trauma to halt HSV-1 activation and reduce the risk of Alzheimer's disease,” Dr. Cairns said.

The issue goes far beyond athletes' concerns. Traumatic brain injury is one of the most common causes of disability and death in adults, affecting approximately 69 million people worldwide each year and resulting in an estimated economic cost of $400 billion annually. Masu.

“Brain tissue models take us to a new level in investigating the connections between injury, infection, and Alzheimer's disease,” said David Kaplan, Stern Family Endowed Professor of Engineering at Tufts University. said. “We can recreate a normal tissue environment similar to the inside of the brain and track viruses, plaques, proteins, gene activity, inflammation, and even measure the level of signaling between neurons. Environmental and other factors There is a lot of epidemiological evidence for this. Tissue models can help clarify associations with Alzheimer's disease risk, put that information on a mechanistic basis, and provide a starting point for testing new drugs.”