Inflammation can reawaken dormant viruses in the brain, which may help explain why concussions often precede dementia, a new study has found.
Brain injuries such as concussions Increases risk of dementiaAnd evidence suggests that the more times someone hits themselves in the head, the higher the risk. Scientists are studying what happens in the brain after damage that can cause changes associated with dementia, such as the buildup of abnormal proteins and brain cell dysfunction and death. Such changes can be seen in alzheimer’s disease and chronic traumatic encephalopathy (CTE) is a recently recognized disorder in high-impact sports.
Some scientists believe these changes may be related to a common virus, herpes simplex virus 1 (HSV-1), the bacteria behind cold sores.
Herpesviruses (a broader group that also includes the viruses behind chickenpox and monopox) have the ability to lie dormant in the body and later reactivate. “They can remain dormant in the body forever,” said the study’s lead author. dana cairnsa postdoctoral fellow at Tufts University. Cairns told Live Science that there is evidence that HSV-1 somehow gets into the brain and lies there waiting.
Related: Lab-created ‘mini-brains’ help explain why traumatic brain injury increases risk of dementia
What’s new here is that researchers have demonstrated that physical damage can activate viruses that are dormant in the brain. Dr. Gorazd StokinHe heads the neuroscience laboratory at the Institute of Molecular and Translational Medicine in the Czech Republic and was not involved in the new study.
The new study relies on a miniature laboratory model of the brain, so further research will be needed to show that the results are relevant to humans. “But it’s a good first step to showing something interesting,” said Stokin, who is also a consultant neurologist at Britain’s Gloucestershire Hospitals NHS Foundation Trust.
Viruses in dementia
The idea that viruses cause dementia is not new. Ruth Izakia co-author of the new paper, brought up this concept. in 1991. Itzaki and his colleagues discovered the virus in the brains of elderly people who died of Alzheimer’s disease. they are Found later People who carry both the virus and ApoE4 — Genetic mutations that increase risk of Alzheimer’s disease — have a higher risk of disease than people who only have ApoE4. They also found that latent HSV-1 can be reawakened by stress and immunosuppression.
“She received a lot of backlash at the time,” Cairns said of Itzaki’s early work. This viral theory of dementia has been niche for decades, but in recent years Interest increased. These days, scientists also have better tools to test theories. Human brain model created in the lab.
The new study was published on Tuesday (January 7) in the journal scientific progressa brain model just 0.2 inches (6 millimeters) in diameter was used. The spongy, donut-shaped structure is made of silk and infused with stem cells. Using certain chemicals, stem cells mature into different brain cells that carry one copy of ApoE4. This genetic trait is ‘relatively common’ among Alzheimer’s patientsStokin pointed out that it is appropriate to include it in brain models.
The researchers infected these models with HSV-1 and used antiviral drugs to force the virus into a dormant state. In previous studies, they showed that: inflammation It is thought that this may have “waked up” the virus, causing changes in brain cells that are also seen in dementia. In the previous workThe researchers caused the inflammation by the varicella-zoster virus, the virus behind chickenpox and shingles.
But “beyond infections, there are other things that can cause inflammation, such as injuries,” Cairns says. “We wanted to know if injury could cause something similar.”
In the new study, the research team subjected the minibrains to models of two types of injury. One is a severe injury in which the skull appears to have broken, and the other is a concussion, in which the brain moves or twists inside the skull. In the concussion experiment, a minibrain was placed in a 3D-printed container filled with a fluid similar to the fluid that cushions the brain inside the skull. Next, we placed the mini-brain in the case on a table where we hit it with a piston.
In both experiments, the brain models were inflamed and HSV-1 reactivated within them. Dementia-related changes, such as protein accumulation, appeared in these infected brain models but not in the lesioned but uninfected model used for comparison.
In the severe injury experiment, the cells were so severely damaged that they died quickly, but in the concussion experiment, the cells survived, allowing the experiment to be repeated. The more this was repeated, the more the dementia-like condition of the infected model worsened.
“People who have been exposed to more chronic damage over longer periods of time often exhibit the worst symptoms of neurodegeneration clinically,” Dr. Cairns noted. “that [the experiment] It matched the concept really well. ”
Additional experiments by the research team suggested that blocking inflammation after injury can prevent HSV-1 from reactivating and prevent the development of dementia symptoms. This discovery strengthened the team’s overall performance, Stockin said. But this result was only shown in minibrains, so “it would be beneficial to try the same thing in animal models,” he added.
Researchers plan to continue experimenting with brain models to see what might block HSV-1’s reawakening — for example, anti-inflammatory and antiviral drugs may be effective. Yes, Cairns said.
“If we could prevent reactivation, or somehow control the viral load…that would be beneficial,” Stokin said, hypothesizing that herpes is indeed the missing link between brain damage and dementia.
