- A new study reveals that two very common viruses that most people carry could interact to cause Alzheimer’s disease.
- Vaccines against one of the viruses appear to reduce the risk of developing Alzheimer’s disease.
- Research suggests that other common viruses can lead to the development of the wasting disease.
A study by researchers at Tufts University in Medford, Massachusetts, reports that a combination of very common viruses could be one of the main causes of Alzheimer’s disease (AD).
The virus responsible for chicken pox and shingles can activate a dormant herpes virus strongly associated with AD into its active state.
Varicella zoster virus (VZV) is the virus that causes chickenpox — or
Corresponding author of the study, Professor David Kaplan of Tufts said Medical News Today this “[m]More than 95% of adults had chickenpox during childhood and adolescence. The virus then remains in the body.
Co-author Dr Ruth Itzhaki, Visiting Professor at the University of Oxford and Emeritus Professor at the University of Manchester, said DTM that “age and the decline of the immune system with age, and immunosuppression” are factors that can awaken VZV as shingles in an adult.
Prior to the new study, “VZV was linked to AD, but the link was unclear and the mechanisms not understood,” Dr Itzhaki said.
The study found that when VZV becomes activated as shingles, it reactivates dormancy
HSV-1 is also extremely common, with 50-80% of American adults carrying the virus. Although the oral or genital form of VZV is active, it can cause painful blisters at the site of infection.
Dr. Itzhaki noted:
“What is now known is that infectious diseases, in general, confer risk for Alzheimer’s disease, and our results explain this for shingles. We are now investigating whether this is the case for certain other infections. If so, this would explain the major risk posed by infectious diseases.
“If we shift the paradigm,” Professor Kaplan said, “to focus more of our efforts on preventative strategies for dealing with these microbial species before they have a chance to wreak this havoc, we might have a better handle on prevention. of this disease”.
The study appears in The Journal of Alzheimer’s Disease.
“Thirty years of evidence by my lab, and subsequently by many others, suggests that HSV-1 is a major cause of AD, although the disease is obviously multifactorial,” Dr. Itzhaki told us.
According to Professor Kaplan, “a range of factors have been reported to reactivate HSV-1 from the latent state, including stresses and disease states”. Dr. Itzhaki added “stress, immunosuppression, UV light and menstruation” as possible triggers.
Dr. Tharick Pascoal, assistant professor of psychiatry and neurology at the University of Pittsburgh School of Medicine who was not involved in the study, commented on the results.
“This study adds to the body of evidence suggesting that HSV-1 can lead to neuroinflammation, which is associated with an increased risk of developing Alzheimer’s disease,” he noted.
“Interestingly,” he added, “this study suggests that this occurs independently of amyloid and tau deposition, which may support the idea that there are independent pathways of neuroinflammation leading to AD, or that the presence of inflammation decreases brain reserve, making patients more susceptible to developing AD.
“If the latter is true,” said Dr. Pascoal, “we can imagine that various viruses may increase the risk of AD, including COVID-19.”
The study authors noted that there is evidence that HSV-1 and VZV can be activated after COVID-19.
Professor Kaplan said DTM that he believes his study “also demonstrates how a 3D tissue model can be used to elucidate such interactions and synergies by relatively rapid methods.” Much AD research uses animal models.
To test the effect of active VZV on inactive HSV-1, Professor Kaplan and his colleagues created brain-like environments embedded in six millimeter-wide doughnut-shaped sponges made of silk proteins and collagen.
Neural stem cells – some of which developed into functioning neurons, and some of which became supporting brain glial cells – were delivered into the sponges.
When researchers introduced VZV into brain tissue, they found that even though neurons were infected, there was no trigger for the development of amyloid plaques or the tau protein tangles characteristic of Alzheimer’s disease. . More importantly, the functionality of the neurons also remained intact.
However, when they introduced VZV into neurons containing dormant HSV-1, HSV-1 reactivated, growth of amyloid and tau proteins increased, and the neurons’ electrical signals began to slow as they would do in AD.
Researchers have put a lot of effort into developing vaccines against HSV-1, but so far no effective vaccine exists. Some have suggested that mRNA vaccines might provide a more productive pathway.
Dr Pascoal suggested there might be reason for hope, saying, “I think we’ve learned a lot about mRNA vaccines during the COVID pandemic in a very short time.”
“I am optimistic that we will have effective mRNA-based vaccines for different targets in the coming years using the insights gained with COVID-19,” he told us.
Dr. Heather M. Snyder, vice president of medical and scientific relations for the Alzheimer’s Association, and not involved in the study, expressed some caution, however.
“Any potential therapy must be evaluated in multiple rigorous human studies. There are several ongoing studies using antivirals, including one funded by the Alzheimer’s Association through our Part the Cloud initiative,” he said. she noted.
Meanwhile, although there is no vaccine for HSV-1, there are vaccines for shingles. The idea that stopping VZV can help people avoid AD is supported by
He found that having had a shingles vaccine is indeed associated with a reduced risk of AD.
Meanwhile, Dr Snyder said: ‘As we age, research suggests certain things are good for our bodies and our brains – getting physical activity, eating a balanced diet and keeping our brains active and engaged. . Learn more about reducing the risk of cognitive decline and dementia on the Alzheimer’s Association website.