- A new study finds that two very common viruses carried by most people may interact to cause Alzheimer disease.
- Vaccines for one of the viruses seem to reduce the chances of developing Alzheimer’s disease.
- Research suggests that other common viruses may drive the development of the debilitating condition.
A study by researchers at Tufts University in Medford, Massachusetts reports that a combination of very common viruses may be a leading cause of Alzheimer’s disease (AD).
The virus responsible for chicken pox and shingles can activate a strongly associated latent herpes virus into its active state with AD.
Study Corresponding Author, Tufts’ Professor David Kaplan saying Today’s medical news that “[m]More than 95% of adults have had chickenpox during childhood and adolescence. The virus remains in the body afterwards.
Co-author Dr. Ruth Itzhakivisiting professor at the University of Oxford and professor emeritus at the University of Manchester, said MNT that “age and the decline of the immune system with age and immunosuppression” are factors that can re-awaken VZV as shingles in an adult.
Prior to the new study, “VZV has been linked to AD, but the link was unclear and the mechanisms were not understood,” said Dr. Itzhaki.
The study found that when VZV is activated as shingles, it reactivates latent
HSV-1 is also extremely common, with 50% to 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 AD risk, and our results explain this for shingles. We are now investigating whether this is the case for some other infections. If so, it would explain the great risk that infectious diseases represent.”
“If we shift paradigms,” said Professor Kaplan, “to focus more efforts on preventative strategies to treat these microbial species before they have a chance to wreak havoc, we might be able to better manage prevention of this disease.”
The study appears in The Journal of Alzheimer’s Disease.
“Thirty years of evidence from my laboratory, and subsequently from many others, suggests that HSV-1 is a major cause of AD, although the disease is obviously multifactorial,” Dr. Itzhaki told us.
According to Prof. Kaplan, “A number of factors have been reported to reactivate HSV-1 from latent state, including stress and disease states.” Dr. Itzhaki added “stressimmunosuppression, ultraviolet light and menstruation” as possible triggers.
Dr Tharick Pascoalassistant professor of psychiatry and neurology at the University of Pittsburgh School of Medicine, who was not involved in the study, commented on the findings.
“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 that leads to AD, or that the presence of inflammation decreases brain reserve, making patients more susceptible to developing AD.”
“If the latter is true,” Dr. Pascoal said, “we can imagine that various viruses may increase the risk of AD, including COVID-19.”
The study authors noted that there is evidence that both HSV-1 and VZV can be activated after COVID-19.
Professor Kaplan said MNT that he feels his study “also demonstrates how a 3D tissue model can be used to elucidate such interactions and synergies in relatively rapid methods.” Much of AD research uses animal models.
To test the effect of active VZV on dormant HSV-1, Professor Kaplan and colleagues created brain-like environments embedded in six-millimeter-wide donut-shaped sponges made from silk protein and collagen.
Neural Mother cells – some of which became functional neurons, and some of which became supporting brain glial cells – were delivered into the sponges.
When the researchers introduced VZV into brain tissue, they found that although the neurons were infected, it did not trigger the development of the hallmark of AD. amyloid plaques or tangles of tau protein. More importantly, the functionality of the neurons also remained intact.
However, when they introduced VZV into neurons with inactive HSV-1 present, HSV-1 reactivated, amyloid and tau protein growth increased, and the neurons’ electrical signals began to decrease as they would in AD.
Researchers have put a lot of effort into developing vaccines for HSV-1, but so far there is no successful vaccine. Some have suggested that mRNA vaccines may provide a more productive way forward.
Dr Pascoal suggested there may be reason for hope, saying, “I think we learned a lot about mRNA vaccines during the COVID pandemic in a very short period of time.”
“I am optimistic that we will have effective mRNA-based vaccines for different targets in the coming years using the knowledge gained with COVID-19,” he told us.
Dr. Heather M. SnyderHowever, , vice president of medical and scientific relations for the Alzheimer’s Association, who was not involved in the study, expressed some caution.
“Any potential therapy needs to be evaluated in multiple rigorous human studies. There are several ongoing studies using antivirals, including a funded by the Alzheimer’s Association through our Part the Cloud initiative.”
Meanwhile, although there is no vaccine for HSV-1, there are vaccines against shingles. The idea that stopping VZV can help people avoid AD is supported by
It has found that having received a shingles vaccine is associated with a reduced risk of AD.
Meanwhile, Dr. Snyder said: “As we age, there are things that research suggests are beneficial for our bodies and our brains: being physically active, eating a balanced diet, and keeping our brains active and engaged. Learn more about reducing your risk of cognitive decline and dementia about him Alzheimer’s Association website.”