- A new study finds that two common viruses most people carry may interact to cause Alzheimer’s disease.
- Vaccines for one of the viruses seem to reduce the chance of developing Alzheimer’s.
- The research suggests that other common viruses may stimulate the development of the debilitating condition.
A study by researchers at Tufts University in Medford, Massachusetts reports that a combination of common viruses may be a major cause of Alzheimer’s disease (AD).
The virus responsible for chickenpox and shingles can activate a dormant herpes virus that in its active state is strongly associated with AD.
Varicella zoster virus (VZV) is the virus that causes varicella — or
Corresponding author of the study, Prof. David Kaplan of Tufts: Medical news today That “[m]more than 95% of adults have 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 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 trigger VZV awakenings like shingles in an adult.
Before the new study, “VZV had been linked to AD, but the linkage was unclear and the mechanisms were not understood,” said Dr. Itzhaki.
The study found that when VZV is activated as shingles, it is reactivated while dormant
HSV-1 is also very 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 carry a risk of AD, and our results explain this for shingles. We are now investigating whether this is also the case with some other infections. If so, that could be the case.” explain the high risk of infectious diseases.”
“If we change paradigms,” said Prof. Kaplan, “to focus our efforts more on preventive strategies to treat these microbial species before they have a chance to wreak this havoc, we may have a better handle on preventing of this disease.”
The study appears in The Journal of Alzheimer’s Disease.
“Thirty years of evidence by my lab, and then by many others, suggests that HSV-1 is a major cause of AD, although the disease is clearly multifactorial,” Dr. Itzhaki us.
According to Prof. Kaplan, “a range of factors that reactivate HSV-1 from the latent state have been reported, including stress and disease states.” dr. Itzhaki added “stress, immunosuppression, UV light and menstruation” as possible triggers.
dr. Tharick Pascoal, an assistant 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 evidence suggesting that HSV-1 may lead to neuroinflammation, which is associated with an increased risk of developing Alzheimer’s disease,” he noted.
“Interestingly,” he added, “this research 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 may reduces brain reserve, making patients more susceptible to developing AD.”
“If the latter is true,” said Dr. Pascoal, “we can imagine that several viruses can 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 believes his research “also shows how a 3D tissue model can be used to elucidate such interactions and synergies in relatively fast methods.” Much AD research uses animal models.
To test the effect of active VZV on inactive HSV-1, Prof. Kaplan and his colleagues created brain-like environments embedded in six millimeter-wide donut-shaped sponges made of silk protein and collagen.
Neural stem cells — some of which developed into functional neurons and some of which became supportive glial cells of the brain — were delivered into the sponges.
When the researchers introduced VZV into the brain tissue, they found that while the neurons became infected, there was no trigger for the development of AD’s characteristic amyloid plaques or tau protein tangles. More importantly, the functionality of the neurons also remained unaffected.
However, when they introduced VZV into neurons with dormant HSV-1 present, the HSV-1 was reactivated, there was increased growth of amyloid and tau protein, and the neurons’ electrical signals began to slow down as in AD.
Researchers have put a lot of effort into developing vaccines for HSV-1, but so far no successful vaccine exists. Some have suggested that mRNA vaccines could provide a more productive way forward.
dr. Pascoal suggested there may be reason to hope, saying, “I think we’ve learned a lot about mRNA vaccines in a very short period of time during the COVID pandemic.”
“I am optimistic that in the coming years we will have effective mRNA-based vaccines for various targets, leveraging the knowledge gained from COVID-19,” he told us.
dr. However, Heather M. Snyder, vice president of medical and scientific relations for the Alzheimer’s Association, and not involved in the study, expressed some caution.
“Any potential therapy needs to be evaluated in multiple, rigorous studies in humans. There are several ongoing studies using antivirals, including one funded by the Alzheimer’s Association through our Part the Cloud initiative,” she noted.
Meanwhile, while there is no vaccine for HSV-1, there are shingles vaccines. The idea that stopping VZV can help people avoid AD is supported by:
Indeed, having a shingles vaccine has been found to be associated with a reduced risk of AD.
Meanwhile, said Dr. Snyder: “As we age, there are things that research suggests are beneficial for our bodies and brains — physical activity, 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.”