People over 65 who received the recombinant herpes virus vaccine (Shingrix) were less likely to be diagnosed with dementia over the next six years, compared with those who received the live, attenuated vaccine (Zostavax) or other vaccines such as the flu and Tdap (tetanus, diphtheria and pertussis). Those are the findings of a study published Thursday in the journal Nature Medicine, adding to a long list of work over the past few decades suggesting — without confirming — that the herpes virus may play a role in the development of dementia.
The team of researchers conducted a natural experiment, taking advantage of the fact that in the United States, people over 65 are vaccinated against herpes and that there was a rapid switch in 2017 between the attenuated vaccine (Zostavax) and the recombinant vaccine (Shingrix). The study compared more than 100,000 people who received the old drug between 2014 and 2017 with another 100,000 people who received the new version between 2017 and 2022.
The researchers then looked at how many of the participants were diagnosed with a form of dementia, such as Alzheimer's disease, in the six years following the injection. The results showed that receiving the Shingrix vaccine was associated with living 17 percent longer without being diagnosed with these diseases, compared with those who received Zostavax.
“This is the equivalent of 164 extra days without a diagnosis of dementia among those who subsequently developed it,” said Paul Harrison, a researcher at the University of Oxford, at a press conference accessed by elDiario. The protection was greater compared to people who had not received the herpes vaccine but had received the flu or Tdap vaccine.
These differences, as previous studies of the Zostavax vaccine have shown, were greater in women: 22% more time without a diagnosis, compared with 13% in men. Harrison noted that this is one of the unknowns left by the research, along with the mechanisms responsible for the seemingly greater protective effect of the new vaccines.
Virus or vaccine
As with previous studies that analyzed the same effect with the old vaccine, the observational design of Harrison’s work does not allow conclusions to be drawn about causality. In other words, it is not possible to know whether the association shown in the scientific literature between dementia cases and the herpes virus is directly due to the virus or its vaccine. However, some researchers believe there is enough published data to suggest there is something behind it.
One of them is Ruth Itzhaki, emeritus professor of Molecular Neurobiology at the University of Manchester (United Kingdom), who has defended this theory since 1991 and already suggested the protective effect of vaccines in 2002. “Infections could cause the herpes simplex virus type 1 to be repeatedly reactivated from its latency in the brains of older people, as a result of the neuroinflammation that infections would cause, and the cumulative damage caused would eventually lead to the development of dementia,” he assures elDiario. . .is.
Herpes viruses, which are also responsible for chickenpox, are annoying because they can persist in the body after the initial infection, hiding from the immune system in the sensory ganglia of neurons. Then they can reactivate, go to the skin and start multiplying again, causing the characteristic sores. For this reason, Itzhaki explains that “vaccines could reduce the risk [de padecer demencia] by reducing the number and severity of infections.”
Correlation does not imply causation
Not everyone is convinced, partly because the herpes virus is common and is found in the brains of people who never develop dementia. Also because many researchers believe that the buildup of beta-amyloid proteins and tau tangles is responsible for Alzheimer's. Proponents of Itzhaki's hypothesis argue that the virus triggers brain cells to produce the proteins, or that cells damaged by an infection produce them as part of an immune response.
“While the herpes zoster virus seems increasingly likely to be the cause of Alzheimer’s, we need to remember that any link of this kind is not straightforward,” explains Andrew Doig, a professor of biochemistry at the University of Manchester, who did not take part in the study published in Nature Medicine. “Most people who are infected with the virus never develop the disease,” says Doig, because “there are many other factors that influence the chance of developing dementia, such as genetics, cardiovascular problems and head trauma.” In fact, the prevalence of dementia in Europe and the United States has decreased by 13% over the past 25 years, despite population ageing, without the cause being known, perhaps due to general improvements in cardiovascular health.
Still, Doig defends that “this is a significant result, comparable in effectiveness to recent antibody drugs” against Alzheimer’s disease. Therefore, administering the recombinant herpes vaccine “could be a simple and inexpensive way to reduce the risk.” According to him, the next step would be to conduct a clinical trial comparing patients who receive the vaccine with those who receive a placebo: “It is the most reliable way to know to what extent the vaccine works. “We also need to see how many years the effect can last and whether we should vaccinate people at a younger age.”
The role of certain viruses ubiquitous in human populations in the development of certain diseases – most of the planet is infected with herpes simplex type 1 without knowing it – is an old debate in which proving causality often becomes a headache. However, it is not impossible: the association of the Epstein-Barr virus – responsible for mononucleosis – with multiple sclerosis was discovered in the 1980s, but it was only in 2022 that a study showed that the pathogen is the “root cause” of this disease. Perhaps herpes vaccines will one day become another tool in the fight against dementia.