People 65 and older who received the recombinant herpesvirus vaccine (Shingrix) were less likely to be diagnosed with dementia in the next six years, compared with those who received the live vaccine (Zostavax) or other vaccines such as influenza and Tdap (tetanus, diphtheria, and pertussis). These are the findings of A study published this Thursday in the journal Nature Medicine, which adds to a long list of works which, in recent decades, seem to suggest – 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, in 2017, there was a rapid switch between the attenuated vaccine (Zostavax) and the recombinant vaccine (Shingrix). The study compared more than 100,000 people who had received the old drug between 2014 and 2017 with another 100,000 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, within six years of getting the shot. The results showed that receiving the Shingrix vaccine was associated with living 17% longer without being diagnosed with these diseases, compared with those who received Zostavax.
“This is the equivalent of 164 additional days without a diagnosis of dementia among those who subsequently suffered from it,” explained the researcher from Oxford University and co-author of the study, Paul Harrison, in a press conference to which elDiario.es has had access. The protection was greater when compared with people who had not received a herpes vaccine, but had received the flu or Tdap vaccine.
These differences, as previous studies with the Zostavax vaccine have shown, were greater in women — 22% longer without diagnosis, compared to 13% for men. Harrison said this is one of the unknowns left by the study, along with the mechanisms responsible for the apparent greater protective effect of the new vaccines.
Virus or vaccine
As with previous studies that looked at the same effect with the old vaccine, the observational design of Harrison’s work does not allow conclusions about causality. In other words, it is not possible to know whether the association shown in the scientific literature between cases of dementia and the herpes virus is directly due to the virus or to its vaccine. However, some researchers believe that there is enough published data to think that there is something behind it.
One of them is the emeritus professor of Molecular Neurobiology at the University of Manchester (United Kingdom) Ruth Itzhaki, who has been defending this theory since 1991 and in 2002 he already suggested the protective effect from vaccines. “Infections could cause the herpes simplex virus type 1 to be repeatedly reactivated from its latency in the brains of older people, due to the neuroinflammation that infections would induce, and the cumulative damage caused would eventually lead to the development of dementia,” he told elDiario.es.
Herpes viruses — which are also responsible for chickenpox — are annoying because they can persist in the body after the first infection by hiding from the immune system in sensory nerve cells. They can then reactivate, travel to the skin and begin replicating again, causing the characteristic sores. For this reason, Itzhaki explains that “vaccines could reduce the risk[of suffering from dementia]by reducing the number of infections and their severity.”
Correlation does not imply causation
Not everyone is convincedpartly because the herpes virus is so 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 either the virus induces brain cells to produce the proteins, or cells damaged by an infection produce them as part of an immune response.
“Although the shingles virus as a cause of Alzheimer’s disease seems increasingly likely, we must bear in mind that any such relationship is not straightforward,” explains Professor of Biochemistry at the University of Manchester Andrew Doig, who was not involved in the study published in Nature Medicine. “Most people infected with the virus never get the disease,” says Doig, because “there are many other factors that influence the likelihood of developing dementia, such as genetics, cardiovascular problems and head trauma.” In fact, in the last 25 years the prevalence of dementia in Europe and the United States has decreased by 13% despite the ageing of the population, although the cause is not known, perhaps because of the lack of knowledge of the cause. overall improvements in cardiovascular health.
Nevertheless, Doig argues that “this is a significant result, comparable in efficacy to recent antibody drugs” against Alzheimer’s. Therefore, administering the recombinant herpes vaccine “could be a simple and cheap way to reduce the risk.” According to him, the next step would be to carry out a clinical trial comparing patients who receive it 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 an earlier age.”
The role played by some omnipresent viruses 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 not until 2022 that the virus was linked to multiple sclerosis. when a study showed that the pathogen is the “main cause” of this disease. Perhaps one day herpes vaccines will become another tool in the fight against dementia.
Source: www.eldiario.es
