The Controversy Over Herpes Vaccine and Dementia: Could a Virus Cause Alzheimer’s?

“We have found clean, causal evidence that the herpes vaccine prevents a good handful of cases of dementia. So, Could a virus cause Alzheimer’s? Yeah!“

That’s how effusive it is show by Twitter Pascal Geldsetzer, a researcher in the Department of Epidemiology at Stanford University. The reason? He has led a study where he compared dementia in the elderly depending on whether they were eligible for the shingles vaccine or not. And he concludes that the vaccine has prevented one in five casesbut neurologists and researchers are skeptical of their results.

To understand this controversy, you have to travel to Wales and go back to September 2, 1933. Those born after that date would be candidates, 80 years later, to receive a vaccine against herpes zoster, the disease known as shingles, caused by a herpesvirus and that mainly affects older people, generating intense pain.

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Geldsetzer and his group took the data from these lucky ones and compared them with those of those elderly people in Wales who were born just before that date. This is what they have defined as “natural randomization”: a population with similar characteristics that only differs by having received or not the vaccine.

In said British nation, the vaccine began to be offered as of 2013. The researchers took it as an opportunity to check if there was a relationship between the vaccine and cases of dementia among the Welsh elderly over seven years.

In this way, they saw that in the population susceptible to being vaccinated, dementia cases had been reduced by 20%. Conclusion? For the authors, this is evidence of the causal relationship between herpesvirus and the development of dementia. “It is extremely unlikely that it was due to pure chance.”

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Others don’t see it that way. “Honestly, I don’t think this pre-publication deserves much attention,” said the head of Neurology at the Hospital Clínic de Barcelona, Raquel Sanchez Valle, to the Science Media Center. “We will see if it is published and how the content appears in its final version. From what I have read, I do not believe it.”

The expert refers to This studio it is still in a step prior to being admitted into the scientific corpus. It has not yet been published in a scientific journal and, to do so, it needs to be reviewed by at least two specialists in the field who are not related to the authors. After that scrutiny, many things can change.

But, in addition, Sánchez Valle emphasizes that the pathology is multicausal and that a seven-year follow-up “is a ridiculous amount of time to date the cause of Alzheimer’s diseasefor example, which starts approximately 20 years earlier”.

Infectious hypothesis of Alzheimer’s

The study has caused a huge stir among specialists. Alberto Ascheriofrom Harvard University, affirms that it is rigorous and of good quality, but “chance remains a possible explanation” for the results. the researcher Kirsten Funkfrom the University of North Carolina, highlights, for his part, that “the diagnosis of Alzheimer’s dementia compared to other dementias was not well defined.”

Although he is not as combative, the head of Neurology at Hospital 12 de Octubre, David Perez Martinezexplains to EL ESPAÑOL that “you have to be cautious” with this work, although it is interesting research.

“The age difference [entre los dos grupos estudiados] It is not very large, but from 75-80 years old a small difference in age can generate relevant differences in the incidence of dementia”. Furthermore, “the incidence grows rapidly from 75 years on. You can’t be sure that here it won’t have an effect on subsequent follow-up.”

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On the other hand, in the vaccinated group, a “care bias on the part of their family doctors” cannot be ruled out, as it is a prevention project within the British national health system. “For example, they might have highlighted the importance of monitoring other well-known risk factors for dementia, such as increased exercise or a healthy diet.”

However, he points out that these data must be taken into account in future research, “it could be of interest to establish a clinical or specific trial in this area.”

Miguel Medinadeputy scientific director of the Center for Biomedical Research in Neurodegenerative Diseases Network (Ciberned), recalls that, “beyond the amyloid hypothesis, the origins of this disease are still unknownit is surely multicausal and there is evidence that some infections, especially herpes, may play a triggering role, at least as one of the multiple causes, although all of them end up leading to amyloid and tau pathology”.

Because the ‘infectious hypothesis’ of Alzheimer’s is not new, but it is experiencing a small boom in recent years, in line with other studies that look for a possible viral origin of other neurodegenerative diseases such as multiple sclerosis.

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In 1991, HSV-1 DNA, one of the nine herpesviruses that infect humans, was discovered in the brains of Alzheimer’s patients, a finding that was later extended to other herpesviruses. This family of microorganisms –causing, for example, chickenpox– has the ability to remain dormant in parts of the body for a lifetimeincluding the nervous system.

It would be a possible inflammatory response of the body to defend itself against the virus which would end up, becoming chronic, being more harmful than beneficial.

In recent years, progress has been made in this hypothesis with studies both in mice and in human tissues. Thus, a relationship has been found between herpesviruses and genetic risk factors such as the APOE4 gene and the classic markers of Alzheimer’s, the accumulation of beta amyloid and tau proteins.

A recent review on Nature account of these and other advances. Although he pointed out that the effect of other risk factors can be modulated through the presence or absence of herpesvirus, he also warned that Viruses most likely potentially contribute to only a small fraction of Alzheimer’s cases.

Pascal Geldsetzer himself admits that, before launching into validating this hypothesis, randomized clinical trials are needed to safely establish the impact of the virus on the pathology. Because, in science, “natural randomization” looks great but is not convincing.