Herpes simplex virus 1 (HSV-1) doubles the risk of dementia, according to a long-term study of more than 1,000 people in their 70s in Sweden. A study published in the Journal of Alzheimer’s Disease found that this association remained constant even after taking into account the two main risk factors for Alzheimer’s disease: older age and the presence of a genetic mutation known as APOE-4. These latest findings may reveal that common viral infections may be an underappreciated cause of cognitive decline.

Herpes simplex virus (HSV) is an extremely common virus that can cause a variety of diseases, including oral and genital herpes. There are two main types of herpes simplex virus: HSV-1 and HSV-2. HSV-1 is mainly associated with oral herpes, which causes painful sores or blisters around the mouth and on the lips. HSV-2 is associated with genital herpes, causing sores or blisters in the genital area.

Herpes is reactivated with reduced immunity

Herpes manifests itself in the form of bubbles with a clear or slightly yellowish liquid, which quickly burst, leaving behind painful erosions. They appear on the infected area and can persist for up to two weeks. Lesions can cause discomfort, itching or burning. With oral herpes, bubbles are formed around the mouth, lips, mucous membrane of the cheeks, palate, gums, or tongue, and with genital herpes, they appear in and around the genitals.

The herpes simplex virus is most contagious when it appears through lesions, but it can be transmitted even if there are no lesions, usually through kissing, sexual contact (genital, oral, or anal), or even through contact with affected skin. . Herpes can also be transmitted from an infected mother to a newborn during childbirth.

After infection with the herpes simplex virus, it does not disappear completely, but remains in the body in a latent state and can appear again at any time in the form of new lesions when it is reactivated. There are several factors that can trigger a recurrence of oral herpes, including immune suppression, respiratory infections such as a cold or flu, fever, prolonged exposure to the sun or cold temperatures, dental procedures, and stress.

Herpes is very common all over the world. According to the World Health Organization (WHO), about 67% of the world’s population under the age of 50 are infected with HSV-1, and about 13% – with HSV-2. These percentages may vary by region and age group, but herpes is considered one of the most common viral infections in the world.

Although many people with oral herpes do not develop symptoms, others have occasional episodes of inflammation and blisters around the mouth and lips. But regardless of how the infection manifests itself on the outside, new findings from a Swedish study suggest that HSV-1 may have an insidious effect on the inside.

The causes of dementia are still not fully understood

“It is encouraging that the results confirm previous studies. There is increasing evidence from studies like this that herpes simplex virus is a risk factor for dementia,” said epidemiologist Erika Westin from Uppsala University in Sweden.

The underlying causes of dementia are one of the biggest mysteries that researchers are still trying to unravel. Alzheimer’s disease, the most common type of dementia, is often associated with the abnormal development of protein clumps in the brain, although this is not always present. For years, neuroscience and pharmaceutical research has focused on preventing or removing these clots in an attempt to slow cognitive decline, with little or no success.

More recently, it has been hypothesized that these clots may play a beneficial role in the immune response of the central nervous system, acting to repair or prevent damage caused by pathogens. In this context, some forms of Alzheimer’s disease can be interpreted as a protective reaction of the body that has gone out of control in the face of the invasion of harmful microorganisms.

The connection between viruses and Alzheimer’s disease

The idea that infections could trigger some forms of Alzheimer’s disease was first proposed as early as 1907, but the scientific community ignored the hypothesis and regarded it “with great hostility” for many decades. Only recently has it been accepted as a real possibility.

In the 1990s, unusual levels of HSV-1 DNA were found in the brains of Alzheimer’s patients who had died for the first time. Later, in 2008, researchers found that HSV-1 DNA was present in 90 percent of the protein plaques in the brains of postmortem Alzheimer’s patients. In addition, it is estimated that 72% of HSV-1 DNA found in the brain is located in these plaques. The results suggest a close relationship between the immune response to the herpes virus and the cognitive decline associated with the disease.

A study this year of about 500,000 medical records found that some serious viral infections, such as encephalitis and pneumonia, may increase the risk of neurodegenerative diseases such as Parkinson’s or Alzheimer’s.

However, to date there is insufficient evidence to support the role of pathogens such as HSV-1 in cognitive decline. Although this idea is gaining acceptance, in the past neuroscience research teams have not typically involved experts in microbiology or virology. In addition, although some studies have shown that antibodies to HSV-1 are associated with an increased risk of dementia, others have not observed such an association.

Double risk of dementia in HSV-1 antibody carriers

Researchers from Uppsala University and Umeå University in Sweden addressed this confound by following younger patients over a longer period of time and matching them by age at the time of analysis.

Of all 1,002 adult participants they followed for 15 years, 82% had antibodies to HSV-1. These patients had twice the risk of developing dementia during the study compared to those who did not have HSV-1 antibodies.

An interesting aspect is that participants who had the APOE-4 gene, which is associated with an increased risk of dementia, were not more likely to have HSV-1 antibody-related cognitive decline.

These findings contradict previous studies suggesting that the APOE genetic variant may enhance the possible effects of HSV-1 on the brain’s immune response.

“This particular study differs from others in that the participants are roughly the same age, which lends greater reliability to the results, as age-related variations that can affect the development of dementia did not influence the results,” Westin noted. .

Westin and his team are calling for randomized controlled trials to investigate whether treating herpes can help prevent or delay the onset of dementia. However, previous applications for antiviral and dementia clinical trials have been rejected by funding agencies.

One of the first, a phase II clinical trial studying the effect of herpes treatment on Alzheimer’s disease, is scheduled to conclude in December 2024. Such results “may push dementia research toward early treatment with conventional antiviral drugs against the herpes virus, or even to prevent the disease before it starts,” the researchers hope.

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