Common Herpes Virus Could Cause 50 Percent of Alzheimer's Disease Cases, Expert Says

The herpes virus, which triggers cold sores, could be the cause of at least half of the cases of Alzheimer’s disease, a leading expert concluded after reviewing existing data on the neurodegenerative condition.

As many as 3.7 billion people under the age of 50, an estimated 67 percent of the world’s population, have the herpes simplex virus type 1 (HSV-1), according to the World Health Organization.

Most commonly transmitted from mouth-to-mouth contact, the infection generally does not result in any symptoms. But it can cause unpleasant blisters, or cold sores, to erupt on the face.

Once a person is infected, it cannot be cured and lies dormant in the body. Symptoms can re-emerge when a person is run-down. By the age of 60, most people have been infected with the virus. A further 417 million people between the ages of 15 and 49 have HSV-2, which is a sexually transmitted disease affecting the genitals.

Owing to the prevalence of herpes, as well as the alarming rates at which Alzheimer’s is being diagnosed (with the number of cases expected to hit 82 million in 2030, and 152 million in 2050) the association between the two is ripe for investigation.

herpes-stock An illustration of the herpes simplex virus, which research has linked to Alzheimer's disease. Getty Images

Read more: What Is Herpes Virus? Alzheimer's Linked to Virus in the Brain

Ruth Itzhaki, a professor in the Division of Neuroscience and Experimental Psychology at the University of Manchester, U.K., has spent more than two decades studying whether herpes and Alzheimer’s disease are linked. On Friday, she published her latest findings in the journal Frontiers in Aging Neuroscience. 

She said in a statement: "HSV1 could account for 50 percent or more of Alzheimer's disease cases.” However, she told Newsweek: "Despite the involvement of a virus, the [Alzheimer's] disease is apparently not contagious."

Previously, Itzhaki found that those who carry the gene variant APOE-e4 experienced more severe effects from the herpes virus, and each reawakening of HSV1 could gradually wear away at the brain until symptoms of Alzheimer’s disease develop. Her research group has also found HSV1 in the brains of elderly people.

As such, Itzhaki believes antiviral drugs could prevent Alzheimer’s disease. But the data to support this are currently sparse. The National Health Insurance Research Database in Taiwan, which 99.9 percent of the Taiwanese population is part of, provides a pool of information on a range of diseases that scientists can draw from.

For this latest research, Itzhaki analyzed existing papers, including three published this year based on the Taiwanese data set. Of the total, two investigated varicella zoster virus (VZV—a type of herpes that causes chicken pox) and its links to cognitive decline. The third homed in on herpes.

These studies focused on what Itzhaki termed “senile dementia” rather than Alzheimer’s disease, as the cause of the symptoms was unclear in some patients.

In what Itzhaki described as the most “striking” of the three studies, the third paper assessed correlations between herpes and Alzheimer’s disease in 8,362 participants who were at least 50 years old in the year 2000. The volunteers visited a doctor with the HSV1 or HSV2 viruses at least three times in the year before the start of study.

The incidences of Alzheimer's disease in this cohort was compared with 25,086 subjects matching their age and gender who did not have herpes.

Those who were infected with HSV and VZV were more likely to develop senile dementia. But antiviral treatments appeared to prompt a “dramatic decrease” in the number of subjects who went on to develop dementia, wrote Itzhaki.  

In the group that took anti-herpes medication, just over 5 percent developed dementia in the decade following, compared with more than 28 percent of those who didn’t consume the drugs. 

What remains unanswered is why the medication appeared to have this effect, and no data were available on whether antivirals can ease the symptoms of the disease. One solution could be that the drugs stop the virus from attacking the central nervous system.

Despite the compelling findings, Itzhaki was emphatic that the participants had what were presumed to be rare cases of severe HSV1 or VZV infections. They had shingles or recurrent cold sores or genital sores or both, rather than the asymptomatic form of the virus.

“But when considered with the over 130 publications that strongly support an HSV1 role in AD [Alzheimer’s disease], they greatly justify usage of anti-herpes antivirals to treat AD,” she wrote.

A short dose of antivirals for those with the APOE-e4 gene variant in those between 30 and 40 years old could therefore prevent what could be dementia, Itzhaki argued.  

While the cause of Alzheimer’s disease is unknown, studies indicate that the buildup of plaque in the brain could play a role.

“Viral DNA is located very specifically within plaques in postmortem brain tissue from Alzheimer's sufferers,” Itzhaki said. “The main proteins of both plaques and tangles accumulate also in HSV1-infected cell cultures—and antiviral drugs can prevent this,” she said.

Itzhaki wrote that she hoped there would eventually be a vaccine for HSV1, although this would be many years away.

To answer the questions raised by the studies, Itzhaki said more work was needed on how Alzheimer’s develops in different groups, known as epidemiological research, including the rates of the disease among those with mild forms of HSV1 and HSV2.

 David Reynolds, chief scientific officer at the charity Alzheimer’s Research U.K., said: "Research into a link between the herpes virus and Alzheimer’s is so far very limited, with only a few scientists studying the association.

"This review presents mainly correlative studies that do not give clear evidence of cause and effect. The evidence presented in this review is not sufficient to suggest that Alzheimer’s disease is contagious and  is passed from person to person like a virus and neither does it mean that having cold sores increases your risk of getting dementia."

James Pickett, head of research at the charity Alzheimer’s Society, described herpes as a "hot topic" in dementia research but not enough is yet known about the relationship between the two.

“More research is needed to find out whether antiviral drugs can reduce dementia risk. We do know there are many things that people can do to reduce their dementia risk, such as eating a healthy diet, exercising regularly, not smoking, not drinking excessively and managing their blood pressure."

John Hardy, a professor of neuroscience at University College London, U.K., said: “Dr Itzhaki has been ploughing a lonely furrow based on her belief that herpes infection is a risk factor for Alzheimer’s disease for a long time and most scientists, including me, have been skeptical."

He argued none of the evidence she cites proved the link, but the putative role of infections in disease was worthy of study. "Certainly, there is clear evidence that there are direct links between inflammatory processes and Alzheimer’s disease,” he said.

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