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The virus behind the common cold sore could put people at greater risk of Alzheimer's disease.
A long-term study of more than a thousand 70-year-olds in Sweden has now found those exposed to the herpes simplex virus type 1 (HSV-1) face double the risk of developing dementia.
The association stuck regardless of the two strongest known predictors of Alzheimer's disease today: age and a genetic variant called APOE-4. The findings are the latest to suggest that some common viral infections may be a neglected source of cognitive decline.
Today, roughly 80 percent of adults in Sweden carry the antibody for HSV-1, whether they know it or not, meaning their immune systems have been exposed to the pathogen at some point in the past.
While many with oral herpes never develop symptoms, others deal with flare-ups of inflammation and blisters around the mouth and lips from time to time. Regardless of how the lifelong infection displays on the outside, the new results from Sweden suggest HSV-1 could be having insidious effects on the inside.
"It is exciting that the results confirm previous studies," says epidemiologist Erika Vestin from Uppsala University in Sweden.
"More and more evidence is emerging from studies that, like our findings, point to the herpes simplex virus as a risk factor for dementia."
The root causes of dementia are one of the most highly investigated mysteries in modern medical science.
Alzheimer's is the most common type of dementia, and it is oftentimes, but not always, marked by abnormal protein clumps in the brain.
For years now, neuroscientists and drug researchers have focused on preventing these clumps to reduce cognitive decline with little to no success.
Some experts now think of them as a red herring. These clumps, they hypothesize, have every reason to exist in the brain. They could very well play a role in the immune response of the central nervous system, repairing damage or preventing pathogens from causing damage.
Some types of Alzheimer's could, therefore, be a sign of an 'out-of-control' defense response to foreign microbes.
The idea that infections might trigger some variations of Alzheimer's disease was first proposed way back in 1907, but the hypothesis was disregarded and treated with "much hostility" by the scientific community for many decades. Only very recently has it emerged as an accepted path forward.
In the 1990s, unusual levels of HSV-1 DNA were found in the brains of deceased Alzheimer's patients for the first time. Later, in 2008, researchers discovered HSV-1 DNA was present in 90 percent of the protein plaques in postmortem brains of Alzheimer's patients. What's more, 72 percent of HSV-1 DNA in the brain was found within these plaques.
The findings suggested that the immune response to the herpes virus was closely tied to cognitive decline.
Just this year, a study of around 500,000 medical records found that some severe viral infections, like encephalitis and pneumonia, may increase the risk of neurodegenerative diseases, such as Parkinson's or Alzheimer's.
Nevertheless, to this day there is still not enough evidence to confirm the role of pathogens like HSV-1 in cognitive decline. While it's becoming more common, historically, neuroscience research teams have not incorporated experts on microbiology or virology.
And while some studies have found the antibodies for HSV-1 are associated with dementia risk, others have found no such link.
Researchers at Uppsala University and Umeå University in Sweden cut through the confusion by following younger patients for a longer period of time, and age-matching them during analysis.
Of all 1,002 adult participants they followed for 15 years, 82 percent were carriers of HSV-1 antibodies. These patients were twice as likely to develop dementia over the course of the study compared to those who did not carry HSV-1 antibodies.
Interestingly, those participants who carried the genetic risk factor, APOE-4, were no more likely to show cognitive decline linked to HSV-1 antibodies.
The findings contradict previous research suggests the APOE genetic variant could exacerbate the possible impacts of HSV-1 on the brain's immune response.
"What's special about this particular study is that the participants are roughly the same age, which makes the results even more reliable since age differences, which are otherwise linked to the development of dementia, cannot confuse the results," says Vestin.
Vestin and colleagues are calling for randomized controlled trials to investigate whether herpes treatment could help prevent or stall the onset of dementia. Previous clinical trial applications on antivirals and dementia, however, have been rejected by funding bodies.
One of the first – an ongoing phase II clinical trial studying the effect of a herpes treatment on Alzheimer's – is due to finish in December of 2024.
Such results "may drive dementia research further towards treating the illness at an early stage using common anti-herpes virus drugs, or preventing the disease before it occurs," hopes Vestin.
The study was published in the Journal of Alzheimer's Disease.
