The virus behind the common cold sore could put individuals at greater risk of Alzheimer’s disease.
In Sweden,a long-term study of more than a thousand 70-year-olds has presently found those exposed to the herpes simplex virus type 1 (HSV-1) face twice the risk of getting dementia.
Recently the association stuck regardless of the two strongest known predictors of Alzheimer’s disease. Age and a genetic variant called APOE-4. The findings are the latest to say that some common viral infections may be a neglected source of cognitive decline.
Recently, in Sweden roughly 80 percent of adults 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.
Though many with oral herpes never develop symptoms, others deal with flare-ups of inflammation and wounds around the mouth and lips from time to time. Irrespective 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 former studies,” says epidemiologist Erika Vestin from Uppsala University in Sweden.
More and more signs are emerging from studies that, like our findings, point to the herpes simplex virus as a risk aspect for dementia.
The main causes of dementia are one of the most extremely studied mysteries in modern medical science.
Alzheimer’s is the most common type of dementia, and it is frequently, but not always, marked by abnormal protein clumps in the brain.
For years now, drug researchers and neuroscientists have mainly focused on preventing these clumps to lessen cognitive decline with little to no success.
Some experts presently think of them as a red herring. These clumps, they hypothesize, have every reason to be in the brain. They could very well play a role in the immune response of the central nervous system, repairing damage or stopping 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 years. Only 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 results suggested that the immune response to the herpes virus was closely tied to cognitive decline.
This year, a study of around 500,000 medical records mentioned that some severe viral infections, like pneumonia and encephalitis may increase the risk of neurodegenerative diseases, such as Parkinson’s or Alzheimer’s.
Nevertheless, to this day there is still not enough proof to confirm the role of pathogens like HSV-1 in cognitive failure. 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 linked with dementia risk, others have found no such link.
In Sweden researchers at Umeå University and Uppsala University cut through the confusion by following younger patients for a longer period of time, and age-matching them during investigation.
Of all 1,002 adult members they followed for 15 years, 82 percent were carriers of HSV-1 antibodies. These patients were more likely to develop dementia during the period of the study compared to those who did not carry HSV-1 antibodies.
Interestingly, those members who carried the genetic risk factor, APOE-4, were no more likely to show cognitive decline connected to HSV-1 antibodies.
The study contradicts previous research that 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 members are almost the same age, which makes the results even more reliable since age differences, which are otherwise associated 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. Former 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 end 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 happens, hopes Vestin.
