Study: Herpes virus doubles the risk of dementia!
A long-term study of more than 1,000 people aged 70 in Sweden found that those exposed to herpes simplex virus type 1 (HSV-1) had double the risk of developing dementia. The association remained regardless of the two strongest known predictors of Alzheimer’s disease today (age and a genetic variant called APOE-4).
These findings are the latest to suggest that some common viral infections may be an overlooked source of cognitive decline. Today, nearly 80% of adults in Sweden carry antibodies to herpes simplex virus type 1, whether they know it or not, meaning their immune systems have been exposed to the pathogen at some time in the past.
While many people with oral herpes never develop symptoms, others deal with bouts of inflammation and blisters around the mouth and lips from time to time.
Regardless of how the infection appears, new findings from Sweden suggest that HSV-1 can have hidden effects on the inside.
For further clarification, epidemiologist Erika Festen from Uppsala University in Sweden says, “It is interesting that the results confirm previous studies. “More evidence is emerging through studies that support our findings that implicate herpes simplex virus as a risk factor for dementia.” This is according to what was reported by the scientific website “Science Alert” from the “Journal of Alzheimer’s Disease”.
The root causes of dementia are one of the most extensively investigated mysteries in modern medical science. Alzheimer’s disease is the most common type of dementia, often, but not always. It is characterized by abnormal protein clumps in the brain.
For years now, neuroscientists and drug researchers have focused on blocking these clumps to reduce cognitive decline with little success.
Some experts assume that these masses have every reason to be in the brain. They can play a role in the immune response of the central nervous system, repairing damage or preventing pathogens from causing damage. Therefore, some types of Alzheimer’s disease could be a sign of an “out of control” defensive response to foreign microbes.
In this context, the idea that infection might lead to some variation in Alzheimer’s disease was first proposed in 1907, but the hypothesis was ignored and treated with “much hostility” by the scientific community for several decades. This path has only recently emerged as an acceptable way 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 that HSV-1 DNA was present in 90 percent of protein plaques in the postmortem brains of Alzheimer’s patients.
Furthermore, 72% of HSV-1 DNA in the brain was found within these plaques. The results indicate that the immune response to the herpes virus was closely linked to cognitive decline.
Just this year, a study of about 500,000 medical records found that some severe viral infections, such as encephalitis and pneumonia, may increase the risk of developing neurodegenerative diseases, such as Parkinson’s or Alzheimer’s. However, to date there is not enough evidence to confirm the role of pathogens such as HSV-1 in cognitive decline.
Although it is becoming more common, neuroscience research teams have historically not included experts in microbiology or virology.
While some studies have found that antibodies to HSV-1 are associated with dementia risk, other studies have found no such association.
To do this, researchers at Uppsala University and Umeå University in Sweden resolved this confusion by following younger patients for a longer period of time, and matching them for their ages during the analysis. Of all 1,002 adult participants followed for 15 years, 82% were carriers of HSV-1 antibodies. These patients were also twice as likely to develop dementia during the study period compared to those who did not carry HSV-1 antibodies. Interestingly, participants carrying the genetic risk factor, APOE-4, were not more likely to show cognitive decline associated with anti-HSV-1 antibodies.
The findings contradict previous research suggesting that the APOE genetic variant could exacerbate the potential effects of HSV-1 on the brain’s immune response.
“The unique thing about this particular study is that the participants are roughly the same age, which makes the results more reliable,” Festen concludes. She and her colleagues are calling for randomized controlled trials to investigate whether herpes treatment can help prevent or stop the onset of dementia. However, applications for previous clinical trials on antivirals and dementia have been rejected by funding bodies. But one of the first experiments is set to end; It is an ongoing phase II clinical trial to study the effect of herpes treatment on Alzheimer’s disease; In December of this year, 2024. She hopes that such results “may push dementia research towards treating the disease at an early stage using common anti-herpes virus drugs, or preventing it before it occurs.”
2024-02-19 13:02:18
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