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. The research, published in Journal of Alzheimer’s Disease, showed that this association remained constant, even after taking into account the two major risk factors for Alzheimer’s disease: advancing age and the presence of a genetic mutation known as APOE-4. These recent findings may reveal that common viral infections may be an underestimated cause of cognitive decline.
Herpes reactivates when immunity is lowPhoto: © Loganban | Dreamstime.com
Herpes simplex virus (HSV) is an extremely common virus that can cause a variety of conditions, including oral herpes 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 reactivates when you have low immunity
Herpes manifests itself as blisters with transparent or slightly yellowish fluid, which quickly burst, leaving behind painful erosions. They appear in the infected area and can persist for up to two weeks. The lesions may cause discomfort, itching or burning. In the case of oral herpes, the blisters form around the mouth, on the lips, mucous membranes of the cheeks, palate, gums or tongue, and in the case of genital herpes, they appear in the genital area and the region around it.
The herpes simplex virus is most contagious when it manifests itself through the appearance of lesions, but it can be transmitted even when there are no lesions, usually through kissing, sexual contact (genital, oral or anal) or even through contact with the affected skin. Herpes can also be passed from an infected mother to her newborn during birth.
After you have been infected with the herpes simplex virus, it does not disappear completely, but remains in the body in a latent state and can reappear at any time in the form of new lesions, when it is reactivated. There are several factors that can trigger the recurrence of oral herpes, including immunosuppression, respiratory infections such as a cold or flu, fever, prolonged exposure to the sun or cold temperatures, dental procedures, and stress.
Herpes is very widespread throughout the world. Conformable World Health Organization (WHO), about 67% of the world’s population aged up to 50 years is infected with HSV-1, and about 13% with HSV-2. These percentages may vary by region and age group, but herpes is considered to be one of the most common viral infections globally.
Although many people with oral herpes do not develop symptoms, others experience occasional episodes of inflammation and blisters around the mouth and lips. But regardless of how the infection manifests itself on the outside, new results from the Swedish study suggest that HSV-1 may have insidious effects on the inside.
The causes of dementia are not yet fully understood
“It is encouraging that the results confirm previous studies. There is increasing evidence from similar studies that herpes simplex virus is a risk factor for dementia,” said epidemiologist Erika Vestin from Uppsala University in Sweden.
The underlying causes of dementia are one of the biggest mysteries 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. Over the years, neuroscience and pharmaceutical research has focused on preventing or eliminating these clumps in an attempt to slow cognitive decline, but with little or no success.
More recently, it has been hypothesized that these clumps 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 could be interpreted as a defensive response of the body that got out of control in the face of the invasion of harmful microorganisms.
The link 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 hypothesis was ignored and treated with “much hostility” by the scientific community for many decades. Only recently has it been accepted as a real possibility.
In the 1990s, unusual levels were identified of HSV-1 DNA in the brains of deceased Alzheimer’s patients, 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. Additionally, an estimated 72% of the HSV-1 DNA found in the brain was located in these plaques. The findings suggest a close link between the immune response to the herpes virus and the cognitive decline associated with the condition.
And study this year based on about 500,000 medical records showed that certain serious viral infections, such as encephalitis and pneumonia, could increase the risk of neurodegenerative diseases such as Parkinson’s or Alzheimer’s.
However, to date, there is insufficient evidence to confirm the role of pathogens such as HSV-1 in cognitive decline. Although this idea is gaining acceptance, in the past, neuroscience research teams did not typically involve experts in microbiology or virology. Furthermore, despite the fact that some studies have suggested that antibodies to HSV-1 are linked to an increased risk of dementia, others have not observed such an association.
Twofold risk of dementia in HSV-1 antibody carriers
Researchers from Uppsala University and Umeå University in Sweden cleared up the confusion by following younger patients for a longer period of time and matching them based on age at the time of analysis.
Of all 1,002 adult participants they followed for 15 years, 82% carried HSV-1 antibodies. 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 – associated with an increased risk of developing dementia – were no more likely to show cognitive decline associated with HSV-1 antibodies.
These findings contradict previous research suggesting that the APOE genetic variant could exacerbate the possible impact of HSV-1 on the brain’s immune response.
“This particular study differs from the rest in that the participants are roughly the same age, which lends greater reliability to the results, as age-related variations, which could influence the development of dementia, did not impact the findings,” Vestin pointed out. .
Vestin and his team are calling for randomized controlled trials to investigate whether treating herpes could help prevent or delay the onset of dementia. However, previous applications for clinical trials on antivirals and dementia have been rejected by funding organisations.
One of the first – one clinical trial in phase II examining the effect of a herpes treatment on Alzheimer’s — is scheduled to conclude in December 2024. Such results “could spur dementia research toward early treatment using common antiviral drugs against the herpes virus or even toward preventing the disease before onset,” researchers hope.
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2024-02-29 12:44:00
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