Link Between Viral Infection(HSV-1/cold sores) and Alzheimer's Emerges in New Data

 

Ask your competent? doctor to test you for this. I had a number of cold sore outbreaks as a kid, no treatment. 

Of course, your incompetent? doctor did nothing with this research from 10 years ago!

Cold sores increases the risk of dementia October 2014 

The latest here?

Link Between Viral Infection and Alzheimer's Emerges in New Data

      Findings implicate HSV-1 but apply only to people with clinical episodes of cold sores

by Judy George, Deputy Managing Editor, MedPage Today May 21, 2025 • 3 min read

Key Takeaways

• People diagnosed with HSV-1 infection had a higher risk of a subsequent Alzheimer's diagnosis.
• Antiherpetic drugs reduced Alzheimer's risk in those diagnosed with HSV-1.
• The findings apply only to people with clinical episodes of cold sores.

People diagnosed with herpes simplex virus type 1 (HSV-1), the virus responsible for cold sores, were more likely to have a subsequent Alzheimer's disease diagnosis, an analysis of U.S. commercial insurance claims suggested.

Across 344,628 Alzheimer's case-control pairs, a history of HSV-1 diagnosis was present in 1,507 people (0.44%) with Alzheimer's disease and 823 matched controls (0.24%), reported Yunhao Liu, PhD, of Gilead Sciences, a pharmaceutical company based in Foster City, California, and colleagues.

This translated to an adjusted odds ratio of 1.80 (95% CI 1.65-1.96), Liu and co-authors wrote in BMJ Openopens in a new tab or window.

Of patients diagnosed with HSV-1, those who used antiherpetic drugs were less likely to develop Alzheimer's compared with those who didn't use antiherpetics (adjusted HR 0.83, 95% CI 0.74-0.92).

"These findings place an even greater emphasis on viewing the prevention of herpesviruses as a public health priority," Liu and colleagues said.

The results confirm previous findings that people with a history of cold sores may have a higher risk of developing Alzheimer's disease, and that this risk may be reduced in people who receive antiviral treatment, noted Alberto Ascherio, MD, DrPH, of the Harvard T.H. Chan School of Public Health in Boston, who wasn't involved with the research.

"This is an observational study based on electronic data of varying quality, so the conclusions cannot be considered definitive," he wrote in a post on the Spanish Science Media Centeropens in a new tab or window website.

"For example, the vast majority of cold sore episodes are not reported in medical records, so the study's conclusions apply to a highly selected subgroup of individuals with clinical episodes of cold sores, perhaps due to clinical severity or the presence of other factors," Ascherio pointed out.

"For this reason, it would be premature for people with cold sores to worry about having an increased risk of Alzheimer's disease," he added. "However, there is growing evidence that viral infections may affect the risk of Alzheimer's disease, and it is important to initiate more definitive research."

At least 22 viruses have been tiedopens in a new tab or window to Alzheimer's, dementia, or other neurodegenerative diseases, and some researchers have proposed that latent viral infectionopens in a new tab or window may provoke Alzheimer's disease. Recent analyses also have linked receiving the herpes zoster (shingles) vaccine with reduced dementia risk in Walesopens in a new tab or window and in Australiaopens in a new tab or window.

Liu and co-authors evaluated diagnostic codes for U.S. patients with records in the IQVIA commercial claims database from 2006 to 2021. They matched patients with an Alzheimer's diagnosis in health records and those without a history of neurologic disease on age, sex, geographical region, database entry year, and number of healthcare visits.

Mean age of the sample was 73 and 65% were women. People with Alzheimer's disease had more comorbidities and a shorter follow-up time compared with controls.

The researchers also identified links between people diagnosed with HSV-2 or varicella zoster virus (chickenpox) and Alzheimer's, but not those diagnosed with cytomegalovirus.

"The molecular mechanisms underlying the role of HSV-1 and other neurotropic viruses in dementia are still not well understood," they observed. Inflammatory alterations in the brain may be important to developing Alzheimer's disease, they noted.

This study captured only a small fraction of the total population with HSV-1 infection, Liu and co-authors pointed out. "Globally, an estimated two-thirds of the population under 50 are infected with HSV-1," they wrote.

The study had other limitations, the researchers acknowledged. People ages 65 and older often are covered by Medicare and are underrepresented in commercial claims data. Due to limited data history, HSV-1 infections prior to the patient's database entry were not included, and some overlap may exist between HSV-1 and HSV-2 diagnoses.

• Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This work was funded by Gilead Sciences.

Liu and most co-authors were employed by and held shares in Gilead. One co-author reported relationships with other pharmaceutical companies.

Primary Source

BMJ Open

Source Reference: opens in a new tab or windowLiu Y, et al "Association between herpes simplex virus type 1 and the risk of Alzheimer's disease: a retrospective case–control study" BMJ Open 2025; DOI: 10.1136/bmjopen-2024-093946.

Cold Sore Virus Linked to Alzheimer’s, Antivirals May Lower Risk

 Ask your competent? doctor to test you for this. I had a number of cold sore outbreaks as a kid, no treatment. 

Of course, your incompetent? doctor did nothing with this research from 10 years ago!

Cold sores increases the risk of dementia October 2014 

The latest here?

 Cold Sore Virus Linked to Alzheimer’s, Antivirals May Lower Risk

Summary: A large study suggests that symptomatic infection with herpes simplex virus 1 (HSV-1)—best known for causing cold sores—may significantly raise the risk of developing Alzheimer’s disease. Researchers found that people with HSV-1 were 80% more likely to have Alzheimer’s, while those treated with antiviral medications had a 17% lower risk.

The findings align with other evidence that HSV-1 may trigger inflammation and amyloid-beta accumulation in the brain, hallmarks of Alzheimer’s pathology. Although the study is observational and can’t prove causation, it highlights the potential for antiviral therapy as a protective strategy and urges greater public health focus on herpes virus prevention.

Key Facts:

• 80% Higher Risk: People with HSV-1 were significantly more likely to develop Alzheimer’s.
• Antiviral Benefit: HSV-1 patients who took antiviral drugs had a 17% lower Alzheimer’s risk.
• Biological Link: HSV-1 may drive brain inflammation and amyloid buildup, contributing to dementia.

Source: BMJ

Symptomatic infection with the virus responsible for cold sores around the mouth–herpes simplex 1, or HSV-1 for short—may have a key role in the development of Alzheimer’s disease, suggests a large pharma industry-funded US study published in the open access journal BMJ Open.

But treatment with antiviral therapy seems to be linked to a lower risk of this type of dementia, suggesting that treatment to quell HSV-1 symptoms may be protective, the findings indicate.

Nearly two thirds (65%) of those with Alzheimer’s disease were women. Credit: Neuroscience News

Currently, around 35.6 million people worldwide live with dementia, and 7.7million new cases are diagnosed every year, say the researchers. Alzheimer’s disease comprises 60%–80% of all dementias, with total costs for its treatment reaching US$305 billion in 2020, they add.

Various infectious agents have been implicated in the development of Alzheimer’s disease, and the most studied of these is HSV-1, which affected more than two-thirds of under 50s around the globe in 2016 alone.

To shed further light on the mooted role of HSV-1 in Alzheimer’s disease and the potential protective effects of antiherpetic drugs, the researchers drew on a large set of US administrative claims data (IQVIA PharMetrics Plus) for the period 2006-21.

People diagnosed with Alzheimer’s disease were matched for age, sex, geographical region, database entry year, and number of healthcare visits with those without any history of neurological disease, resulting in a total of 344,628 case–control pairs.

Nearly two thirds (65%) of those with Alzheimer’s disease were women. Their average age was 73 and they tended to have more co-existing conditions—all risk factors.

In all, 1507 (just under 0.5%) people with Alzheimer’s disease had been diagnosed with HSV-1 (0.44%) compared with 823 (just under 0.25%) of those in the comparison (control) group.

Unsurprisingly, the risk of Alzheimer’s disease rose in tandem with age. But, overall, the likelihood of an HSV-1 diagnosis was 80% higher among those with Alzheimer’s disease, after adjusting for potentially influential factors. 

Among the 2330 people with a history of HSV-1 infection, 931 (40%) used antiherpetic medication after their diagnosis. And they were 17% less likely to develop Alzheimer’s disease than those who didn’t use these treatments.

The researchers also looked at the potential role of other herpes viruses, including HSV-2, varicella zoster virus, and cytomegalovirus. Both HSV-2 and varicella zoster virus infections were also associated with a heightened risk of Alzheimer’s disease.

Exactly how HSV-1 and other neurotropic viruses might heighten the risk of dementia isn’t clear, point out the researchers. 

“However, studies have shown that inflammatory alterations in the brain caused by HSV infection are pivotal in [Alzheimer’s disease] development,” they explain. 

“It has been reported that Aβ peptides are deposited in response to HSV infection and protect host cells by blocking viral fusion with the plasma membrane, pointing to HSV as a potential risk factor for [Alzheimer’s disease]. Consistently, Aβ exhibits antimicrobial properties against various pathogens, including HSV-1,” they add.

HSV-1 DNA is also found in the plaques characteristic of Alzheimer’s disease, and people carrying the ApoE ε4 allele, the most common genetic risk factor for the disease, are more susceptible to HSV infections, they note.

This is an observational study, and as such, no firm conclusions can be drawn about cause and effect. And the researchers acknowledge that HSV-1 infections before the patient’s inclusion in the database weren’t known, added to which many people with the infection don’t have symptoms, while others might not seek treatment when they do–all factors that might influence the findings.

But their findings are in line with those of other studies. And they suggest: “While the molecular mechanisms remain to be fully elucidated, these results are indicative of a possible role for antiherpetic therapy in mitigating dementia risk.”

And they conclude: “These findings place an even greater emphasis on viewing the prevention of herpes viruses as a public health priority. 

About this virology and Alzheimer’s disease research news

Author: Emma Dickinson
Source: BMJ
Contact: Emma Dickinson – BMJ
Image: The image is credited to Neuroscience News

Original Research: The findings will appear in BMJ Open

Yet More Evidence that Viruses May Cause Alzheimer's Disease

You better hope like hell that your doctors and hospital follow up this research. You will need it.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

I had cold sores when I was a kid, haven't had one in decades, wonder if I need to be concerned.

https://gizmodo.com/yet-more-evidence-that-viruses-may-cause-alzheimers-dis-1827511539

For decades, the idea that a bacteria or virus could help cause Alzheimer’s disease was dismissed as a fringe theory. But not so much anymore. On Wednesday, a team of researchers from Harvard Medical School reported in the journal Neuron the latest bit of evidence suggesting herpesviruses can spark the cascade of events that leads to Alzheimer’s disease, a fatal form of dementia that afflicts at least 5 million Americans.

The researchers studied how neurons in mice responded to the presence of herpes simplex 1 (HSV-1), the virus that causes cold sores. In a separate experiment involving a 3D model of the human brain grown in a dish, they also studied human herpesvirus 6 (HHV-6), the germ responsible for causing the childhood skin disease roseola. These viruses are usually caught early on in life and stay dormant somewhere in the body, but as we age, they almost always migrate up to the brain.

Some of the mice used in the experiment were genetically bred to have neurons that could create the human version of amyloid beta (or amyloid-β). Amyloid-β is a protein normally produced in the brain. But in Alzheimer’s patients, it clumps together to form the plaques that are thought by many experts to slowly destroy the brain. Many scientists had long assumed that amyloid-β was essentially a waste product, with no meaningful purpose. But the researchers had earlier shown that amyloid-β might actually serve as a first line of defense against fungal and bacterial infection.

In the current study, both viruses seemed to provoke an identical reaction. The mice’s brains grew new deposits of amyloid-β plaques practically “overnight,” according to senior author Rudy Tanzi, a geneticist specializing in the brain at Massachusetts General Hospital as well as Harvard Medical School. And the mice bred with these human-like neurons were able to better fend off brain infection than mice without them. The same effects were also seen in the petri dish.

“The seeding of amyloid is what causes the deposition of plaque,” Tanzi told Gizmodo, “and herpesviruses and other microbes can rapidly seed amyloid-β.”

The study is the second in recent weeks to support the role of viruses in Alzheimer’s disease. That first study, also published in Neuron and led by researchers from the Icahn School of Medicine at Mount Sinai, found evidence that certain herpesviruses are more abundantly present in the brains of people who died with Alzheimer’s; it also suggested that genes belonging to these viruses directly interact with human genes that raise the risk of the disease.

The timing is no accident, Tanzi said. His team has corresponded with the Mount Sinai team for years, and they had originally planned to release their results at the same time (both will be published in the same print July edition of the journal). It was the Mount Sinai team, Tanzi notes, that suggested the Harvard team look at HHV-6 as well as HSV-1 in their experiments, since that was the virus they had started to zero in on in their work.

While Tanzi and his team acknowledge the long-ignored work by other researchers supporting the viral hypothesis of Alzheimer’s, as it’s known, he said their research takes things in a slightly different direction. It’s an attempt to reconcile various theories about what causes Alzheimer’s.

Supporters of the viral theory have often speculated that germs such as HSV-1—the most commonly blamed culprit—directly goad the brain into spiraling out of control through inflammation, with amyloid-β only being a bystander. But in Tanzi’s version, amyloid-β still is the key cog behind the disease. Neurons use the protein to either kill or safely trap viral or bacterial particles in a “nano-net,” as Tanzi put it. In Alzheimer’s disease, this process goes off the rails, leading to the uncontrolled buildup of plaques. From there, Tanzi’s work has shown, the plaques trigger the production of tangles—clumps of another brain protein called tau seen in the later stages of Alzheimer’s—which together then trigger chronic inflammation. All of these moving parts align to wither the brain, eventually causing death.

In this scenario, it’s not so much the germ, but the immune system that’s at fault. “The microbes are the prequel to the amyloid hypothesis,” Tanzi said.

Viruses are only one of the things that could set off Alzheimer’s, he pointed out. The same sort of seeding might happen in people whose genes cause them to make too much amyloid-β, in the absence of infection. And genetics might help explain why only some people’s infections cause the brain to start producing amyloid-β en masse. “Just having the virus isn’t enough,” Tanzi said.

But given the widespread failure of Alzheimer’s treatments that have focused on stopping amyloid-β production, the viral link provides a new, clear direction for future clinical trials: Preventative antimicrobial drugs or vaccines that can stop these germs from ever reaching the brain in the first place. Some recent, if observational research (meaning, not controlled trials) has already suggested that these drugs can lower the risk of dementia.

These sorts of definitive studies are likely still a while away, but there’s certainly a change in the headwinds.

“I think we’ve gotten past the point where this idea is ridiculed, but some might be still violently opposing it,” Tanzi said, referring to the 19th century German philosopher Arthur Schopenhauer’s maxim about the three stages of truth (first ridicule, then violent opposition, and finally acceptance as self-evident).

The Herpes Virus Can Affect Your Brain In Surprising Ways

I had two forms of the virus as a kid; chicken pox and cold sores. 

The Herpes Virus Can Affect Your Brain In Surprising Ways

If you’ve had mononucleosis, chicken pox, or cold sores, then you’ve had the herpes virus. Weird, isn’t it? Anna Rothschild explains in the YouTube channel Gross Science that the virus actually stays in your body for a lifetime and goes through a period where it lies dormant in neurons, hiding from the immune system. It turns out, however, it can even sneak into your brain.

Before you freak out about that, it’s important to note that this happens to about two in a million people. The virus can sneak into your temporal lobe and affect you in peculiar ways. For instance, those who survived the viral attack on the brain had specific damage that didn’t allow them to make normal class categorizations that we normally make on a daily basis, like colors or animals.

More at link.

Cold sores increases the risk of dementia

And is your doctor addressing this along with your 33% dementia chance post-stroke from an Australian study?  I remember having cold sores as a kid.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=146364&CultureCode=en
Infection with herpes simplex virus increases the risk of Alzheimer's disease. Researchers at Umeå University, Sweden, claim this in two studies in the journal Alzheimer’s & Dementia.
"Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer's disease. This also means that we have new opportunities to develop treatment forms to stop the disease," says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study. 
Alzheimer's disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer's disease.  A majority of the population carries this virus.  After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer's disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain.  There this can in turn start the process which results in Alzheimer's disease.
Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies.  In one study, which is based on the Betula project, a study on ageing, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer's disease. This study had 3,432 participants who were followed for 11.3 years on average.  In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer's disease were examined and as many matched people who had not developed dementia.  The samples were taken on average 9.6 years before diagnosis.  This study showed an approximately doubled risk of developing Alzheimer's disease if the person was a carrier of the herpes virus.
"Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer's disease," says Hugo Lövheim.