Swedish researchers started wondering whether cold sores increase the risk for dementia more than a decade ago (Alzheimer’s & Dementia, online, Oct. 7, 2014). They identified patients diagnosed with Alzheimer’s disease (AD) at the Memory Clinic of the University Hospital in Umeå. These were people who had blood samples stored in the Medical Biobank there 10 years before their AD diagnosis. Those with evidence of HSV1 (herpes simplex virus type 1) infection were more likely to develop Alzheimer’s disease.
That study generated scary headlines:
“Studies Link Cold Sore Virus to Alzheimer’s Risk” WebMD
“Cold Sores may DOUBLE the Risk of Developing Alzheimer’s Disease” Daily Mail
This message was not popular with some neuroscientists. Researchers who had staked their careers on amyloid plaque as the cause of AD and anti-amyloid drugs as the “cure” did not want to hear about herpes infections. Such an explanation did not fit with their model of dementia.
New Swedish Study: Cold Sores Increase Dementia Risk
Fast forward to February, 2024. Once again Swedish scientists have linked herpes simplex virus (HSV) to Alzheimer’s disease (Journal of Alzheimer’s Disease, Feb. 2, 2024). A different group of Swedish scientists from Uppsala University reports that:
“Herpes Simplex Viral Infection Doubles the Risk of Dementia in a Contemporary Cohort of Older Adults: A Prospective Study”
In this study, scientists recruited about a thousand 70-year-old Swedes without dementia. These volunteers provided blood samples so the researchers could test whether they had antibodies to HSV1. Their medical records also indicated if they had taken prescription antivirals such as acyclovir.
Over the next 15 years, 4% of these participants developed Alzheimer disease and 7% were diagnosed with dementia. People with a specific antibody to HSV (IgG) were twice as likely as those without the antibody to develop dementia.
Will Antiviral Herpes Drugs Be Helpful Against Dementia?
The Swedish scientists cite Italian researchers (Current Opinion in Pharmacology, April, 2022) by noting:
“Anti-herpesvirus treatment may mitigate the HSV-related AD risk.”
The Italian researchers conclude:
“A growing body of evidence support recurrent HSV-1 infection as a potential risk factor for AD, and clinical trials repurposing anti-herpetic drugs to treat this disease and its earlier stages are ongoing. However, there is a huge need for additional research to unravel when and how the virus may reach the brain of susceptible individuals and which HSV-1-infected population suffers recurrent infection targeting the brain.”
The Swedish investigators call for randomized controlled trials to determine whether antiviral drugs against herpes could be protective. To support their plea for research into inexpensive and safe antiviral drug treatment, they cite other Swedish colleagues (Alzheimer’s & Dementia, June 9, 2021).
Those scientists wrote:
“It [antiviral treatment] reduced this risk [of AD] by 70% in anti–HSV-1 IgG–positive persons and reduced the AD or dementia risk among people with symptomatic HSV infection.”
Why Aren’t Drug Companies and Neuroscientists Excited?
You might think that pharmaceutical manufacturers would be jumping for joy to learn that antiviral drugs might be helpful against Alzheimer’s disease. We have seen no such excitement. (Antiviral herpes medications such as acyclovir, famciclovir and valacyclovir are now available generically and are inexpensive.) Most of the researchers who have been involved in amyloid-beta drug development have also been strangely silent about the virus/AD research.
Billions of dollars have been spent developing anti-amyloid drugs that have a checkered track record. Most have been ineffective. And even the ones that have recently been approved by the FDA have marginal benefits and substantial risks. You can read my latest overview of such medications at this link.
The Wayback Machine: Cold Sores Increase the Risk of AD
Over the last two decades, most people have become familiar with the concept of the microbiome. It refers to the trillions of bacteria, fungi and viruses living primarily in our digestive tracts. In recent years, however, researchers have discovered a microbiome on our skin, in our lungs and even in our brains.
Judging from what you have just read, you might think that the link between viruses and dementia is something new. If you climb into the Wayback machine with us for a few minutes, you will learn that this story has been around for a much longer time. As far back as 1974, researchers writing in the British Journal of Psychiatry noted that people with dementia had a greater likelihood of having antibodies to the herpes simplex virus that causes cold sores.
In 1982, Melvyn J. Ball, MD, a pathologist at the Oregon Health and Science University, proposed that herpes simplex virus (HSV) type 1 could be contributing to the brain lesions (plaques and tangles) of Alzheimer dementia (The Canadian Journal of Neurological Sciences). Dr. Ball theorized that the virus “hibernates” in the trigeminal ganglia, a neuronal structure within the brain. In its dormant state, the virus resides within this nerve tissue without seeming to cause mischief. When activated, the virus travels down nerves to the lips and triggers the familiar cold sore lesion.
Dr. Ball suggested that the virus might also travel in another direction, deeper into the brain:
“It is suggested that reactivation of the same dormant viral material travelling centripetally instead might be the cause of the ‘degenerative’ lesions typical both of Alzheimer’s Disease and of the normal aged human brain.”
Dr. Ball Persisted in Studying His Hypothesis:
Most neuroscientists and Alzheimer’s disease researchers ignored Dr. Ball’s hypothesis, but over the last three decades Dr. Ball has tirelessly pursued this idea. In 2006 in the Journal of Alzheimer’s Disease, he noted that most research on Alzheimer disease had failed to determine the most important neurological abnormalities of the disease.
In his words:
“However, during my elusive search, evidence has been slowly gathered that reactivation of latent Herpes simplex virus, traveling from trigeminal ganglia into neighbouring mesial temporal cortex, might best explain the limbic predilection for and earliest site of neurofibrillary tangle formation.”
Other investigators discovered that the herpes virus could be detected within the brain lesions of Alzheimer disease patients (Journal of Pathology, Jan. 2009).
They wrote:
“We discovered a striking localization of herpes simplex virus type 1 DNA within plaques: in Alzheimer’s disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques…”
The Latest Research on the HSV Type 1 and Alzheimer’s Disease
Although funding agencies and mainstream researchers pretty much dismissed this line of research, some epidemiologists began digging deeper. The Swedes in particular noted that there seemed to be an increased risk of Alzheimer disease after herpes simplex virus reactivation (Alzheimer’s & Dementia, June, 2015). Researchers tracked 3,432 subjects for over 11 years. They found that reactivated herpes infections were linked to a doubling of the risk for Alzheimer disease compared to individuals who were not infected.
That research came from Umeå University in Umeå, Sweden (Alzheimer’s & Dementia, June, 2015). These investigators identified 360 individuals with a diagnosis of Alzheimer’s disease and 360 cases of dementia-free controls. All patients had given blood long before (on average 9.6 years earlier), and it had been stored in a medical “Biobank.” The scientists analyzed the blood for antibodies to herpes simplex virus type 1.
The presence of the antibodies was associated with a two-fold increased risk for dementia:
“Among persons with a follow-up time of 6.6 years or more, HSV infection was significantly associated with AD [Alzheimer’s disease]. This may indicate a role of HSV in early AD development…”
“It has been hypothesized that immune system weakening in older individuals might contribute to HSV reactivation and spread to the brain, which then may explain the connection seen among persons older than 60 years in this study whereas causes of AD other than HSV might be relatively more common among those younger than 60 years of age…”
“Converging evidence now supports a relationship between HSV and the early development of at least some cases of AD.”
What’s the Bottom Line and What to Do?
First, you will likely read that researchers in the Alzheimer disease mainstream reject this research. I characterize this as the “not invented here” phenomenon. Funding agencies have spent billions of dollars pursuing other avenues, but so far they have proven almost worthless. The idea that they may have overlooked this approach for at least 50 years will be hard to swallow.
Dr. Hugo Lovheim, the lead author of some of the Swedish research, has been quoted:
“The identification of a treatable cause [herpes simplex] of the most common dementia disorder is a breakthrough…Whether treatment of herpes infection with antiviral drugs may slow the Alzheimer’s progression is not known, but is certainly worth investigating in clinical studies.”
“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.”
Many people may not want to wait years and years for such clinical trials to be funded and for the results to be published. As Dr. Lovheim noted, there are effective prescription antiviral medications against herpes simplex virus type 1. They include acyclovir (Zovirax), famiclovir (Famvir), penciclovir (Denavir) and valacyclovir (Valtrex). Such drugs are surprisingly effective against herpes viruses and reasonably safe. They do require a prescription. And clearly, such drugs have not yet been tested for preventing or treating Alzheimer disease in large, well-controlled trials. Consequently, we simply cannot tell whether they will be able to inhibit virus that may already have entered the brain.
What About L-Lysine?
You might want to think about a simple over-the-counter approach. Again, we have no evidence that this will help, but the risks are low. For decades, we have been hearing from readers of our syndicated newspaper column, listeners to our syndicated radio show and visitors to this website that L-lysine works against a number of herpes infections.
One reader wrote about using L-lysine for shingles, a painful rash associate with a different herpes virus, herpes zoster:
“In a recent column you answered a question about L-lysine and shingles. I have been taking L-lysine for various forms of herpes for over 20 years, and it has kept me virtually outbreak-free.
“It is also important to avoid nuts and chocolate. Dietary restraint together with L-lysine have worked better for me than acyclovir, which I took for a year as part of a study at the University of Rochester.
“I have read about both nut avoidance and L-lysine, but often when I speak to physicians about it they are not aware of it. A lot of pain and discomfort could be avoided if they were.”
JS agrees that L-lysine can be helpful:
“I too am a firm believer in L-Lysine. At the very first tingle I will take anywhere from 2 to 5 1000 mg pills. If I know I will have lots of sun exposure, or that I am stressed out or run down, I will take a couple in the morning and a couple before sleep preemptively.
“I keep lysine in my glove box, in my day bag, golf bag, gym bag, and at home. It is so helpful that I literally will not go anywhere without it, so that I can take it immediately if i feel a cold sore coming on, or if I am consciously stressed, tired, sick, etc. I’ve also learned to avoid caffeine, chocolate, most nuts, and other foods that are rich in arginine.
“There are tons of articles explaining how food and diet can assist in preventing and limiting the extent of breakouts. With this current approach, I usually do not get any sores that are visible, and am able to keep them in check.”
Sharon got advice on L-lysine from her dentist:
“My dentist told me many years ago to use Lysine as soon my lip starts to sting. I take three Lysine immediately and the sore will not go on and develop. The second and third days, I take three more. No blisters for me.”
Would you like to read more about controlling recurrent cold sores with L-lysine? Here is a link to some fascinating stories. You’ll find other commentary about whether L-lysine might help protect our brains from Alzheimer disease here.
No one knows whether antiviral drugs or L-lysine will prevent or help Alzheimer’s disease. But anything that can keep the virus from reactivating is probably worth a try. Since L-lysine seems surprisingly safe, it might be an experiment worth considering. Let us know your thoughts and experience with herpes simplex type virus 1 in the comment section below.
Could Alzheimer Plaques Be Protecting the Brain?
Research demonstrates that two of the beta amyloid compounds that form plaques in the brains of people with Alzheimer disease have antiviral activity (Bourgade et al, Biogerontology, Feb. 2015). In cell cultures, these beta-amyloid peptides inhibit herpes simplex virus growth.
The investigators conclude:
“Overproduction of Aβ peptide to protect against latent herpes viruses and eventually against other infections, may contribute to amyloid plaque formation, and partially explain why brain infections play a pathogenic role in the progression of the sporadic form of AD.”
We don’t know if Dr. Ball is still alive, and if so, whether he feels vindicated. But increasingly, other neuroscientists are coming around to his view. One review referred to “a compelling argument for a pathogen-based etiology of AD” [Alzheimer Disease] (McNamara & Murray, Current Alzheimer Research, 2016).
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