Alzheimer’s and Herpes simplex virus

The Discovery: Herpes Virus DNA Found Inside Alzheimer’s Plaques

In 2009, a research team led by Dr. Ruth Itzhaki at the University of Manchester published a finding that should have changed the course of Alzheimer’s research. Using advanced molecular techniques, they examined brain tissue from Alzheimer’s patients and made a striking discovery: herpes simplex virus type 1 (HSV-1) DNA was found directly inside amyloid plaques — the hallmark pathological feature of Alzheimer’s disease.

The numbers were remarkable. In Alzheimer’s disease brains, 90% of amyloid plaques contained HSV-1 DNA. And 72% of all HSV-1 DNA found in these brains was located within the plaques themselves. The virus was not merely present in the brain alongside the plaques. It was embedded within them.

We published this article in 2010 because the implications were too significant to overlook. If a common virus was directly contributing to the formation of Alzheimer’s plaques, it meant that the disease might be preventable — and treatable — through antiviral approaches, including frequency-based protocols.

What the Study Found

The research, published in the Journal of Pathology (2009, Vol. 217, Issue 1, pages 131-138), was conducted by Wozniak, Mee, and Itzhaki at the Faculty of Life Sciences, University of Manchester.

The Method

The researchers used a technique called in situ polymerase chain reaction (PCR) to detect HSV-1 DNA directly within brain tissue sections. They combined this with immunohistochemistry and thioflavin S staining to identify and visualize amyloid plaques. This dual approach allowed them to see exactly where the viral DNA was located relative to the plaques — not just whether both were present in the same brain, but whether they occupied the same physical space.

The Key Findings

The results were consistent across multiple brains and showed a clear pattern.

In Alzheimer’s disease brains, 90% of amyloid plaques contained herpes simplex virus type 1 DNA. Additionally, 72% of all viral DNA detected was physically associated with plaque deposits.

In aged normal brains — which also develop some amyloid plaques, though at a lower frequency — 80% of plaques still contained HSV-1 DNA. However, only 24% of the total viral DNA was plaque-associated. This difference was statistically significant (p < 0.001).

The researchers interpreted this difference as evidence that healthy aging brains are better at clearing amyloid beta (Aβ), so less of the viral DNA ends up trapped within plaque deposits. In Alzheimer’s brains, the accumulation and impaired clearance of amyloid means more viral DNA becomes permanently embedded in the growing plaques.

What This Means

The study’s authors stated their conclusion directly: HSV-1 “is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer’s disease.” They recommended pursuing antiviral agents as treatment and potentially vaccination as prevention.

This was a bold conclusion in 2009. The Alzheimer’s research establishment was heavily invested in the “amyloid hypothesis” — the idea that amyloid plaques are the primary cause of the disease and that removing them should cure it. The suggestion that a virus was driving plaque formation challenged this framework at its foundation.

Why This Was Ignored — And Why It Matters Now

Despite the strength of Itzhaki’s findings, the infectious theory of Alzheimer’s was largely sidelined by the mainstream research community for years. Billions of dollars continued to flow into amyloid-targeting drug development, most of which failed in clinical trials. Meanwhile, the evidence connecting HSV-1 to Alzheimer’s continued to accumulate quietly.

The Frequency Research Foundation recognized the significance of this research immediately. When we published this article in 2010, the herpes-Alzheimer’s connection was considered fringe. Today, it is one of the most actively investigated areas in Alzheimer’s science.

2025 Update: 15 Years of Validation

Since the Wozniak, Mee, and Itzhaki study, the evidence linking herpes simplex virus to Alzheimer’s disease has grown from a single provocative finding into a substantial body of research involving millions of patients.

Large Population Studies Confirm the Link

Multiple large-scale epidemiological studies have now demonstrated that people with HSV-1 infections have a significantly higher risk of developing Alzheimer’s disease. Crucially, several of these studies have shown that antiviral treatment reduces that risk. A landmark 2018 study from Taiwan involving over 33,000 subjects found that individuals treated with anti-herpes medications had a dramatically lower incidence of dementia compared to untreated HSV carriers. This was the type of evidence that moves a theory from “interesting” to “actionable.”

The Mechanism Is Now Well Understood

Research since 2009 has clarified how HSV-1 drives Alzheimer’s pathology. The current understanding involves a cyclical process. HSV-1 resides dormantly in nerve tissue, including the trigeminal ganglion near the brain. When the virus reactivates — which can happen repeatedly throughout life due to stress, immune suppression, or aging — it travels to the brain and causes direct neuronal damage. The brain’s immune response to viral reactivation includes the production of amyloid beta, which has antimicrobial properties. Amyloid beta effectively traps the virus but accumulates over repeated cycles of reactivation, eventually forming the characteristic plaques of Alzheimer’s disease. Each cycle of viral reactivation triggers neuroinflammation, compounding the damage.

This means amyloid plaques may not be the cause of Alzheimer’s — they may be the brain’s defensive response to a chronic viral infection. This reframing explains why drugs designed solely to remove amyloid plaques have largely failed: they address the symptom, not the cause.

The APOE-ε4 Connection

Itzhaki’s earlier research had shown that HSV-1 is a particularly strong risk factor for Alzheimer’s in people who carry the APOE-ε4 gene variant — the best-known genetic risk factor for the disease. Subsequent research has confirmed this interaction. The APOE-ε4 allele appears to impair the brain’s ability to control HSV-1 reactivation, leading to more frequent viral flare-ups and faster plaque accumulation. This explains why some people with HSV-1 develop Alzheimer’s while others do not — the combination of the virus and the genetic variant creates the highest risk.

The Antimicrobial Hypothesis Gains Mainstream Support

What was once called the “herpes hypothesis” has evolved into the broader “antimicrobial protection hypothesis” of Alzheimer’s disease, championed by researchers at Harvard and other major institutions. This framework recognizes that amyloid beta functions as an antimicrobial peptide — part of the brain’s innate immune system — that responds to pathogens including HSV-1, bacteria, and fungi. Alzheimer’s, in this view, is the result of chronic, repeated immune activation in the brain.

The Connection to Other Chronic Infections

HSV-1 is not the only infectious agent linked to Alzheimer’s. The broader pattern is that chronic, brain-infiltrating infections drive the neuroinflammatory cycle that produces Alzheimer’s pathology. At the Frequency Research Foundation, we have been tracking these connections across multiple pathogen types.

Mycoplasma infections can cross the blood-brain barrier and contribute to ongoing neuroinflammation. Our research on mycoplasma is documented in Mycoplasma: A Key Component in Lyme and Other Diseases and Mycoplasma – Why the Lyme Flu Goes On and On.

Lyme disease spirochetes can directly invade brain tissue and trigger immune responses similar to those caused by HSV-1. Our Lyme disease frequency protocols address this neurological component.

The common thread across all these infections is chronic neuroinflammation. Managing this inflammatory burden is critical to slowing or preventing Alzheimer’s progression. Our article Eliminating Inflammation Is a Top Priority for Disease Prevention explains why this is the foundational strategy.

How Frequency Therapy Addresses the HSV-1 Connection

This research has direct and practical implications for frequency therapy. If HSV-1 is a significant driver of Alzheimer’s pathology, then addressing the virus with targeted frequencies — rather than waiting for plaque formation and trying to clear plaques after the fact — represents a fundamentally different treatment strategy.

At the Frequency Research Foundation, Dr. Jeff Sutherland has developed frequency protocols that target multiple aspects of the HSV-1/Alzheimer’s connection. Antiviral frequencies target HSV-1 directly, potentially reducing the frequency and severity of viral reactivation episodes in the brain. Anti-inflammatory frequencies address the neuroinflammation triggered by each reactivation cycle. Gamma frequency restoration, particularly 40 Hz stimulation, supports the brain’s natural clearance mechanisms for amyloid beta. Immune support frequencies help the body maintain better viral suppression over time.

This multi-layered approach addresses the cause (the virus), the mechanism (neuroinflammation), and the consequence (amyloid accumulation and cognitive decline) simultaneously. It is the type of comprehensive strategy that the research now supports.

Our flagship protocol, Alzheimer’s Disease – Version 2.0, incorporates antiviral frequency components alongside gamma stimulation and neuroinflammatory targeting. For the complete picture of how frequency therapy addresses Alzheimer’s from every angle, read our complete guide to Alzheimer’s disease and frequency therapy.

If you or a loved one is dealing with Alzheimer’s or cognitive decline, a consultation with Dr. Jeff Sutherland can assess whether chronic viral infections may be a contributing factor and develop a personalized frequency protocol to address it. Book Your Consultation

Frequently Asked Questions

Does having herpes simplex virus mean you will get Alzheimer’s?

No. HSV-1 is extremely common — an estimated 50-80% of adults carry the virus. The majority will not develop Alzheimer’s. The risk appears to be highest in people who carry both HSV-1 and the APOE-ε4 gene variant. Other factors including overall immune health, frequency of viral reactivation, and the presence of other chronic infections also influence risk. Frequency therapy aims to reduce viral reactivation and the neuroinflammation it triggers.

How does HSV-1 get into the brain?

HSV-1 typically infects through oral contact and establishes a lifelong latent infection in the trigeminal nerve ganglion, which is located close to the brain. When the virus reactivates — often triggered by stress, illness, or immune suppression — it can travel along nerve pathways into the brain itself. The brain’s immune response to the virus includes producing amyloid beta, which traps the virus but accumulates over time into plaques.

Can antiviral treatment prevent Alzheimer’s?

Large population studies suggest it may help. The most significant evidence comes from a Taiwanese study of over 33,000 subjects showing dramatically lower dementia rates in HSV carriers who received antiviral treatment compared to those who did not. This supports the principle that controlling the virus may slow or prevent Alzheimer’s development. Frequency-based antiviral approaches offer an alternative pathway for addressing HSV-1 without the side effects of pharmaceutical antivirals.

Why was this research ignored for so long?

The Alzheimer’s research field was heavily invested — both scientifically and financially — in the amyloid hypothesis, which focused on plaque removal rather than asking what causes plaque formation. Billions of dollars in drug development were committed to amyloid-clearing therapies. Acknowledging that a virus might be driving plaque formation would have fundamentally disrupted this approach. It took repeated clinical trial failures of amyloid-targeting drugs and growing population-level evidence for antiviral protection to shift mainstream attention toward the infectious theory.

How does frequency therapy differ from antiviral medication for HSV-1?

Antiviral medications like acyclovir and valacyclovir target viral replication through a single biochemical mechanism. Frequency therapy takes a broader approach, using targeted frequencies to address the virus directly while simultaneously reducing neuroinflammation, supporting immune function, and restoring healthy brain wave patterns (including 40 Hz gamma oscillations). This multi-target strategy addresses the full cascade from viral reactivation through to cognitive decline.

Take the Next Step

The herpes-Alzheimer’s connection is no longer a fringe theory — it is supported by 15 years of research involving millions of patients. If chronic viral infection is driving Alzheimer’s pathology, then addressing that infection early and comprehensively is one of the most important steps you can take.

Dr. Jeff Sutherland has spent decades developing frequency protocols that target the infections, inflammation, and brain wave disruptions that contribute to Alzheimer’s disease. A paid consultation is the most direct way to explore what frequency therapy can offer for your specific situation.

Book Your Consultation with Dr. Jeff Sutherland

This article is part of our comprehensive Alzheimer’s resource library. Herpes simplex virus is one of several chronic infections linked to Alzheimer’s disease. Read our complete guide to Alzheimer’s disease and frequency therapy for the full scope of research, from 40 Hz gamma science to nutritional strategies and personalized frequency protocols.

© Frequency Research Foundation. This content is for educational and informational purposes only. It is not intended to diagnose, treat, cure, or prevent any disease. Always consult with qualified healthcare professionals regarding medical conditions.

XMRV Virus Causes Chronic Disease Syndrome

Dr. Schimpff, former CEO of the University of Colorado Medical Center, has an interesting book on the future of medicine. He and I were coinvestigators on an Operation Room of the Future grant designed to upgrade information technology in the new surgery center the University opened a few years ago.

He also has a good blog with a recent posting on the XMRV virus. Frequency Foundation subscribers have already received the frequency set as part of the Swine Flu series. Most of you don’t realize that XMRV is one of the many viruses that are part of what is called “Swine Flu” as conventional medicine has a tough time even confirming that you have the 1918 swine flu virus and doesn’t determine what other organisms are making you sick. After you get the swine flu you will likely be chronically infected with XMRV unless the virus is eliminated with frequencies.

Chronic Fatigue Syndrome Shown to be Caused by Virus

A very recent discovery may lead to significant advances for the estimated 4 million Americans and 17 million worldwide who suffer with chronic fatigue syndrome. CSF is, like its name suggests, a persistent extreme level of fatigue that does not resolve with rest or sleep. It may also be accompanied by memory lapses and other neurological issues. All too many individuals have been branded as having a “psychological problem” and as not really being ill. No cause had been known although viral infection, immune dysfunction or both had been thought possible. There has been no specific treatment.

Now researchers at the Whittemore Peterson Research Institute in Reno, Nevada have shown that CFS is likely caused by a virus. Known as xenotrophic murine leukemia virus – related virus, or XMVR, it is a retrovirus that is suspected of being transmitted by intimate human contact. The discovery means that a definite diagnostic rest can be created. And hopefully it means that scientists will be able to shortly find or create drugs to both prevent the disease and to treat those who have it. It also means that no loner will these patients be labeled as not having a real medical problem.

The researchers’ early studies suggest that perhaps 4% of us carry the virus. If proven correct, then an immediate goal is for a quick and inexpensive test to screen donated blood so that the virus is not transmitted inadvertently via transfusions. And it raises the intriguing question of why some but not all of those infected go on to develop CSF.

In study done at the Cleveland Clinic, scientists have found the same XMRV virus in prostate cancer samples. It is too soon to say that the virus is causative; if might be just a “passenger.” Additional research will be done to make a clear determination.

Meanwhile, the Whittemore Peterson researchers have suggested a new name – x-associated neuroimmune disease [XAND], a name that clarifies that this is a real disease and suggests some of its implications.

This finding of XMRV as the likely cause of CFS is a major medical advance.

Stephen C. Schimpff, M.D.

Feb 2007 Flu Frequency Update: Version 2.01

Flu season is here and the CDC flu charts are headed straight up! All the flu outbreaks I have seen during years where I have been analyzing frequencies have been transmitted by parasites infected with viruses, fungi, bacteria, insects, and smaller parasites inside larger parasites. The infected parasites keep reinfecting you so the symptoms linger. They also stir up other pathogens that might be quietly lingering in your body, particularly Lyme infections which exist in the majority of the population.

For those who got a good case of this year’s flu, it was the worst in recent memory – a month of congestion, sneezing, coughing, asthma symptoms, headaches, joint, and muscle aches and pains, with repeated reinfection. This is the most complex flu observed to date by the Frequency Foundation as it is carried by dozens of Lyme organisms. For those already infected with Lyme (more than 50% of people tested) it stirs up a dormant Lyme infection and makes the flu worse than ever.

The latest version of this flu frequency set contains:
· 2 flu viruses
· 13 helper viruses
· over a dozen insect frequencies
· at least half a dozen strains of the Lyme babesia parasite
· over a dozen strains of other Lyme parasites
· and the Gregory cancer “virus” (a type of nanobacteria) [1]

To make things worse, many of the parasites are infected with the other flu organisms so killing them with frequencies or otherwise releases more flu organisms and the brucella bacteria which is major component of Lyme disease.

Frequency sets are provided in the F100 programming language for use on F165 or other frequency generators, and for transmission by Advanced BioPhoton Analyzers (APBAs). Details on how to translate them to FSCAN devices are provided. Programs for plasma devices that operate under 10,000 hz are also included.

Gregory “Cancer Virus” Frequencies

“Cancer virus” in carcinoma of the uterus – Gregory, 1952

Remarkable findings are routine in electronic medicine. However, some are more useful than others. After recent discussions in the Rife newsgroups, I bought a copy of:

Gregory, John E. Pathogenesis of Cancer, Second Edition. Fremont Foundation, 1952.

Dr. Gregory was a surgeon who studied the pathology of tumors under one of the first electron microscopes. He found the same organism in all cancer patients and called it a “cancer virus” because of its small size. It would not be called a virus today because it replicates by cell division.

The frequency of the “cancer virus” in the circle in the photo above is 11666766. After testing a number of individuals with cancer, I have found this and other forms of the “cancer virus” in all of them.

It is easy to knock out malignant cells with electromagnetic frequencies as shown by Gorgon. However, it is not so easy to prevent development of new malignant cell populations. Previously, I have shown new populations related to the SV40 virus, parasites, baccilus licheniformis, and nanobacteria. Yet eliminating all of these organisms does not necessarily stop recurrence.

The Gregory “cancer virus” may be a key factor. Dr. Gregory comments:

Is this virus a product of cancer or the cause of the disease? To answer this question, cultures of malignant melanoma virus were injected into mice and baby chickens. In 25 per cent of the injected animals there developed cancers which included cancer of the ovary, adrenal, breast and stomach, spindle cell sarcoma, myosarcoma, and leukemia. A control group, ten times larger, developed no malignancies. Further, the virus isolated from the developed malignancies was the same as that injected. The virus was also re-cultured from the tumor and again it was the same as that injected. This carries out all the criteria of Koch’s Postulate. I have now carried out this experiment and have fulfilled Koch’s Postulate over fifty times.

It is interesting to note that in the group of tumors developed, less than 10 per cent were the same type of tumor as that from which the original virus came. This proves that the cancer cells were not transplanted, producing the tumors…

One research group at a medical school has carried out this experiment through nine consecutive animals, producing nine different malignancies. The virus was cultured from each tumor, and the virus culture was then injected into the next animal, producing another cancer. When the last experiment was finished the final re-cultured virus was found to be the same as that used to start the experiment.

This proves that human cancer virus, which has been found in 100 per cent of human cancers, actually causes the cancers and is not present as a secondary invader.

An additional experiment was performed to rule out the possibility that the tumors were caused by the transmission of a chemical agent. This virus was heated to 56 degrees C. for one hour and then injected into twice as many animals as before, but no malignancy developed. This proves that it is living virus which produced the malignancies.

While there are many organisms, genetic programs, cellular problems, and immune issues related to malignancy, the “cancer virus” appears to be the only organism present in 100% of the cases. Removing it should certainly lower risk. With a little luck, it might be equivalent to the pump handle that John Snow removed from the Broad Street water supply during the 1854 London cholera epidemic. It stopped the epidemic immediately.

More recent information (2019) indicates that this is the organism found in all tumor cells that was DNA sequenced and found to be bacillus licheniformis. Frequencies are available to subscribers.

Pseudoscience: Ignorance about Borna Virus

One of my friends called me last night. He had checked himself into the hospital because of his bipolar disease. He told the physicians he had the Borna virus and it was flaring up. We had used frequency transmission to deal with it on multiple occasions. The hospital physicians asked, “What’s the Borna virus?” They then proceeded to give him too much Lithium resulting in a two week hospital stay.

Ignorance masquerading as science is pseudoscience and medical error is the third leading cause of death, mostly based on “scientists” who are supposed to know what they are doing. When they used to do autopsies in real medicine to find out what was going on, physicians in the U.S. and the U.K. discovered a third of the patients that died in hospitals died of an undiagnosed disease. So they have pretty much stopped doing autopsies as it puts them at risk of being sued for malpractice.

If my friends physicians consulted PubMed they would have found over 862 papers in the medical journals on the borna virus. It is associated with a wide variety of mental illness, particularly bipolar disease and depression.

Why didn’t the physicians consult his medical records at his primary physician’s office? They would have found out that he had tested positive for the borna virus and the primary physician was handling it, including the appropriate does of lithium. This failure to review available medical information on a patient will be viewed as malpractice in the not too distant future. There is a national initiative to enable sharing of this critical patient care information. While we are waiting for computer systems to do it automatically, how about using an old fashion phone call?

The physicians should have immediately queried the internet about the patient’s problem. Every bipolar person I have ever tested has it, and so do most members of the family. The virus is very widespread and causes all kinds of problems in addition to bipolar disease.

They wanted to know how he caught it. They could have done a Google search on “borna virus.” They would have found that 8% of our DNA is actually borna virus DNA. Or they might read a comprehensive review of the borna virus from the National Institutes of Health We used to teach science in medical schools. I wonder what they are teaching students these days?

The effects of Borna virus were first noticed in Saxony in Germany in 1766 in horses – first they got sad, and then hyperactive, and then most of them died. But the virus got its name about a century ago, when it killed some 2,000 cavalry horses in the town of Borna in Germany. But only recently, in the 1990s, have we found a link between this virus and depression. Depression is a disorder of your mood or emotions. It affects some 5% of the population at any given time. There’s actually a bunch of diseases that go under the single name of “depression”, and they tend to come and go during your life. They do more than just make you a little bit unhappy. They can cause severe disability, greater than is caused by heart disease, diabetes or even arthritis. In fact, it’s thought that 70% of suicides happen in people suffering from depression. But what’s the evidence that this strange new virus called Borna virus can cause depression?

Well, much of this research has been done by two virologists, Hanns Ludwig from the Free University of Berlin, and Liv Bode from the Robert Koch Institute (also in Berlin). In 1994, they found that clinically depressed people were more likely to have some of the proteins associated with Borna virus in their blood. The next year, they found traces of the actual RNA of the Borna virus as well. In 1996, these virologists took some Borna virus from clinically depressed patients, and when they injected this Borna virus into rabbits, the rabbits became apathetic, sluggish, withdrawn and stopped their normal grooming – in other words, the rabbits started suffering depression. And in January 1997, they found that if they used the anti-virus drug amantadine in depressed patients, as the virus disappeared from the blood stream, so did the symptoms of depression.

When I was teaching medical students at the University of Colorado Medical School from 1975-1983, we did not go home with a question like this unanswered. And we had to do real work in the medical library to get the answer. Today it takes three minutes on the internet.

The current issue of Health Affairs discusses the appalling 17 year gap between evidence based findings in the leading medical journals and information that is resident in the typical physicians head:

Implementing Evidence

Evidence-Based Decision Making: Global Evidence, Local Decisions

Carolyn M. Clancy and Kelly Cronin

Despite the notable progress to date, evidence-based decision making has been largely overshadowed by the persistence of poor-quality care in the United States. Elizabeth McGlynn’s landmark report on U.S. health care quality, AHRQ’s National Healthcare Quality Report, and a recent cross-national report on quality indicators raise important questions about the gap between the promise of evidence-based health care and its current level of adoption. All stakeholders in the health care system presumably find the current seventeen-year delay from evidence to practice unacceptable. This translation chasm is even more intolerable, given the increased array of choices resulting from large public and private investments in biomedical science. Although many factors, including local professional norms and patients’ values and preferences, contribute to deviations from evidence-based care, a fundamental question remains: Why does the gap persist?

Limited resources. Investments in biomedical science have resulted in a wide variety of diagnostic and therapeutic options for clinicians and patients. The extant infrastructure for conducting systematic reviews–including AHRQ’s Evidence-based Practice Centers (EPCs), the worldwide Cochrane Collaboration, and independent private-sector organizations–has led to much progress in developing methods and conceptual enhancements for systematic reviews. Nevertheless, the field is not advancing as rapidly as it could because of limited resources.

Knowledge chasm. Moreover, by definition, systematic reviews rely on available studies. Since the link between decisionmakers’ needs and establishment of clinical research priorities is somewhat circuitous, the net result is that decision-makers have few resources for learning quickly which patients are likely to benefit from new options and which patients will experience marginal benefits or outright harm. Payers and consumers confront the same knowledge chasm and lack good information for coverage decisions, cost sharing, and treatment choices.

Need for a systems approach. We now know that knowledge about best practice is necessary but not sufficient to effect change in practice and policy. Impatient purchasers are testing innovations to identify incentives and programs that reward evidence-based (“best”) practice, but they have a limited knowledge base on which to derive or evaluate new approaches. Although the Institute of Medicine’s reports on medical errors and quality have reinforced the importance of a systems approach to improvement, major support for research to inform such an approach has only recently become available.

Poor accessibility. Finally, evidence is infrequently available in a form that can be acted upon at the time decisions must be made. From clinical encounters to policy decisions, there are few clear pathways between the evidence that is available through peer-reviewed literature reviews and the point of decision making. Clinicians searching for information all too often find that existing knowledge is not accessible in real time and may not necessarily map to the issue at hand. Also, although consumers are increasingly active in seeking information about health and specific conditions, most of this activity is peripheral to care delivery. Personalized decision making, including provider and treatment selection as well as self-management, looms on the horizon. Development and adoption of personal health records could support individual choice based on current information.