Infections and Dementia: Are Viruses and Bacteria Driving Alzheimer Disease?

Scientists have known about an infection connection with dementia since the 1820s. That was when French physicians described neurosyphilis (Revue Neurologique, April, 2018). This condition occurs when the bacterium Treponema pallidum gets into the brain and causes irritability, mood swings, confusion, forgetfulness and memory loss, along with many other symptoms. Over the intervening 200 years, evidence has accumulated connecting infections and dementia. And yet to this day, most neuroscientists have seemingly downplayed the relationship between viruses and bacteria in the brain to cognitive decline.

Amyloid and Alzheimer Disease: The Chicken or the Egg?

Drug companies, the Alzheimer’s Association and the FDA have placed almost all their chips on the beta-amyloid theory of Alzheimer’s disease. Billions have been spent on anti-amyloid drugs such as aducanumab (Aduhelm), lecanemab (Leqembi). and donanemab (Kisunla). What they have not asked is why beta-amyloid builds up in the brain.

Read more about this controversy at this link. While beta-amyloid may indeed be part of the story, we have long wanted to know what amyloid is actually doing in the brain. What triggers the formation of this sticky protein in the first place?

Some researchers have long suggested that there is a connection between infections and dementia. They believe that beta-amyloid formation in the brain is the body’s natural reaction to invasion. They postulate that it may be part of an immune response that runs amok. Could tau tangles have a similar origin?

Infections and Dementia:

Evidence has been accumulating that infections might play a role in the development of dementia ever since the French physicians discovered the syphilis bacterium in the brains of patients. In addition to the previous research we describe below, two new studies have drawn attention to the connection between infections and dementia.

Chlamydia pneumoniae and Alzheimer Disease:

A study published in Nature Communications (January 22, 2026) is intriguing.

The authors introduce their research this way:

“Alzheimer’s disease (AD) is a debilitating neurodegenerative condition and the leading cause of dementia in the elderly, currently ranked as the seventh most common cause of death worldwide…The potential role of infectious agents in AD pathogenesis has gained increasing attention, with Chlamydia pneumoniae, an obligate gram-negative bacterium primarily responsible for community-acquired pneumonia, emerging as a significant pathogen.”

When people read the word Chlamydia, they may think sexually transmitted infection. That is Chlamydia trachomatis. These investigators were looking at a different bacterium, Chlamydia pneumoniae. This germ causes sinus infections and pneumonia.

We have long been intrigued by this bacterial bad boy because of a physician researcher, David Hahn, MD, MS. Dr. Hahn has been studying C. pneumoniae for more than 25 years. He wrote a fascinating book titled A Cure for Asthma? What Your Doctor Isn’t Telling You–And Why. (Full disclosure: The People’s Pharmacy Press published this book in 2013). In it he describes why hard-to-treat asthma could be linked to the same bacterium, C. pneumoniae. Because this germ is hard to eradicate, Dr. Hahn came up with an intriguing dosing schedule that involves intermittent and long term treatment (3 months) with the antibiotic azithromycin. You can read about this research at this link:

Azithromycin for Asthma AMAZES!
Many doctors are unaware of the science supporting azithromycin for asthma. Why would this antibiotic help?

C. pneumoniae can linger for long periods of time in the lungs and nose and cause a lot of mischief. That’s because it can create an inflammatory response within the body. The researchers who described their work in Nature Communications (January 22, 2026) point out that the same bacterium can linger in the retina of the eye and in the brain. When it sets up housekeeping, C. pneumoniae can trigger an immune response and inflammation.

An overview of this research describes it this way (Cedars Sinai, January 30, 2026):

“They found significantly higher levels of Chlamydia pneumoniae in the retinas and brains of people with Alzheimer’s disease than they found in people with normal cognition. The higher the bacterial levels detected, the more severe the brain changes and cognitive decline investigators found.”

This doesn’t prove that Chlamydia pneumoniae causes Alzheimer’s—but it strengthens the broader theme: infections and dementia may be biologically connected through chronic inflammation and immune dysfunction.

Another Piece in the Puzzle: Shingles (Varicella-Zoster) & Alzheimer Disease:

You have no doubt heard of chickenpox. It is caused by the varicella-zoster virus (VZV). Once you catch chickenpox as a child, the virus does not disappear. Even though your immune system initially beats back this infection, the virus goes into hibernation in the brain and spinal column. It hides in the trigeminal ganglia and the dorsal root ganglia. These nerve cells allow the virus to lie dormant for decades.

Scientists have developed two vaccines against the varicella-zoster virus (VSV). The first was was Zostavax. It was approved in 2006. It has been replaced by a newer and more effective virus called Shingrix. Three “natural experiments” point to shingles vaccination as potentially protective against dementia.

The first two experiments happened unintentionally in Wales and Australia. In those countries public health authorities established arbitrary eligibility dates for people to receive the Zostavax vaccine. People only slightly older did not differ in other important respects, but they could not be vaccinated.

As a result of the cutoff, researchers could compare the people who were vaccinated to those were were unvaccinated. As a result of this accidental protocol, investigators discovered that there were protective effects of the VSV vaccine against dementia. Those who had been vaccinated were 20 percent less likely to be diagnosed with dementia over the next several years.

The most recent study comes from Canada and involves people born between 1930 and 1960 (Lancet Neurology, Feb. 2026). In Ontario, eligibility for the shingles vaccine was set for people born on or after Jan. 1, 1946. Electronic health records from private practices in Ontario were analyzed from 1990 to 2022.

The absolute difference in dementia diagnoses for more than 200,000 patients was 2 percentage points between those eligible for the shingles shot and those who missed it by a few weeks or months. Elsewhere in Canada, where there was no shingles vaccination program, there is no clear difference in risk of dementia by birth date.

The investigators report:

“Microbes have long been suggested to have a role in the pathogenesis of dementia. Neurotropic herpesviruses have received particular attention because they preferentially target the nervous system, their reactivation becomes more common with age and can cause encephalitis, and they are highly prevalent.

“Being born immediately after versus immediately before the date-of-birth eligibility threshold for Ontario’s herpes zoster vaccination programme led to a large difference in receipt of herpes zoster vaccination. These groups, who are not expected to differ systematically, also had a large difference in the probability of receiving a new dementia diagnosis over a 5·5-year follow-up.

“In conclusion, this study provides strong evidence of a protective effect of herpes zoster vaccination on incident dementia…These results suggest that herpes zoster vaccination could be an effective tool to prevent, or delay, dementia and has implications for research into the pathogenesis of dementia and maintenance of neuroimmune health in older age.”

Cytomegalovirus Linked to Alzheimer Disease:

Researchers have also reported finding antibodies to cytomegalovirus (CMV) in many donated organs from people who died with Alzheimer disease (Alzheimer’s & Dementia, Dec. 19, 2024). These antibodies were especially prevalent in the digestive tract. The scientists found evidence of the virus itself in the vagus nerve connecting the gut to the brain.

Cytomegalovirus is a member of the herpes virus family, and is nearly as widespread. Half to four-fifths of Americans have antibodies to CMV by the time they reach their 40s. Consequently, it is not a surprise that the researchers detected antibodies in organs. However, when they exposed brain tissue to CMV, both amyloid and phosphorylated tau proteins increased and neurons died. All this suggests a link between CMV infection and the degeneration typical of Alzheimer disease.

Herpes Infection Associated with Alzheimer Disease Markers:

A study published in Cell Reports shows that a protein from the herpes simplex virus (HSV-1) that causes cold sores increases with abnormal levels of tau (Cell Reports, Dec. 26, 2024). Neurofibrillary tangles made of phosphorylated tau are typical of Alzheimer disease pathology. As a result, scientists use tau levels as an important marker for Alzheimer disease.

In laboratory experiments using brain organoids, cells that produce p-tau (that is, phosphorylated tau) help protect neurons from this infection. The researchers suggest that tau phosphorylation may be part of the brain’s innate immune response to infection.

Earlier Research on Viral Infections and Dementia:

One significant study included data from nearly 150,000 people over many decades. Researchers followed participants in the Nurses’ Health Study, the Nurses’ Health Study II and the Health Professionals Follow-up Study (Alzheimer’s Research & Therapy, Aug. 14, 2024).

People who had a bout of shingles were 20% more likely to report subjective cognitive decline subsequently than people who did not have shingles. Men with an APOE4 gene had a greater risk. For some reason, that did not show up in women.

The investigators note that the data on these healthcare cohorts show that shingles is associated with an almost 40% higher chance of stroke, with the risk lasting more than a decade. They suggest that shingles vaccination might prove protective for both stroke and dementia, but they call for further studies to confirm that link.

By the way, one of the people involved in this study was Walter Willett, MD, Dr. P.H. He is one of the most well regarded epidemiologists and nutrition scientists in the world. He has been a frequent guest on The People’s Pharmacy syndicated radio show and was also the first recipient of The People’s Pharmacy Award for Excellence in Research and Communication for the Public Health.

Here is how the authors of the study, including Dr. Willett, introduce their research.

“There is growing evidence that herpesviruses may influence the risk of cognitive decline and dementia. Herpes zoster (HZ), commonly known as “shingles,” is caused by reactivation of the neurotrophic varicella-zoster virus (VZV)…HZ may potentially contribute to dementia risk through neuroinflammation, cerebral vasculopathy, or direct neuronal damage, but current evidence regarding the relationship between HZ and subsequent risk of cognitive decline is conflicting.

“In three large independent cohorts, HZ was associated with an approximately 20% higher long-term risk of SCD [subjective cognitive decline].

The Take Home Message About Viral Infections and Dementia in Alzheimer’s Research & Therapy, Aug. 14, 2024:

“To our knowledge, this is the first large study to examine HZ and the risk of early subjective cognitive decline, which may be the earliest manifestation of age-related cognitive decline and may be especially sensitive among individuals who received higher education. Given the long preclinical phase of dementia, identifying a potential association between HZ and early cognitive decline is important as it may provide insight into the complex and possible causal relationship between viral infections and cognitive health, as well as offer opportunities for early risk reduction and improved public health strategies.”

More Evidence Linking Viral Infections and Dementia:

NIH researchers also reported earlier on a relationship between viral infections and neurodegenerative diseases (Neuron, Jan. 11, 2023). They analyzed data from over 300,000 people in a Finnish biobank (FinnGen) and almost 500,000 people in the UK biobank.

These were individuals who had been diagnosed with a variety of neurodegenerative diseases such as Alzheimer disease, generalized dementia, vascular dementia, ALS, Parkinson’s disease and multiple sclerosis. Investigators compared these people to individuals who did not have any such neurological diseases.

The Associations Between Viral Infections and Dementia:

The authors introduce their research this way:

“Recent research has shown a definitive association between an increased risk of multiple sclerosis and prior infection with the Epstein-Barr virus (EBV). Additional concerns regarding the potential short and long-term cognitive impact of the current coronavirus pandemic have raised the priority of investigating the potential connection between viral exposures and neuroinflammation and/or neurodegeneration.”

They found that exposure to viral diseases was associated with an increased risk of neurodegeneration. Viral encephalitis was closely linked to Alzheimer disease. When patients had influenza with pneumonia, they were more likely to develop 5 of the 6 neurodegenerative diseases studied.

Shingles, caused by the varicella-zoster herpes virus, and intestinal viral infections were also associated with brain disorders.

The authors point out that this can be a delayed process:

“Some of these exposures were associated with an increased risk of neurodegeneration up to 15 years after infection.”

What About Herpes Viral Infections and Dementia?

The authors of this research linking viral infections and dementia point out that:

“The results described above are supported by recent findings in the literature, which suggest an association between herpes simplex virus (HSV) encephalitis and AD [Alzheimer’s disease], AD and hepatitis, genital warts and dementia, EBV and dementia, and MS and HSV. Since the discovery of an association of the 1918 flu pandemic, caused by H1N1 influenza A, with postencephalitic parkinsonism, a link between influenza and PD has been debated. A recent study using Danish data found an association between influenza and PD with an odds ratio of 1.73 up to 10 years after virus exposure. This is very similar to the hazard ratio for influenza and pneumonia in FinnGen which was 1.72.”

Preventing Viral Infections and Dementia:

The NIH investigators go on to note that “vaccines are currently available for some of these viruses, including influenza, shingles (varicella-zoster), and pneumonia.”

They suggest that vaccination might partially reduce the risk of developing neurodegenerative diseases:

“Influenza and pneumonia vaccination has been found to reduce risk for AD and PD. Shingles (varicella-zoster) vaccination is associated with a reduced risk of dementia, AD, and PD in both the United States and Wales.”

They also suggest that antiviral drugs might be beneficial:

“These findings also suggest additional avenues to explore for both the treatment and prevention of NDDs. In addition to vaccination, some studies suggest that using antivirals may reduce the risk of dementia in HSV positive patients25 or in patients with varicella-zoster virus.”

This Is NOT New!

We have written a lot about the possible connection between viral infections and dementia. Several years ago we interviewed a Harvard researcher who believed that beta-amyloid has both antiviral and antimicrobial properties. He suggested that the formation of amyloid plaque was the body’s way of fighting off infection. You can listen to this intriguing interview at this link.

More recently, we interviewed Donald Weaver, MD, PhD. He is a senior scientist at the Krembil Brain Institute at the University Health Network, Toronto, Ontario, Canada. He is a professor of Medicine (Neurology), Chemistry, and Pharmaceutical Sciences at the University of Toronto and a neurologist at the Toronto Western Hospital. His research suggests that Alzheimer’s disease might be an autoimmune disease and that many things could trigger this reaction, including viral infections. You can listen to this podcast at this link.

Final Words on Infections and Dementia:

We think it is time to think differently about Alzheimer’s disease and dementia. Most of the drugs that have been developed to rid the brain of amyloid plaque have fizzled. Even the newest ones that have been approved by the FDA, Aduhem, Leqembi and Kisunla have not restored memory or been proven to reverse dementia.

Perhaps it is time to explore the connection between infections and dementia. Why does the body form amyloid plaque? Could vaccination help prevent some cases of Alzheimer disease? Would an antibiotic such as azithromycin be helpful against Chlamydia pneumoniae infections that linger in the lungs, eyes or brain? If the NIH and the Alzheimer’s Association begin funding novel approaches to preventing or treating dementia, perhaps we might make more progress against this devastating disease!

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