Can People Catch Alzheimer’s Disease? New Research Raises Questions

Here is an uncomfortable question: Can people catch Alzheimer’s disease? Most neurologists would still say absolutely not! Alzheimer’s disease (AD) is not contagious like the flu. You cannot “catch” it from sitting next to someone with dementia. And we absolutely agree. But new research published in a prestigious journal, Nature Communications (Jan. 22, 2026), suggests something far more complicated and unsettling.

Scientists have found strong evidence that a common respiratory bacterium, Chlamydia pneumoniae, may infect the brain and retina of the eye, lie dormant for years, and then amplify the inflammation and amyloid buildup associated with Alzheimer’s disease.

You may not catch Alzheimer’s disease itself. But you might catch a pathogen that helps trigger it.

A Common Bacterium That Can Cause a

The bacterium in question is Chlamydia pneumoniae. It is pronounced a couple of ways, but experts we have consulted pronounce it: kluh-MID-ee-uh    new-MO-nee-yay. Others pronounce pneumoniae: new-MO-nee-eye. Researchers often abbreviate it C. pneumoniae.

Please do not confuse the above bacterial infection with Chlamydia trachomatis, which is a common sexually transmitted infection. C. pneumoniae is a respiratory germ. It is widespread and enters the body through the nose and mouth. This pathogen can cause sinus infections, bronchitis, pneumonia, and has been linked to hard-to-treat asthma and COPD.

I personally went through a bout of hard-to-treat bronchitis and asthma. What cured me was a novel treatment regimen with the antibiotic azithromycin. Here is an account of that ordeal:

How I Overcame Asthma That Would Not Quit
A long-term course of the antibiotic azithromycin helped me shake off recurrent bouts of asthma that would not quit.

If People Can “Catch” C. Pneumoniae, Could They “Catch” Alzheimer’s Disease?

Many people are infected at some point in their lives with C. pneumoniae. In fact, by older adulthood, exposure rates are extremely high.

The new study published in Nature Communications (Jan. 22, 2026) shows that:

• Chlamydia pneumoniae was found in the retinas and brains of people who died with Alzheimer’s disease.
• The bacterial burden was much higher in people with dementia than in cognitively normal individuals.
• The infection was strongly associated with amyloid-beta buildup, neuroinflammation, and worse cognitive performance.
• In mouse models, this infection worsened memory and increased amyloid plaque formation.

Importantly, the bacteria appear capable of lying dormant in nervous tissue for years. This research opens up new opportunities for research. For one thing, it raises the possibility that patients with detectable C. pneumoniae bacteria might benefit from antibiotic-based treatment.

Can People Catch Alzheimer’s Disease Through Infection?

Let’s be very clear. You cannot catch Alzheimer’s disease from a handshake. But what if certain infections set off a chain reaction in vulnerable brains?

The researchers describe a process involving something called the NLRP3 inflammasome — essentially a molecular alarm system in immune cells. When triggered by infection, it produces inflammatory chemicals that can damage tissue.

In Alzheimer’s disease:

1. Infection may activate this inflammatory system.
2. Inflammation promotes amyloid-beta accumulation.
3. Amyloid buildup further drives inflammation.
4. A destructive feedback loop begins.

This study suggests Chlamydia pneumoniae could help ignite that loop.

Have Scientists Suggested Infection Before as a Contributor to Dementia?

Yes — for over a century!

Syphilis

The bacterium Treponema pallidum was identified over 100 years ago. Neurosyphilis was a common cause of dementia in Europe early in the 20th century. That was before the age of antibiotics.

Scientists have known for a very long time that this sexually transmitted disease could cause cognitive impairment, confusion and ultimately dementia. Would doctors in 1910 say you could catch a brain disorder? Probably not in those words. But clearly an individual could “catch” syphilis from an infected person during intercourse. If that bacterium got into the brain, it caused a lot of misery.

Once we could cure this STD with penicillin, neuroscientists seemingly forgot about the infection connection with Alzheimer’s disease.

Creutzfeldt-Jakob disease

We have known about a neurodegenerative disease called CJD (Creutzfeldt-Jakob disease) for more than 100 years.

It is described this way (StatPearls, March 9, 2022):

“Creutzfeldt-Jakob disease (CJD) is a rapidly progressive, rare, transmissible, universally fatal, neurodegenerative condition caused by prion proteins.”

“It belongs to a group of transmissible spongiform encephalopathies that can affect people worldwide with an incidence of one case per million per year.”

What Is a “Prion?”

The article above in StatPearls describes CJD:

“The infectious agent is ‘prion’ (a protein) that can be transmitted either by direct contact with contaminated tissue (iatrogenic) or via inheriting a mutation in the prion protein gene (familial)…The word ‘prion” derives from the words ‘proteinaceous’ and ‘infectious…”

Mad Cow Disease?

Perhaps you remember headlines about Mad Cow Disease, also known as BSE or bovine spongiform encephalopathy. Researchers believe that this progressive neurodegenerative disease is caused by prions. It can be spread from cow to cow or through contaminated meat-and-bone meal (MBM).

It can take years for cows to develop symptoms of BSE.

A review from the CDC reports:

“Strong evidence indicates that classic BSE has been transmitted to people primarily in the United Kingdom, causing a variant form of Creutzfeldt-Jakob disease (vCJD)… Since vCJD was first reported in 1996, a total of only 231 patients with this disease, including 3 secondary, blood transfusion-related cases, have been reported worldwide. The risk to human health from BSE in the United States is extremely low.”

We interpret that as good news and bad news. The good news is that CJD is “extremely” rare. The bad news is that some forms of neurodegenerative diseases are indeed transmissible. That is why the latest research has captured headlines.

What About Herpes? Could You Catch Alzheimer’s Disease from this Virus?

We first stumbled upon the idea that Alzheimer’s disease might be infectious when we read articles by Melvyn J. Ball, MD. He was a pathologist at the Oregon Health Science University. In an article in the Canadian Journal of Neurological Sciences (Aug. 9, 1982), Dr. Ball proposed that the herpes simplex virus (HSV) that causes cold sores might also damage brain tissue.

Everyone knows that the herpes virus can travel down from the trigeminal ganglia in the brain to the lips and cause a cold sore. Dr. Ball proposed that hibernating viruses could also travel deeper into the brain and cause AD-like lesions.

He wrote:

“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.”

Sadly, very few neurologists paid any attention to Dr. Ball’s hypothesis. But he did not give up.

In 2006 he wrote in the Journal of Alzheimer’s Disease:

“…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 Researchers Suggest an Infectious Cause for AD:

Although most neurologists ignored Dr. Ball’s findings, he is not the only one to posit pathogens as a risk factor for dementia. We have written extensively about infections and Alzheimer’s disease. Here is an article that we wrote tracing some early research back to 1974.

Many years ago we were honored to interview Dr. Robert Moir, a Harvard scientist who studied the role of infections as a causative factor in the development of Alzheimer’s disease. You can listen to this radio show at this link. You can also read about more recent research linking infection to AD at this link.

More recently, scientists have explored links between dementia and:

• Herpes viruses
• Gum disease bacteria
• Chronic systemic infections

Now this new work in Nature Communications (Jan. 22, 2026), strengthens the infectious hypothesis by identifying bacterial infection directly inside retinal and brain tissue from Alzheimer’s patients.

Didn’t We Already Learn People Could Catch Alzheimer’s Disease?

A study published in Nature Medicine (Jan. 29, 2024) sent ripples through the Alzheimer’s research community.  The research was kicked off because clinicians in the UK discovered a number of patients who had developed Alzheimer’s disease (AD) before they were 60.

That in itself might not have garnered attention. There are cases of early-onset AD.

But some of the cases were in their 40s and 50s:

“Symptom onset was between the ages of 38 years and 49 years in four patients (cases 3, 4, 5 and 8) and at age 55 years in the remaining patient (case 2). In three of these five patients (cases 3, 4 and 8), a diagnosis of Alzheimer’s disease had been made before referral to the NPC; two individuals presented with typical amnestic symptoms (cases 4 and 8) and met National Institute on Aging and Alzheimer’s Association (NIA-AA) diagnostic criteria for probable Alzheimer’s disease, and the other individual (case 3) presented with non-amnestic (language) symptoms.”

The researchers reviewed medical records from these patients. They did not have the known genetic mutations that are thought to cause early-onset dementia. What they did have in common, however, was a history of childhood injections of human growth hormone (HGH) that had been extracted from the pituitary glands of cadavers. This led to the suggestion that Alzheimer’s pathology could be transmitted under very rare circumstances.

The authors concluded that amyloid-beta can behave in ways similar to prions — misfolded proteins that propagate disease, like those responsible for Creutzfeldt-Jakob disease (CJD) and “mad cow” disease.

What we can conclude from all this research is that under specific conditions, Alzheimer-related pathology can be transmitted. Infection may help drive or worsen the disease process.

Catch Alzheimer’s Disease — Or Catch the Trigger?

Here’s the key distinction. You probably cannot catch Alzheimer’s disease the way you catch measles.

But you might catch pathogens that:

• Invade nervous tissue
• Trigger chronic inflammation
• Accelerate amyloid accumulation
• Impair microglial cleanup mechanisms
• Worsen cognitive decline

The 2026 study even suggests that impaired immune clearance in the retina may allow bacterial persistence, meaning some people may carry this infection silently for years.

Interestingly, the bacterial burden was higher in people who carried the APOE-ε4 gene — the strongest known genetic risk factor for Alzheimer’s disease. That raises the possibility of a gene–infection interaction.

If Infection Plays a Role, What Does That Mean?

The authors of the new research suggest that:

• Early antibiotic treatment targeting Chlamydia pneumoniae could be studied.
• Therapies aimed at dampening NLRP3 inflammasome activation might slow disease progression.
• Retinal imaging could potentially detect infection-related biomarkers before severe cognitive decline.

A Taiwanese nationwide study previously reported that patients treated appropriately for Chlamydia pneumoniae infections had a lower subsequent risk of Alzheimer’s disease.

That does not prove causation. But it is intriguing.

If You Could Catch Alzheimer’s Disease, Can you Prevent AD?

Here is a question that most neuroscientists and drug companies seem to shy away from:

Would Vaccines Work to Prevent AD?

If there is a possibility that infections could trigger the destruction that leads to Alzheimer’s disease, could vaccination prevent the process from starting? I want to reinforce the idea that most neuroscientists find such an idea preposterous. And yet there are data to support this hypothesis. The most recent was published in (Lancet Neurology, Feb. 2026). The data come from Canada and it is the third such study to reinforce the idea that a shingles vaccine can reduce the risk of dementia.

Would Antibiotics Work to Prevent AD?

The authors of the recent research in Nature Communications (Jan. 22, 2026) point out that:

“Notably, a recent nationwide cohort study in Taiwan demonstrated that antibiotic treatment targeting Chlamydia pneumoniae significantly reduced the risk of AD onset. These findings suggest that Chlamydia pneumoniae infection may exacerbate AD pathology and that therapeutic strategies targeting Chlamydia pneumoniae could potentially slow or mitigate AD progression.”

The infectious hypothesis remains controversial, but it is no longer fringe. Data are accumulating to suggest that infections play a role in dementia.

Final Words: Can People Catch Alzheimer’s Disease?

Most neurologists would still say no! And in the everyday sense, they are right. You cannot catch Alzheimer’s disease by being near someone with dementia.

But science is increasingly showing that:

• Misfolded proteins can propagate under rare conditions.
• Pathogens may amplify neurodegeneration.
• Chronic infection and inflammation may contribute to risk.

Perhaps the more accurate question is not:

Can people catch Alzheimer’s disease?

But rather:

Can people catch infections that increase the likelihood of developing Alzheimer’s disease years or decades later?

That question now deserves serious attention. And if this line of research holds up, it could radically reshape how we think about prevention and even treatment of one of the most devastating diseases of our time.

There is also the looming question: will people who caught COVID-19, especially those who developed long COVID, be more vulnerable to cognitive dysfunction down the road? Hopefully, some brave young investigators break new ground in the fight against dementia.

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