Common respiratory infection may be linked to Alzheimer’s

Alzheimer’s disease keeps spreading as families age, while its root cause remains unsettled, leaving prevention and treatment stuck in uncertainty.

New evidence now points toward an unexpected suspect, a routine respiratory infection that may be shaping changes inside the brain.

In the United States alone, about 7.2 million older adults were living with Alzheimer’s dementia in 2025, and scientists are still unclear about what first sets the disease in motion.

A possible contributing factor

Chlamydia pneumoniae is a pneumonia bacterium that shows up in some Alzheimer’s brain samples, and a 2024 review assessed the evidence. 

Researchers at Cedars-Sinai Medical Center pulled together human tissue studies, animal experiments, and cell work to map possible links.

The work was led by Dr. Maya Koronyo-Hamaoui in the Neurosurgery Department at Cedars-Sinai.

Her research focuses on immune stress in brain and eye tissue, so the review treats infection as a contributory factor, not a sole cause.

An infection that persists

Microbiologists have tracked how Chlamydia pneumoniae, or Cp, spreads by entering cells.

It switches between a tough traveling form and a growing form, and that switch helps it survive antibiotics and immune attacks.

Under pressure, Cp can slow down and linger for months inside a host cell, which makes detection and treatment more difficult.

That kind of persistence matters in aging bodies, where repeated respiratory infections can keep restarting the same inflammatory signals.

Paths into brain tissue

For Cp to matter in dementia, it must reach the brain or at least disturb the immune system far beyond the lungs.

Researchers have proposed a nasal route and a blood route, and both could carry Cp toward brain tissue.

Infected immune cells may slip through the blood-brain barrier, a wall of cells controlling brain entry, and spread infection.

A nasal infection could also ride nearby nerves, but researchers still debate how often that happens in people.

Clues from the brains of patients

Brain tissue donated after death has offered the clearest hints in Alzheimer’s disease, as researchers can look directly for bacterial material.

In 1998, a report described Cp in brain regions that also showed classic Alzheimer’s damage.

Some experts found Cp inside neurons and immune-like cells, sometimes beside the protein clumps that mark the brains of Alzheimer’s sufferers.

Other labs did not detect Cp at all, which keeps the evidence correlative and sensitive to methods and sampling.

What animal studies show

Researchers moved beyond human samples by infecting mice through the nose, and then watching the brain for later changes.

A 2004 study found Alzheimer-like amyloid plaques in mouse brains after experimental nasal Cp infection.

Those plaques include amyloid beta, a sticky protein fragment that can clump, but mouse timelines do not match human aging.

Many models also stop short of measuring memory or reasoning, so the link to cognitive decline remains untested.

Proteins react to infection

Some scientists now see amyloid beta as part of the immune response, not only as a waste product in Alzheimer’s disease.

In a 2016 paper, researchers reported that amyloid beta can trap some microbes, which may require it to clump.

If the brain keeps sensing infection, it may keep making amyloid beta, and clearing the clumps may become harder over years.

That logic fits the infection hypothesis, but it still cannot clarify whether bacteria cause disease or simply gather in damaged tissue.

Inflammation can do damage

Even without heavy bacterial growth, the immune system can harm neurons when it stays switched on for too long.

Infected cells release cytokines, small messenger proteins that rally immune cells, and those signals can spill into the brain.

Brain-resident immune cells respond by changing shape, producing toxic molecules, and sometimes failing to clear amyloid beta efficiently.

This kind of collateral injury could speed degeneration, yet it may depend on age, genetics, and the intensity of infection.

Genes may tune Alzheimer’s risk

A major genetic risk factor for Alzheimer’s comes from APOE4, a gene variant. Lab data suggest APOE4 can change how cells handle fats, and some microbes use those fats to grow.

Researchers have also linked APOE4 to higher burdens of Cp in brain tissue, which could amplify immune stress.

Genetics may not start the infection, but may set the conditions that determine whether an exposure leaves lasting damage.

Future research directions

To move from suspicion to proof, scientists need studies that follow people over time and track infection markers.

“No definitive studies have been performed proving or disproving Cp’s role as a causative or accelerating agent in AD pathology and cognitive decline,” wrote Dr. Koronyo-Hamaoui.

Teams must standardize tissue sampling, genetic testing, and detection tools, because small choices can flip a sample from positive to negative.

Until those results arrive, doctors should not use antibiotics to prevent dementia, since harms can outweigh unproven benefits.

Taken together, the evidence suggests Cp could act as an accelerant in susceptible brains by sustaining inflammation and amyloid production.

The review also underlines how much uncertainty remains, and it points toward careful, long-term studies that can settle cause and effect.

The study is published in Frontiers in Neuroscience.

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