A common bacterial infection known for causing pneumonia and sinus issues may also play a surprising role in worsening Alzheimer’s disease, research suggests.

Scientists at Cedars-Sinai have discovered that Chlamydia pneumoniae, known for causing pneumonia and sinus infections, can linger in neural tissue for years, triggering immune responses that may worsen nerve damage and dementia symptoms.

Researchers found significantly higher levels of C. pneumoniae in the retinas and brains of people with Alzheimer’s disease. Higher bacterial levels were linked to more severe brain changes and faster cognitive decline.

“This discovery raises the possibility of targeting the infection-inflammation axis to treat Alzheimer’s,” co-corresponding study author Timothy Crother, a research professor at Cedars-Sinai Guerin Children’s and the Department of Biomedical Sciences at Cedars‑Sinai, said in a statement.

“It’s an intriguing finding because it strengthens the idea that infections and inflammation may play a bigger role in Alzheimer’s than previously assumed,” Christopher U. Missling, president and CEO of Anavex Life Sciences, a biotechnology company developing medicine solutions for central nervous system disorders, and not involved in the study, told The Epoch Times.

Bacteria Infect Retina to Worsen Disease

The study, published in Nature Communications, involved examining retinal tissue from 104 people, including those with normal cognition, mild cognitive impairment, and Alzheimer’s disease, using advanced imaging, genetic testing, and protein analysis.

In patients with Alzheimer’s disease, researchers found higher levels of C. pneumoniae in brain and eye tissues. The presence of these bacteria often came with inflammation in the surrounding tissue, which researchers theorize could damage the brain and cause cognitive decline over time.

For the first time, researchers found that Chlamydia bacteria can reach the retina and trigger the body’s first line of defense against infections—the innate immune response—activating inflammatory pathways involved in infections.

C. pneumoniae is a common respiratory pathogen, with most people being infected by the bacteria by 20 years of age.

Researchers found elevated levels of immune proteins associated with inflammation in the eyes of people with Alzheimer’s, indicating an ongoing immune response. Proteins involved in detecting bacteria were also increased in both the brain and eyes of people with Alzheimer’s.

Higher bacteria levels were also more common in people carrying the APOE4 gene, a known genetic risk factor for Alzheimer’s.

Mouse Models Confirm the Link

To validate their findings, researchers studied human neurons in the lab and mice with Alzheimer’s disease.

Injecting C. pneumoniae into the nose of mice led to a clear increase in bacterial presence in the brains of mice with Alzheimer’s within seven days. Researchers observed a significant rise in certain immune cells and inflammatory markers in brain regions involved in memory.

“Seeing Chlamydia pneumoniae consistently across human tissues, cell cultures, and animal models allowed us to identify a previously unrecognized link between bacterial infection, inflammation, and neurodegeneration,” Maya Koronyo-Hamaoui, senior study author and a professor at Cedars-Sinai, said in the statement.

Notably, the infection also increased production of amyloid-beta, the protein that builds up in the brains of people with Alzheimer’s.

Previous research has detected C. pneumoniae in the brains of Alzheimer’s patients and confirmed that the amyloid beta associated with this disease can be produced in response to infections.

Potential Treatment Implications

The findings show that a long-lasting bacterial infection can cause the production of amyloid, activate an immune response, and speed up brain cell damage, Missling, who has a doctorate in organic chemistry, said.

The research could point toward new treatment approaches, including early antibiotic use and anti-inflammatory therapies. The findings also support the use of the retina as a noninvasive diagnostic tool for Alzheimer’s.

The research “strengthens the idea that infections and inflammation may play a bigger role in Alzheimer’s than previously assumed,” Missling said.

He suggested the findings could even lead to preventative strategies for at-risk populations, such as APOE4 carriers.

“That might include earlier screening for chronic infections, targeted anti‑inflammatory approaches, or interventions that reduce microbial burden before neurodegeneration begins.”

However, Dr. Rajesh Burela, neurology resident physician at Northwell Health in Poughkeepsie, New York, and Drugwatch.com, told The Epoch Times that while the study findings are “compelling,” further research is needed to prove the theory.

“Regardless, it shows that there is potential for significant progress in understanding the infection’s role in AD [Alzheimer’s Disease] pathogenesis,” he noted, and explained that even if infection does not directly cause Alzheimer’s, it may act as a disease accelerator, making anti-infectious strategies potentially valuable.

“I think it’s still too early to say that these therapies and this type of research will lead to preventative strategies,” he said. “Simply because we need more longitudinal studies.”