Researchers have found that Chlamydia pneumoniae, a widespread bacterium best known for causing pneumonia and sinus infections, may persist in both the eye and the brain for many years, potentially worsening Alzheimer’s disease. According to a new study from Cedars-Sinai, the bacterium appears capable of intensifying disease-related changes rather than merely coexisting with them. The research, published in Nature Communications, points towards new therapeutic possibilities, including early antibiotic intervention and treatments designed to reduce chronic inflammation.
The study demonstrates for the first time that Chlamydia pneumoniae can travel to the retina, the delicate layer of tissue at the back of the eye responsible for processing visual information. Once present there, the bacterium activates immune responses associated with sustained inflammation, nerve cell damage and progressive cognitive decline. This finding is particularly significant because the retina is closely connected to the brain, making it a valuable window into neurological health.
By observing the bacterium consistently across human tissue samples, laboratory-grown cells and animal models, the researchers were able to establish a previously unrecognised connection between bacterial infection, inflammation and neurodegeneration. The senior author of the study, Maya Koronyo-Hamaoui, emphasised that the eye can act as a surrogate for the brain. She noted that retinal infection and long-term inflammation appear to mirror changes occurring in the brain itself, suggesting that retinal imaging could one day help identify individuals at higher risk of Alzheimer’s disease through a noninvasive approach.
To carry out the research, the team used advanced imaging techniques, genetic analyses and protein profiling to study retinal tissue from 104 individuals. This group included people with normal cognitive function, those with mild cognitive impairment and individuals diagnosed with Alzheimer’s disease. By comparing these samples, the investigators were able to assess how bacterial presence varied across different stages of cognitive health and decline.
The analysis revealed that levels of Chlamydia pneumoniae were significantly higher in both the retinas and brains of people with Alzheimer’s disease than in those with normal cognition. Moreover, the severity of bacterial presence closely tracked the extent of brain pathology and cognitive deterioration. In other words, higher bacterial levels were associated with more pronounced neurological damage and greater loss of cognitive ability.
The researchers also observed that elevated bacterial levels were more common among individuals carrying the APOE4 gene variant, which is already recognised as a major genetic risk factor for Alzheimer’s disease. Further experiments using human neurons in laboratory settings and mouse models of Alzheimer’s showed that infection with Chlamydia pneumoniae increased inflammation, promoted nerve cell death and accelerated cognitive decline. The infection also stimulated the production of amyloid-beta, the protein that accumulates abnormally in the brains of people with Alzheimer’s.
These findings, led by co-first authors Bhakta Gaire and Yosef Koronyo, suggest that targeting chronic bacterial infection and the inflammatory processes it triggers could represent a new treatment strategy. Co-corresponding author Timothy Crother noted that the work highlights the infection–inflammation axis as a promising therapeutic target. Taken together, the results also strengthen the case for using the retina as a practical, noninvasive tool to help diagnose, track and potentially predict the progression of Alzheimer’s disease.
More information: Bhakta Prasad Gaire et al, Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer’s disease retina, Nature Communications. DOI: 10.1038/s41467-026-68580-4
Journal information: Nature Communications Provided by Cedars-Sinai Medical Center
