A common bacterium known for causing pneumonia and sinus infections may significantly contribute to the progression of Alzheimer’s disease. Researchers at Cedars-Sinai Medical Center discovered that Chlamydia pneumoniae can invade both the retina and brain, leading to inflammation, nerve cell death, and an increase in amyloid-beta levels, which are associated with Alzheimer’s. This finding, published on February 21, 2026, in the journal Nature Communications, highlights a potential new avenue for treatment that could involve early antibiotic intervention and strategies aimed at reducing inflammation.
The study reveals that Chlamydia pneumoniae can persist in the eye and brain for extended periods, exacerbating the damage linked to Alzheimer’s disease. Researchers found that individuals diagnosed with Alzheimer’s exhibited significantly higher levels of this bacterium in both retinal and brain tissues compared to those with normal cognitive function. Notably, higher concentrations of the bacterium correlated with more severe cognitive decline, especially in individuals carrying the high-risk APOE4 gene variant.
Linking Infection and Neurodegeneration
For the first time, scientists demonstrated that Chlamydia pneumoniae can reach the retina, the light-sensitive tissue at the back of the eye. This invasion activates immune responses connected to inflammation and nerve cell loss, which are critical factors in cognitive decline. Dr. Maya Koronyo-Hamaoui, the study’s lead author and professor of Neurosurgery, Neurology, and Biomedical Sciences at Cedars-Sinai Health Sciences University, stated, “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.”
The research team analyzed retinal tissue samples from 104 participants, encompassing individuals with normal cognition, mild cognitive impairment, and Alzheimer’s disease. The findings indicated that the presence of Chlamydia pneumoniae was notably higher in the retinas and brains of Alzheimer’s patients, suggesting a direct relationship between bacterial levels and the severity of cognitive deficits.
Potential for New Treatment Strategies
To further investigate this connection, researchers conducted experiments on human nerve cells and studied Alzheimer’s disease models in mice. In both scenarios, infection with Chlamydia pneumoniae resulted in increased inflammation, greater nerve cell death, and a decline in cognitive functions. The bacterium also prompted the production of amyloid-beta, which is a characteristic protein that accumulates in the brains of Alzheimer’s patients.
Dr. Timothy Crother, a co-corresponding author of the study and research professor at Cedars-Sinai, noted, “This discovery raises the possibility of targeting the infection-inflammation axis to treat Alzheimer’s.” The findings suggest that addressing long-standing bacterial infections and their associated inflammation may represent a promising new therapeutic approach for Alzheimer’s disease.
The implications of this research also underscore the potential for using retinal imaging as a noninvasive method to identify individuals at risk for developing Alzheimer’s. By monitoring retinal health, healthcare providers could gain valuable insights into brain pathology and disease progression.
The study involved contributions from multiple authors, including Bhakta Gaire, Yosef Koronyo, and several others associated with Cedars-Sinai, as well as external collaborators like Julie A. Schneider and Lon S. Schneider. Funding for this research was provided by various grants from the NIH/NIA and the Alzheimer’s Association.
These findings present a compelling case for further exploration into the role of chronic bacterial infections in neurodegenerative diseases, potentially paving the way for innovative treatments that could alter the course of Alzheimer’s disease.
