A study from researchers at Cedars-Sinai Medical Center has uncovered a potential link between a common bacterium, Chlamydia pneumoniae, and the progression of Alzheimer’s disease. This bacterium, typically known for causing pneumonia and sinus infections, may invade both the retina and brain, leading to inflammation, nerve cell death, and the accumulation of amyloid-beta, a protein associated with Alzheimer’s. The findings, published on February 21, 2026, in the journal Nature Communications, indicate that this chronic infection could contribute to cognitive decline, particularly in individuals carrying the high-risk APOE4 gene.
In their research, scientists discovered that Chlamydia pneumoniae can persist in the eye and brain for extended periods. This persistence may exacerbate the damage associated with Alzheimer’s. As the study’s lead author, Maya Koronyo-Hamaoui, PhD, emphasized, the presence of this bacterium across various human tissues and animal models highlights a previously unrecognized connection between bacterial infection, inflammation, and neurodegeneration.
Impact of Bacterial Presence on Cognitive Health
The research team analyzed retinal tissue from 104 participants, employing advanced imaging techniques, genetic testing, and protein studies. This cohort included individuals with normal cognitive function, mild cognitive impairment, and Alzheimer’s disease. Notably, those diagnosed with Alzheimer’s demonstrated significantly higher levels of Chlamydia pneumoniae in both their retinas and brains compared to their cognitively healthy counterparts. Furthermore, the study found that elevated bacterial levels correlated with increased brain damage and more severe cognitive decline, especially among individuals with the APOE4 gene, which is known to heighten Alzheimer’s risk.
To deepen their investigation, the researchers examined human nerve cells in laboratory settings and studied mice models of Alzheimer’s disease. In both instances, infection with Chlamydia pneumoniae resulted in heightened inflammation, increased nerve cell mortality, and deteriorating cognitive function. The bacterium also stimulated the production of amyloid-beta, further linking it to Alzheimer’s pathology.
Potential Therapeutic Approaches
These findings raise intriguing possibilities for new therapeutic strategies targeting the infection-inflammation axis in Alzheimer’s treatment. Timothy Crother, PhD, co-corresponding author of the study, noted that addressing chronic infections and their inflammatory consequences might represent a novel approach to managing the disease. This research also underscores the potential of using retinal imaging as a noninvasive method for identifying individuals at risk for Alzheimer’s.
The collaborative study included contributions from various Cedars-Sinai researchers, such as Bhakta Gaire, Yosef Koronyo, and others. It received funding from the National Institutes of Health and the Alzheimer’s Association, supporting ongoing efforts to understand and combat this debilitating condition.
These insights into the relationship between Chlamydia pneumoniae and Alzheimer’s disease not only advance scientific knowledge but may also pave the way for innovative treatment options, potentially transforming the landscape of Alzheimer’s care in the future.
