Researchers Link Pneumonia-Causing Bacterium to Alzheimer's Disease Risk
Could a common respiratory infection quietly contribute to Alzheimer's disease? A new study suggests that Chlamydia pneumoniae-a bacterium best known for causing pneumonia and sinus infections—may invade the retina and brain, triggering inflammation and accelerating neurodegeneration. The research, led by scientists at Cedars-Sinai, was published in Nature Communications.
Alzheimer’s disease is characterized by the buildup of amyloid-beta plaques in the brain, along with chronic inflammation and progressive nerve cell loss. While genetics and aging are well-established risk factors, scientists have increasingly explored whether infections might also contribute to disease progression.
In this study, researchers analyzed retinal tissue from 104 individuals, including people with normal cognition, mild cognitive impairment, and Alzheimer’s disease. Using advanced imaging, molecular testing, and protein analysis, they found significantly higher levels of Chlamydia pneumoniae in both the retinas and brains of patients with Alzheimer’s compared to cognitively healthy individuals. Higher bacterial levels were also linked to more severe cognitive decline.
The association was especially strong in individuals carrying the APOE4 gene variant, a known genetic risk factor for Alzheimer’s. This suggests a possible interaction between infection and genetic vulnerability.
To test causality, the team conducted laboratory experiments using human nerve cells and Alzheimer’s mouse models. Infection with Chlamydia pneumoniae led to increased inflammation, greater neuronal death and elevated production of amyloid-beta. Notably, researchers demonstrated for the first time that the bacterium can travel to and persist in the retina—activating immune responses that mirror changes occurring in the brain.
These findings support the concept of an “infection-inflammation axis” in Alzheimer’s disease. The retina, often described as a window to the brain, may serve as a noninvasive site for early detection through retinal imaging.
While further research is needed to confirm long-term causality, the study raises the possibility that early antibiotic treatment or anti-inflammatory therapies targeting chronic infection could represent novel strategies to slow or prevent Alzheimer’s progression.
REFERENCE: Bhakta Prasad Gaire, Yosef Koronyo, Jean-Philippe Vit, Alexandre Hutton, Lalita Subedi, Dieu-Trang Fuchs, Natalie Swerdlow, Altan Rentsendorj, Saba Shahin, Daisy Martinon, Edward Robinson, Alexander V. Ljubimov, Julie A. Schneider, Lon S. Schneider, Debra Hawes, Stuart L. Graham, Vivek K. Gupta, Mehdi Mirzaei, Keith L. Black, Jesse G. Meyer, Moshe Arditi, Timothy R. Crother, Maya Koronyo-Hamaoui. Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer’s disease retina. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-68580-4
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