Common pneumonia bacterium linked to Alzheimer's disease

Researchers have discovered that Chlamydia pneumoniae, a bacterium commonly causing pneumonia and sinus infections, may contribute to Alzheimer's disease by invading the retina and brain. The study found higher levels of the bacterium in Alzheimer's patients, particularly those with the APOE4 gene variant, associated with greater cognitive decline. This suggests potential new treatment avenues targeting infection and inflammation.

A team at Cedars-Sinai Medical Center has identified a possible connection between Chlamydia pneumoniae and Alzheimer's disease. The bacterium, known for respiratory infections, can persist in the eye and brain, triggering inflammation, nerve cell death, and accumulation of amyloid-beta protein, a key feature of Alzheimer's.

The research, published in Nature Communications, analyzed retinal tissue from 104 individuals, including those with normal cognition, mild cognitive impairment, and Alzheimer's. Results showed significantly higher levels of Chlamydia pneumoniae in the retinas and brains of Alzheimer's patients compared to those with normal cognition. These elevated levels correlated with more severe brain damage and accelerated cognitive decline, especially in carriers of the APOE4 gene variant, which raises Alzheimer's risk.

In laboratory tests on human nerve cells and in mouse models of Alzheimer's, infection with the bacterium increased inflammation, promoted nerve cell loss, and boosted amyloid-beta production, worsening cognitive issues.

"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," stated Maya Koronyo-Hamaoui, PhD, professor of Neurosurgery, Neurology, and Biomedical Sciences at Cedars-Sinai and senior author.

She added, "The eye is a surrogate for the brain, and this study shows that retinal bacterial infection and chronic inflammation can reflect brain pathology and predict disease status, supporting retinal imaging as a noninvasive way to identify people at risk for Alzheimer's."

Co-corresponding author Timothy Crother, PhD, noted, "This discovery raises the possibility of targeting the infection-inflammation axis to treat Alzheimer's."

The findings, led in part by co-first authors Bhakta Gaire, PhD, and Yosef Koronyo, MSc, propose that addressing chronic bacterial infections and resulting inflammation could offer new therapeutic strategies. They also bolster the use of retinal imaging for early detection and monitoring of Alzheimer's. The study received funding from the NIH/NIA and the Alzheimer's Association.

ተያያዥ ጽሁፎች

Scientific illustration showing AI tool SIGNET mapping disrupted gene networks in Alzheimer's brain neurons.
በ AI የተሰራ ምስል

AI tool maps causal gene-control networks in Alzheimer’s brain cells

በAI የተዘገበ በ AI የተሰራ ምስል እውነት ተፈትሸ

Researchers at the University of California, Irvine report that a machine-learning system called SIGNET can infer cause-and-effect links between genes in human brain tissue, revealing extensive rewiring of gene regulation—especially in excitatory neurons—in Alzheimer’s disease.

A new genomic analysis suggests that Alzheimer's disease may begin with inflammation in organs like the skin, lungs, or gut, potentially decades before brain symptoms appear. Researchers analyzed genetic data from hundreds of thousands of people and found risk genes more active outside the brain. This perspective could reshape prevention and treatment strategies.

በAI የተዘገበ

A large study of nearly 28 million older Americans has found that long-term exposure to fine particle air pollution increases the risk of developing Alzheimer's disease, primarily through direct effects on the brain. The research, led by Yanling Deng at Emory University, indicates that individuals with a history of stroke may face heightened vulnerability. Published in PLOS Medicine, the findings highlight the importance of cleaner air for protecting cognitive health in aging populations.

Researchers have demonstrated that restoring levels of a key brain energy molecule can reverse advanced Alzheimer's disease in mouse models, repairing damage and restoring cognitive function. The study, published on December 22, challenges the long-held view that the condition is irreversible. Findings from human brain tissue support the approach's potential relevance to patients.

በAI የተዘገበ

Researchers at the University of California, San Francisco, have discovered a mechanism by which exercise helps protect the brain from age-related damage associated with Alzheimer's disease. Physical activity prompts the liver to release an enzyme that repairs the blood-brain barrier, reducing inflammation and improving memory in older mice. The findings, published in the journal Cell, highlight a body-to-brain pathway that could lead to new therapies.

A large study published in Neurology finds that impaired kidney function is linked to higher levels of Alzheimer’s biomarkers in the blood, without increasing overall dementia risk. However, among people who already have elevated biomarker levels, poor kidney health may hasten when dementia symptoms appear, underscoring the need to factor kidney function into interpretation of Alzheimer’s blood tests.

በAI የተዘገበ

Scientists at Northwestern University have identified a toxic subtype of amyloid beta oligomers that triggers early Alzheimer's changes in the brain. Their experimental drug, NU-9, reduced this damage and inflammation in pre-symptomatic mice, suggesting potential for preventing the disease before symptoms appear. The findings highlight a new strategy for early intervention.

 

 

 

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