Alzheimer's & Dementia

Common eye bacteria linked to dementia and Alzheimer's

Common eye bacteria linked to dementia and Alzheimer's
Bacteria and infection appear to impact the onset of cognitive decline, but we're not sure how
Bacteria and infection appear to impact the onset of cognitive decline, but we're not sure how
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Bacteria and infection appear to impact the onset of cognitive decline, but we're not sure how
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Bacteria and infection appear to impact the onset of cognitive decline, but we're not sure how

Scientists have uncovered an intriguing link between infection and brain health, finding that a common bacterium in the eye appears to be linked to cognitive decline and Alzheimer’s disease. It's the newest evidence suggesting bacteria and infections play a significant and poorly understood role in destroying the brain as we age.

Researchers at Cedars-Sinai found traces of Chlamydia pneumoniae – a bacterium that's best known for causing respiratory infections – in the eye's retinal tissue, and higher levels of this pathogen correlated with advanced degeneration in Alzheimer’s disease patients. While this don't show causation by any means, the findings add to a growing body of evidence suggesting chronic infections play some role in neurodegenerative disease over time.

“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,” said Maya Koronyo-Hamaoui, a professor at Cedars-Sinai Health Sciences University and the lead author of the study. “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.”

The team found that higher levels of the bacterium were more common in people with the problematic APOE4 gene variant, a well-established risk factor for AD. And in human neurons and AD mice models, infection with C. pneumoniae elevated inflammation, increased nerve cell death and in turn contributed to cognitive decline. The infection also boosted the production and accumulation of amyloid-beta plaques.

It is still unclear whether the bacterium plays a direct role in disease progression or is simply more likely to appear as the brain and immune system become compromised with age.

Why this study is important is when it's seen in the context of existing evidence that bacteria and infection may play a role in cognitive decline. Previous studies have shown that the gum-disease bacterium Porphyromonas gingivalis has been detected in AD brains and appears to accelerate the build-up of amyloid-beta plaques in animal models. However, it's important to note that these findings remain debated and do not confirm a source of cognitive decline. Meanwhile. herpes simplex virus type 1 (HSV-1) has also been implicated in doubling the risk of developing AD. These studies, however, are observational and cannot fully rule out other underlying health factors that trigger cognitive breakdown.

Other research has explored whether respiratory pathogens like Chlamydia pneumoniae might reach the brain through nasal or olfactory pathways, but results have been mixed and the mechanisms are still poorly understood.

Nonetheless, the pattern of infection and bacteria and an elevated risk of cognitive decline is understandably something that scientists want to know more about. In particular, many are now studying the broader role of systemic inflammation and the gut–brain axis' role in harming the brain. Differences in gut microbiome makeup have been reported in AD studies, but it's still unclear whether these shifts contribute to disease or reflect other age-related changes in metabolism and immune function.

In this latest retinal study, it's worth noting that the eye may now be a handy focus for monitoring brain-related disease risk, potentially offering a less invasive way to track early changes linked to cognitive decline.

“This discovery raises the possibility of targeting the infection-inflammation axis to treat Alzheimer’s,” said Timothy Crother, PhD, co-corresponding author of the study.

The research was published in the journal Nature Communications.

Source: Cedars Sinai

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