Changes in gut, mouth bacteria tied to Parkinson’s cognitive decline
Researchers: Guts of patients with dementia enriched with mouth bacteria
Changes in the bacterial communities in the gut and mouth are associated with cognitive impairment in people with Parkinson’s disease, a study suggests.
Some oral bacteria and related virulence factors, such as molecules that help bacteria colonize the body — many of which can trigger a potent inflammatory response — were significantly enriched in the guts of Parkinson’s patients with cognitive impairment.
“Our findings suggest that promoting a healthy microbiome through consistent oral care, a balanced diet, and potentially targeted probiotic interventions could support improved disease management in Parkinson’s,” Saeed Shoaie, PhD, the study’s lead at King’s College London in the U.K., said in a university news story. The study, “Microbiome signatures of virulence in the oral-gut-brain axis influence Parkinson’s disease and cognitive decline pathophysiology,” was published in Gut Microbes.
People with Parkinson’s can have a range of nonmotor symptoms, including gastrointestinal problems such as constipation or nausea, in the years before motor symptoms appear. Changes in the gut may play a role in Parkinson’s development via the communication system between the gut and the brain, called the gut-brain axis.
While the oral health of Parkinson’s patients also impacts the course of their disease, the contribution of mouth bacteria has been largely overlooked. In fact, Porphyromonas gingivalis, a well-studied oral bacterium, has been found in the brain of people with Alzheimer’s disease, and active gum disease, or periodontitis, has been reported to impact cognitive abilities.
“The human gut and oral bacterial communities are increasingly linked to neurodegenerative diseases,” Shoaie said. “Disruptions in the gut-brain axis could trigger inflammation and immune responses that contribute to neuronal damage.”
Gut, oral microbiome effect on cognition
The researchers examined gut and mouth bacteria collected from the stool and saliva samples of Parkinson’s patients with mild cognitive decline and dementia to explore the role of gut and oral microbiomes on cognitive impairment. A group of healthy people served as controls.
Parkinson’s patients with dementia had significantly less gut microbiome diversity than those with mild cognitive impairment. There was also a decrease in microbial diversity and the metagenomic species richness, or the total number of different species within a microbial community, in the oral microbiome of those with dementia.
In a species analysis, there was a limited number of overlapping bacterial species across all three groups, meaning many species were uniquely enriched or depleted in patients with mild cognitive impairment or dementia. This suggests “these microbial changes are likely associated with [cognitive impairment],” the researchers wrote.
In a predictive assessment, the changes in microbial species were sensitive enough to differentiate between Parkinson’s patients with varying clinical features, and adding data like age and sex significantly improved the predictions.
“We don’t yet know if the bacteria are causing the cognitive decline or if changes in the body due to Parkinson’s allow these bacteria to grow,” said Frederick Clasen, PhD, the study’s first author and research associate at King’s College London. “But our findings suggest they may play an active role in worsening symptoms.”
When oral bacteria move to the gut
Researchers then investigated so-called oral-gut translocation, wherein oral bacteria move into the gut, where they don’t usually live. Data showed the guts of patients with dementia were significantly enriched with mouth bacteria. Moreover, those with cognitive impairment or dementia had significantly higher levels of oral-specific virulence factors in the gut, that is, molecules that help the bacterium colonize the body.
The identified virulence factors had various functions, including stress, immune modulation, adherence, biofilm formation, invasion, and metabolism. Some are important for bacteria to infect cells that line the blood vessels in the brain. At the same time, several other factors related to immune modulation were involved in producing LPS, a molecule on bacterial surfaces that triggers inflammation.
“These toxins could be used as biological markers to identify patients at higher risk of dementia in Parkinson’s,” Clasen said. “In the future, they might also be targets for new treatments that protect the brain by changing the gut environment.”
Researchers also saw a drop in several types of bacteria in the mouth of patients with dementia or cognitive impairment compared with healthy people, which could suggest a loss of healthy bacterial balance, making it easier for harmful bacteria to take over.
“Our study provides compelling evidence that the interplay between oral and gut microbiomes significantly influences [Parkinson’s] and [cognitive impairment],” the researcher wrote. “The translocation of oral microbial species to the gut, along with their associated [virulence factors], highlights new avenues for understanding disease mechanisms and developing potential biomarkers and therapeutic avenues.”
Shoaie said the “emerging evidence underscores the potential importance of maintaining oral and gut health in mitigating or slowing neurodegenerative processes. As people with Parkinson’s become increasingly reliant on carers, routine practices such as oral hygiene and nutritional intake may be neglected.”
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