Study in India links gut bacteria differences to Parkinson’s disease
Pro-inflammatory gut microbes are more abundant in patients
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- Parkinson's disease is linked to significant differences in gut microbiome composition, according to a study in India.
- Patients show elevated levels of pro-inflammatory bacteria, alongside reduced levels of beneficial microbes.
- These findings highlight candidate microbial signatures that may influence Parkinson's severity in specific populations.
People with Parkinson’s disease have different bacteria in their gut, the predicted functions of which differ from those in healthy people, according to a study from southern India that adds further evidence for a possible link between the gut, inflammation, and the disease.
“These findings identify candidate microbial signatures and predicted functional patterns that provide a valuable resource for future investigations,” researchers wrote in “Integrative microbiome and functional profiling decodes pro-inflammatory gut microbiome signatures in South Indian patients with Parkinson’s disease,” which was published in npj Parkinson’s Disease.
Population-specific studies needed
Parkinson’s occurs due to the loss of nerve cells that produce dopamine, a chemical messenger involved in movement. Growing evidence suggests that an unhealthy gut populated by an imbalanced bacterial community may disrupt the normal functioning of the gut-brain axis, a two-way communication pathway between the gut and the brain, contributing to symptoms of Parkinson’s.
To provide a detailed picture of the composition of the gut microbiome — that is, the community of all microbes living in the gut — among patients in the Indian state of Kerala, the researchers compared stool samples from 65 adults with Parkinson’s and 65 healthy adults.
“As gut microbial composition varies geographically, population-specific studies are essential to understand this relationship,” they wrote.
The researchers analyzed genetic material from the stool samples using 16S ribosomal RNA gene sequencing. This technique identifies bacteria by examining a specific part of their genetic material. After removing low-quality and unreliable sequences, they identified 14,929 groups of genetic sequences.
Both the number and types of bacteria differed between patients and healthy adults, who served as controls. Species richness, which refers to the number of different bacterial types present, differed significantly. However, Shannon and Simpson diversities, which consider both the number of types and their relative abundances, were similar.
Several groups of bacteria were more abundant in patients than in controls. These included Akkermansia, Bifidobacterium, Escherichia–Shigella, Collinsella, and bacteria belonging to the Enterobacterales group. Some of these bacteria have been associated with inflammation or changes in the gut’s lining.
Other bacteria were less abundant in patients, including Bacteroides, Prevotella, Lachnospira, Agathobacter, and certain bacteria belonging to the Erysipelotrichaceae family. Some bacteria in these groups can help the gut stay healthy by breaking down food and producing substances that control inflammation.
Greater fragmentation seen among bacteria in patients
Network analysis, which the researchers applied to understand how bacteria interact with one another, showed fewer connections and greater fragmentation among bacteria in patients. On the contrary, healthy control networks showed “a dense, well-balanced topology indicative of complex and stable microbial interactions,” the researchers wrote.
PICRUSt2, a computer-based tool that predicts microbial activities from genetic data, suggested changes in how carbohydrates (sugars) are broken down, how energy is produced, and how proteins and genetic material are processed. Some predicted pathways differed between groups even though their overall functional profiles were somewhat similar.
This study provides one of the most comprehensive characterizations of the gut microbiome in [Parkinson’s] from an underrepresented South Indian population, expanding the geographical diversity of [Parkinson’s] microbiome research and suggesting that population-specific factors may influence disease-associated microbial profiles.
Several predicted pathways related to the production of brain chemicals were also altered. These included pathways associated with dopamine, glutamate, and gamma-aminobutyric acid, which are chemical messengers involved in movement and communication between nerve cells. The researchers also found changes in pathways involving phenylalanine and tyrosine, which the body uses to produce dopamine.
When the researchers compared the relative abundance of bacteria with clinical measures, they found that certain bacterial groups were associated with more severe symptoms or with higher doses of levodopa, a medication that is converted into dopamine in the brain and is commonly used to treat Parkinson’s. However, other bacterial groups showed the opposite pattern.
“Taken together, this study provides one of the most comprehensive characterizations of the gut microbiome in [Parkinson’s] from an underrepresented South Indian population, expanding the geographical diversity of [Parkinson’s] microbiome research and suggesting that population-specific factors may influence disease-associated microbial profiles,” the researchers concluded.
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