Study shows a subtle shift in gut bugs with Parkinson’s gene mutation

People with Parkinson’s disease who carry mutations in the GBA1 gene tend to have higher levels of inflammation-promoting gut bacteria and fewer protective microbes than patients without the mutation, according to a new study.

While the overall diversity of gut bacteria remained similar between both groups, researchers uncovered key differences in specific bacterial strains that could influence how the disease progresses.

“This study suggests a subtle shift toward a more pro-inflammatory gut microbial profile in [Parkinson’s patients carrying GBA1 mutations], characterized by fewer butyrate-producing and more pro-inflammatory bacteria,” researchers noted.

The study, “Pathogenic GBA1 Variants and their Interaction with the Gut-Microbiota-Brain Axis in Parkinson’s Disease,” was published in Movement Disorders.

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Genetics and the gut microbiome

The causes of Parkinson’s disease are not fully understood, but genetics is thought to play a role in determining disease risk. Mutations in the GBA1 gene are a well-established risk factor for Parkinson’s, and they can also cause a separate disorder called Gaucher disease.

The human digestive tract is home to billions of bacteria and other microscopic organisms, collectively known as the gut microbiome. A growing body of evidence suggests that the gut microbiome is dysregulated in Parkinson’s disease and may play a role in its development. However, much about the microbiome and its role in Parkinson’s remains unclear.

In the study, a team of U.S. scientists sought to determine whether the microbiome is altered in people with Parkinson’s who carry a mutation in the GBA1 gene. To find out, they conducted detailed analyses of stool samples from 36 patients: 16 with a GBA1 mutation and 20 without known Parkinson’s risk mutations.

Analyses showed that the gut microbiome’s overall diversity and community composition were comparable in Parkinson’s patients with or without GBA1 mutations. However, the researchers noted “subtle but potentially biologically relevant … differences.”

Bacterial shifts and gut inflammation

Specifically, patients with GBA1 mutations tended to have lower levels of anti-inflammatory bacteria, particularly those that produce the anti-inflammatory signaling molecule butyrate. At the same time, mutation carriers also had elevated counts of certain types of bacteria with pro-inflammatory effects.

In line with these bacterial shifts, mutation carriers tended to have higher levels of fecal calprotectin, a marker of intestinal inflammation, although this difference between groups did not reach statistical significance.

The researchers noted that this analysis was limited to a small number of patients, and the observed differences might have been influenced by other variables. For instance, the mutation carriers in this study had generally been living with Parkinson’s for longer, and treatment patterns differed between the two groups.

“Despite these limitations, our findings suggest that GBA1 variants have limited effects on overall [microbiome] disruption after [Parkinson’s] onset,” the researchers concluded, noting a need for further studies to validate and expand on the results.