April 23, 2026, 10:48 am | Read time: 6 minutes
Typical symptoms of Parkinson’s disease include tremors, slowed movements, and muscle stiffness. However, by the time these symptoms appear, many nerve cells have often already been lost. This is unfavorable for early treatment, which is crucial for slowing the progression of the disease. In search of warning signs before the first symptoms, researchers have now found early indicators of Parkinson’s in the gut. FITBOOK evaluates the study and explains its potential significance.
Study Investigates Early Indicators of Parkinson’s
The goal of a new international study focused on early detection was to identify people through an examination of the gut microbiome who are still healthy but have an increased risk of developing Parkinson’s disease.1 The idea is based on the assumption that certain changes in the gut microbiome can be detected in individuals with an increased risk of Parkinson’s. This may apply to both carriers of a significant risk gene and a portion of the general population.
The researchers explain that variants in the GBA1 gene are considered a particularly important genetic risk factor. The gene encodes an enzyme needed for the “cleaning” and recycling of cell components. Individuals with these variants have up to a 30-fold increased risk of developing Parkinson’s. However, only about 10 percent develop the disease by age 60, and about 19 percent by age 80. Why many carriers remain healthy despite genetic predisposition is still unclear. This is precisely the question the research team pursued.
Details of the Study
The hypothesis centered on the idea that the gut microbiome–the entirety of all bacteria and microorganisms in the gut–might be involved in early disease processes. Previous studies have already shown that the gut flora of Parkinson’s patients differs significantly from that of healthy individuals.2 There is also increasing evidence of the involvement of the so-called microbiota-gut-brain axis, which is the reciprocal communication between the gut, immune system, nervous system, and brain.
The researchers aimed to determine whether symptom-free GBA1 carriers already exhibit Parkinson’s-like changes in the gut microbiome. The study also sought to find out whether these changes are associated with early symptoms and whether similar patterns occur in people without genetic risk. If so, early markers could potentially be derived.
Methods and Study Procedure
For the study, the researchers analyzed clinical data and stool samples from a total of 464 participants from the United Kingdom and Italy. This included 271 Parkinson’s patients, 43 symptom-free carriers of GBA1 variants, and 150 healthy control individuals.
The team then examined the entire genetic material of the gut microorganisms using so-called shotgun metagenomics. This method does not just look for individual bacteria but sequences the entire genome of all microorganisms. This allows for a particularly detailed capture of the microbiome’s composition. A total of 627 microbial species units (MSP) were analyzed.
Additionally, the researchers assessed bacterial metabolic functions, or potential biological activities of the microorganisms. The statistical approach was also new: In addition to classic frequency comparisons, they examined whether changes between the groups were coherent, meaning they moved in the same direction. They used Cliff’s Delta as a measure of the direction and strength of the differences.
Additional Health Data Collected
Extensive clinical parameters were also recorded, including mobility, constipation, autonomic complaints (such as bladder or circulatory problems), depressive symptoms, sense of smell, cognitive performance, dietary habits, and disease duration.
Results
The analysis showed significant differences in the gut microbiome between Parkinson’s patients and healthy control individuals. Overall, the researchers identified 176 microbial species that differed significantly between the two groups.
In Parkinson’s patients, certain bacteria were more prevalent, including some species of streptococci and bifidobacteria. At the same time, other bacteria were significantly reduced, particularly members of the Lachnospiraceae and Ruminococcaceae families. These are considered important producers of butyrate, a short-chain fatty acid with anti-inflammatory effects and significance for the gut barrier.
Intermediate Profile in Symptom-Free Carriers of GBA1 Variants
Notably, symptom-free carriers of GBA1 variants showed an intermediate microbiome profile. This means that their composition was between that of healthy control individuals and Parkinson’s patients. Even here, weak but recognizable changes typical of Parkinson’s were found.
The more pronounced these microbiome changes were, the more frequently early symptoms occurred, which are considered prodromal symptoms. These included, in particular, autonomic disorders such as digestive or circulatory problems, as well as initial motor abnormalities, depressive symptoms, and cognitive impairments.
Similar patterns were also observed in a portion of the healthy control individuals without known genetic predisposition. This suggests that individuals with increased risk could potentially be identified in the general population through the gut microbiome.
Heterogeneous Picture of the Disease
The results also showed a large individual variability. The microbiome followed more of a continuum than a clear separation: Some individuals showed only minor changes, while others had significant deviations. These differences were related to disease duration and medication dosage and suggest that the microbiome continues to change over the course of the disease.
Functionally, a clear pattern also emerged: In Parkinson’s patients, metabolic pathways associated with protein breakdown and potentially pro-inflammatory processes were more active. At the same time, functions involved in carbohydrate utilization and the formation of protective metabolic products were reduced. This overall indicates altered metabolic activity of the gut microbiome.
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Possible Significance of the Results
The data support the assumption that Parkinson’s does not originate solely in the brain, but that the gut and peripheral nervous system may also be involved early in the disease process. It is particularly relevant that microbiome changes occur not only in those affected but also in genetically predisposed individuals and a portion of healthy people.
In combination with early non-motor symptoms, the gut microbiome could potentially serve as part of a risk stratification in the future. Especially in conjunction with genetic and clinical data, this offers a possible approach for earlier identification of at-risk individuals.
Limitations
The study is cross-sectional (a snapshot) and therefore does not allow for conclusions about cause and effect. It remains unclear whether the observed microbiome changes contribute to the development of the disease or are merely a side effect. Additionally, individual subgroups–particularly the GBA1 carriers–were relatively small, which limits the significance. Long-term data are still completely lacking, so it is not clear which of the identified individuals will actually develop Parkinson’s later.