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Emerging research highlights the connection between the gut and Parkinson’s disease (PD), shedding light on how imbalances in the microbiome may influence this debilitating condition. This post discusses how changes in gut bacteria might contribute to PD progression and what these findings mean.

Parkinson’s disease, historically seen as a brain disorder, may begin in the gut long before motor symptoms appear. Constipation, one of the earliest and most prevalent non-motor symptoms of PD, can precede diagnosis by decades. In a recent large-scale study by Wallen and colleagues at the University of Alabama at Birmingham, researchers investigated stool samples from 490 individuals with PD and 234 neurologically healthy controls using metagenomics, a high-resolution method to analyze genetic material expressed by gut microbes. The findings revealed widespread dysbiosis, with over 30% of the bacterial species identified in PD patients showing significant differences from those observed in healthy controls.

Specifically, the study found that bacteria Bifidobacterium dentium and Streptococcus mutans, were significantly more abundant in individuals with PD. For instance, Bifidobacterium dentium showed a sevenfold increase compared to healthy controls, while Streptococcus mutans was elevated sixfold. In contrast, bacterial species with anti-inflammatory and neuroprotective properties, such as Roseburia intestinalis and Faecalibacterium prausnitzii, were depleted in PD. This imbalance in microbial populations may reflect alterations in gut brain interactions..

The study also highlighted the role of the gut in PD pathology through its connection to alpha-synuclein, a protein linked to neurodegeneration. Alpha-synuclein aggregates, a hallmark of PD in the nervous system, were often found in the gut during the early stages of the disease. This supports the hypothesis that PD may originate in the gut, with pathological proteins spreading to the brain via the sensory branches of the vagus nerve. Experimental evidence in mice has shown that alpha-synuclein fibrils injected into the gut can induce similar pathology in the brain, a process that can be arrested by vagotomy (cutting of the vagus nerve). Similarly, in a previous study, patients who had undergone a complete vagotomy were found to have a lower likelihood to be diagnosed with PD than those without such a surgery.

Another important finding was the dysregulation of metabolic pathways within the gut microbiome of PD patients. The altered microbial composition was associated with an increased production of neurotoxic compounds and a reduction in short-chain fatty acids which play a key role in preventing or reducing inflammation and maintaining gut health.

While the study by Wallen and coworkers provides valuable insights, it does have limitations. The cross-sectional design means that causality between the gut microbiome and a diagnosis of PD cannot be established. Additionally, the study population was geographically restricted to the southern United States, limiting the generalizability of the findings to other regions or ethnic groups. Nevertheless, these findings support the growing understanding of the role of altered communication between the gut, its microbes and the brain in PD and point towards novel microbiome-targeted therapies for this brain disorder.

While the science is still evolving, there are practical steps that individuals can take to support the diversity and richness of their gut microbiome. A diet rich in fiber from a variety of fruits, vegetables, and whole grains can nourish beneficial bacteria. Incorporating a variety of fermented foods such as fermented dairy products and kimchi introduces probiotics that help maintain a diverse microbiome.

Together with evidence from a growing number of preclinical and clinical studies the study by Wallen and coworkers supports the evolving paradigm shift in understanding Parkinson’s disease—not just as a brain disorder, but as a condition with potential origins in the gut.