The link between the gut microbiota and Parkinson’s disease points to a possible therapeutic route

A study led by the Nagoya University Graduate School of Medicine in Japan has revealed a link between the gut microbiota and Parkinson’s disease (PD). The researchers found a reduction in intestinal bacteria of genes responsible for the synthesis of the essential B vitamins B2 and B7.

They also identified a link between the lack of these genes and the low levels of agents that help maintain the integrity of the intestinal barrier. This barrier prevents toxins from entering the bloodstream, which causes the inflammation seen in Parkinson’s. Their findings, published in np Parkinson’s diseasesuggest that treatment with B vitamins to address these deficiencies could be used to treat PD.

Parkinson’s is characterized by a variety of physical symptoms that interfere with daily activities and mobility, such as tremors, slow movements, stiffness and balance problems. Although the frequency of Parkinson’s can vary between populations, it is estimated to occur in approximately 1-2% of individuals aged 55 years or older.

Several physiological processes are strongly influenced by the microorganisms in the intestines, which are collectively known as the gut microbiota. Under ideal conditions, the gut microbiota produces SCFAs and polyamines, which maintain the intestinal barrier and prevent toxins from entering the bloodstream. Toxins in the blood can be transported to the brain, where they cause inflammation and affect neurotransmission processes critical to maintaining mental health.

To better understand the relationship between intestinal microbial characteristics in Parkinson’s, Hiroshi Nishiwaki and Jun Ueyama of Nagoya University Graduate School of Medicine conducted a meta-analysis of stool samples from patients with Parkinson’s from Japan, the United States, Germany, China and Taiwan.

They used shotgun sequencing, a technique in which all the genetic material in a sample is sequenced. This is an invaluable tool as it provides researchers with a better understanding of the microbial community and genetic makeup of the sample.

They observed a decrease in the bacterial genes responsible for the synthesis of riboflavin (vitamin B2) and biotin (vitamin B7) in patients diagnosed with Parkinson’s. Riboflavin and biotin, sourced from both food and gut microbiota, have anti-inflammatory properties, which can counteract the neuroinflammation seen in diseases like Parkinson’s disease.

B vitamins play a crucial role in the metabolic processes that affect the production and functions of short-chain fatty acids (SCFAs) and polyamines, two agents that help maintain the integrity of the intestinal barrier and prevent toxins from entering the bloodstream. A study of fecal metabolites revealed a decrease in both in patients with Parkinson’s disease.

The findings indicate a possible explanation for the progression of Parkinson’s. “Deficiencies in polyamines and SCFAs can lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in Parkinson’s disease,” Nishiwaki explains.

“This higher permeability exposes nerves to toxins, contributing to the abnormal aggregation of alpha-synuclein, which activates immune cells in the brain and leads to long-term inflammation.

“Supplementation therapy targeting riboflavin and biotin shows promise as a potential therapeutic avenue for alleviating Parkinson’s symptoms and slowing disease progression.”

The results of the study highlight the importance of understanding the complex relationship between gut microbiota, metabolic pathways and neurodegeneration. In the coming years, therapy may be able to be tailored based on each patient’s unique microbiome profile. By altering bacterial levels in the microbiome, doctors may be able to delay the onset of symptoms associated with diseases such as Parkinson’s disease.

“We could perform gut microbiota analyzes on patients or fecal metabolite analyses,” Nishiwaki said. “Using these findings, we can identify individuals with specific deficiencies and administer oral riboflavin and biotin supplements to those with reduced levels, potentially creating an effective treatment.”