summary: New research uncovers a link between gut bacteria and Parkinson’s disease (PD). Researchers found that genes responsible for the synthesis of essential B vitamins are reduced in PD patients. This reduction may weaken the intestinal barrier and lead to brain inflammation. This finding suggests that B vitamin supplementation may be a potential treatment for PD.
Key Facts:
- The bacteria that synthesizes vitamin B in the intestines of Parkinson’s disease patients is reduced.
- A weakened intestinal barrier caused by vitamin B deficiency can lead to brain inflammation.
- Vitamin B supplementation may be a potential treatment for PD.
sauce: Nagoya University
A study led by the Nagoya University Graduate School of Medicine has uncovered a link between the gut microbiome and Parkinson’s disease (PD). Researchers found that genes responsible for the synthesis of the essential B vitamins B2 and B7 were reduced in gut bacteria.
The researchers also found a link between defects in these genes and lower levels of substances that help maintain the integrity of the intestinal barrier. This barrier prevents toxins that cause the inflammation seen in PD from entering the bloodstream.
The results of their research are npj Parkinson’s diseasesuggests that treatment with B vitamins that address these deficiencies could be used to treat PD.
PD is characterized by a variety of physical symptoms that interfere with daily activities and mobility, including tremors, slowness of movement, stiffness, balance problems, etc. The frequency of PD varies across populations, but it is estimated to affect approximately 1-2% of people aged 55 years or older.
Many physiological processes are heavily influenced by the microbes that live in the gut (collectively known as the gut microbiota), which, under ideal circumstances, produce short-chain fatty acids and polyamines and maintain the intestinal barrier that prevents toxins from entering the bloodstream.
Toxins in the blood are carried to the brain, where they can cause inflammation and affect neurotransmitter processes that are important for maintaining mental health.
To gain a deeper understanding of the relationship of gut microbial characteristics in Parkinson’s disease, Professors Hiroshi Nishiwaki and Jun Kamiyama of the Nagoya University Graduate School of Medicine conducted a meta-analysis of stool samples from Parkinson’s disease patients from Japan, the United States, Germany, China, and Taiwan.
They used shotgun sequencing, a technique that sequences all of the genetic material in a sample, an invaluable tool because it allows for a deeper understanding of the sample’s microbial community and genetic makeup.
The researchers found that bacterial genes responsible for the synthesis of riboflavin (vitamin B2) and biotin (vitamin B7) were reduced in patients diagnosed with PD. Riboflavin and biotin, available from both food and the gut microbiota, have anti-inflammatory properties and may reduce the neuroinflammation seen in diseases like PD.
B vitamins play a key role in metabolic processes that affect the production and function of short-chain fatty acids (SCFAs) and polyamines, two substances that maintain the integrity of the intestinal barrier and prevent toxins from entering the bloodstream. Examination of fecal metabolites has revealed a decrease in both in PD patients.
The findings suggest a potential explanation for the progression of Parkinson’s disease: “Deficiencies in polyamines and short-chain fatty acids may lead to a thinning of the intestinal mucus layer and increased intestinal permeability, both of which have been observed in Parkinson’s disease,” Nishiwaki explained.
“This increased permeability exposes neurons to toxins, contributing to the abnormal aggregation of alpha-synuclein and activating immune cells in the brain, leading to long-term inflammation.”
“Supplementation targeting riboflavin and biotin holds promise as a potential therapeutic avenue to alleviate Parkinson’s disease symptoms and slow disease progression,” he added.
The findings highlight the importance of understanding the complex relationship between gut microbiota, metabolic pathways, and neurodegeneration. In the coming years, it may be possible to customize treatments based on each patient’s unique microbiome profile. By modifying the levels of bacteria in the microbiome, doctors may be able to delay the onset of symptoms associated with diseases such as Parkinson’s.
“We can conduct analyses of the patient’s intestinal microbiota and fecal metabolites,” Nishiwaki said.
“These findings could be used to identify individuals with specific deficiencies and potentially develop effective treatments by administering oral riboflavin and biotin supplements to those with reduced levels.”
About this Parkinson’s research news
author: Matthew Coslett
sauce: Nagoya University
contact: Matthew Coslett – Nagoya University
image: Image courtesy of Neuroscience News
Original Research: Open access.
Hiroshi Nishiwaki et al. “Meta-analysis of shotgun sequencing of gut microbiota in Parkinson’s disease” npj Parkinson’s disease
Abstract
A meta-analysis of shotgun sequencing of gut microbiota in Parkinson’s disease
We aimed to identify gut microbial signatures in Parkinson’s disease (PD) in each country by meta-analyzing a fecal shotgun sequencing dataset of 94 Parkinson’s disease patients and 73 controls in Japan with five previously reported datasets from the United States, Germany, China1, China2, and Taiwan. We established GC-MS and LC-MS/MS assays to quantify fecal short-chain fatty acids (SCFAs) and fecal polyamines, respectively. Alpha diversity was increased in PD across the six datasets.
Taxonomic analysis revealed that the species Akkermansia muciniphila It increased in PD, but Roseburia intestinalis and Faecalibacterium prausnitzii It decreased in PD.
Pathway analysis showed that riboflavin and biotin biosynthetic genes were significantly decreased in PD after adjusting for confounding factors.Five out of six categories of carbohydrate-active enzymes (CAZymes) were decreased in PD.
Metabolomic analysis of fecal samples revealed that fecal SCFAs and polyamines were significantly decreased in PD, and riboflavin and biotin biosynthetic genes were positively correlated with fecal SCFA and polyamine concentrations.
The bacteria responsible for the decline in riboflavin biosynthesis in Japan, the United States, and Germany were different from those in China 1, China 2, and Taiwan. Similarly, the bacteria responsible for the decline in biotin biosynthesis in the two country groups were also different.
We hypothesize that decreased SCFAs and polyamines reduce the intestinal mucus layer, thereby promoting the formation of abnormal α-synuclein fibrils in the enteric plexus in PD, which also leads to neuroinflammation in PD.
