Lack of vitamin B in the gut may lead to Parkinson’s disease

Summary: A new study reveals a link between gut bacteria and Parkinson’s disease (PD). Researchers found a deficiency in the genes responsible for the synthesis of essential B vitamins in PD patients, which may weaken the intestinal barrier and cause inflammation in the brain. This finding suggests that B vitamin supplementation may be a potential therapeutic route for PD.

Important facts:

  • The number of vitamin B-synthesizing bacteria in the gut of PD patients was decreased.
  • A weakened intestinal barrier due to vitamin B deficiency can cause inflammation in the brain.
  • B vitamin supplementation may be a potential treatment for PD.

Source: Nagoya University

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

They also identified a link between a lack of these genes and 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 PD.

Their findings, published in NPJ Parkinson’s Diseasesuggest that treatment with B vitamins to correct these deficiencies could be used to treat PD.

Various physiological processes are significantly influenced by the microorganisms found in the gut, collectively known as the gut microbiota. Credit: Neuroscience News

PD is characterized by a variety of physical symptoms that interfere with daily activities and mobility, such as tremors, slowness of movement, stiffness, and balance problems. While the frequency of PD may vary among different populations, it is estimated to affect approximately 1–2% of individuals aged 55 years or older.

Various physiological processes are greatly influenced by the microorganisms found in the gut, collectively known as the gut microbiota. Under ideal conditions, gut microbiota produce SCFAs and polyamines, which maintain the intestinal barrier that prevents toxins from entering the bloodstream.

Toxins present in the blood can reach the brain, where they cause inflammation and affect neurotransmission processes, which are vital for maintaining mental health.

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

They used shotgun sequencing, a technique that sequences all the genetic material in a sample. This is an invaluable tool because it gives researchers a better understanding of the microbial community and genetic structure of a sample.

They found a decrease in bacterial genes responsible for the synthesis of riboflavin (vitamin B2) and biotin (vitamin B7) in patients with PD. Riboflavin and biotin, derived from both food and gut microbiota, have anti-inflammatory properties, which may counteract the neuroinflammation seen in diseases such as PD.

B vitamins play important roles in 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, preventing toxins from entering the bloodstream. Examination of fecal metabolites revealed decreased levels of both in patients with PD.

The findings indicate a possible explanation for PD progression. “Polyamine and SCFA deficiency may cause the intestinal mucosal layer to thin, leading to increased intestinal permeability, both of which have been observed in PD,” Nishiwaki explained.

“This increased permeability exposes nerves to toxins, leading to abnormal aggregation of alpha-synuclein, activation of immune cells in the brain, and chronic inflammation.”

He added, “Complementary therapy based on riboflavin and biotin is promising as a potential therapeutic route to alleviate PD symptoms and slow disease progression.”

The study results highlight the importance of understanding the complex relationships between gut microbiota, metabolic pathways, and neurodegeneration. In the coming years, therapy could potentially be customized based on each patient’s unique microbiome profile. By altering the levels of bacteria in the microbiome, doctors could potentially delay the onset of symptoms associated with diseases like PD.

“We can perform gut microbiota analysis or stool metabolite analysis on patients,” Nishiwaki said.

“Using these findings, we can identify individuals with specific deficiencies and prescribe oral riboflavin and biotin supplements to those with low levels, potentially leading to effective treatment.”

About this Parkinson’s disease research news

Author: Matthew Cosslett
Source: Nagoya University
contact: Matthew Cosslett – Nagoya University
image: Image credit: Neuroscience News

Original Research: open access.
,Meta-analysis of shotgun sequencing of the gut microbiota in Parkinson’s diseaseBy Hiroshi Nishiwaki et al. NPJ Parkinson’s Disease


abstract

Meta-analysis of shotgun sequencing of the gut microbiota in Parkinson’s disease

We aimed to identify gut microbial characteristics in Parkinson’s disease (PD) in different countries by performing a meta-analysis of our fecal shotgun sequencing dataset of 94 PD patients and 73 controls in Japan, combined with five previously reported datasets from the USA, Germany, China1, China2 and Taiwan. GC-MS and LC-MS/MS assays were established to quantify fecal short-chain fatty acids (SCFAs) and fecal polyamines, respectively. α-diversity was increased in PD in the six datasets.

Taxonomic analysis revealed that the species Akkermansia muciniphila increased in P.D., while the species Roseburia intestinalis And Faecalibacterium prausnitzii PD decreased.

Pathway analysis showed that genes in the biosynthesis of riboflavin and biotin had significantly decreased PD after adjusting for confounding factors. Five of the six categories of carbohydrate-active enzymes (CAZymes) had decreased PD.

Metabolomic analysis of our stool samples showed that SCFA and polyamine contents in feces were significantly decreased in PD. Genes in riboflavin and biotin biosynthesis were positively correlated with fecal concentrations of SCFA and polyamines.

The bacteria responsible for the reduction of riboflavin biosynthesis in Japan, the US and Germany were different from those in China1, China2 and Taiwan. Similarly, different bacteria were responsible for the reduction of biotin biosynthesis in the two country groups.

We believe that the reduction in SCFAs and polyamines leads to the degeneration of the intestinal mucosal layer, which subsequently facilitates the formation of abnormal α-synuclein fibrils in the intestinal nerve plexus in PD, and also causes neuroinflammation in PD.

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