A study recently published in npj Parkinson’s Disease reveals a link between gut microbiota and Parkinson’s Disease (PD), discovering that a decrease in bacterial genes is related to the synthesis of vitamins B2 and B7. The study also identified a relationship between the 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. The findings suggest that treatment with B vitamins to address these deficiencies could be used to treat PD.
Parkinson’s Disease is characterized by a range of symptoms that hinder daily activities and mobility. The frequency of Parkinson’s Disease varies between different populations, however, it is estimated to affect around 1-2% of people aged 55 years old and older.
A range of physiological processes are influenced by gut microorganisms collectively known as gut microbiota. In ideal conditions, gut microbiota produce SCFAs and polyamines, which help to maintain the intestinal barrier that prevents toxins from entering the bloodstream. Toxins in the blood can be carried to the brain where they cause inflammation and affect processes critical to maintaining mental health.
For this study, shotgun sequencing was used to offer the researchers a better understanding of the microbial community and genetic makeup of the sample. The sequencing revealed a decrease in the bacterial genes responsible for the synthesizing of riboflavin (vitamin B2) and biotin (vitamin B7) in patients diagnosed with Parkinson’s Disease.
Riboflavin and biotin, derived from both food and gut microbiota, have anti-inflammatory properties, which may counteract the neuroinflammation seen in diseases like PD. B vitamins play important roles in the metabolic processes that influence 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. An examination of fecal metabolites revealed decreases of both in patients with Parkinson’s Disease.
“Deficiencies in polyamines and SCFAs could lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in PD,” Hiroshi Nishiwaki explained. “This higher permeability exposes nerves to toxins, contributing to abnormal aggregation of alpha-synuclein, activating the immune cells in the brain, and leading to long-term inflammation.” Adding that “Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression.”
“We could perform gut microbiota analysis on patients or conduct fecal metabolite analysis,” Nishiwaki said. “Using these findings, we could identify individuals with specific deficiencies and administer oral riboflavin and biotin supplements to those with decreased levels, potentially creating an effective treatment.”
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https://www.nagoya-u.ac.jp/researchinfo/result-en/2024/06/20240618-01.html