An important discovery that may lead to a potential treatment for Parkinson's disease

A study conducted by Nagoya University School of Medicine in Japan revealed a link between gut microbes and Parkinson's disease.

The researchers found a decrease in gut bacteria in the genes responsible for manufacturing the essential B vitamins B2 and B7.

They also identified a relationship between deficiency of these genes and low levels of factors that help maintain the integrity of the intestinal barrier.

This barrier prevents toxins from entering the bloodstream, causing the inflammation seen in Parkinson's disease.

Their findings, published in the journal npj Parkinson's Disease, suggest that treatment with B vitamins to address these deficiencies could be used to treat Parkinson's disease.

Parkinson's disease is characterized by a variety of physical symptoms that impair daily activities and movement, such as tremors, slow movement, stiffness, and balance problems.

While the frequency of Parkinson's disease may vary between different population groups, it is estimated to affect about 1-2% of individuals aged 55 years or older.

Various physiological processes are strongly influenced by the microorganisms present in the intestine, which are collectively known as the gut microbiota.

Under ideal conditions, the intestinal microorganisms produce short-chain fatty acids (SCFA) and polyamines, which maintain the intestinal barrier that prevents toxins from entering the bloodstream. Toxins in the blood can travel to the brain, where they cause inflammation and affect neurotransmission processes that are essential for maintaining mental health.

To better understand the relationship between gut microbial characteristics in Parkinson's disease, Hiroshi Nishiwaki and Jun Aoyama of Nagoya University Graduate School of Medicine conducted a statistical analysis of stool samples from patients with Parkinson's disease from Japan, the United States, Germany and China.

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

They noticed a decrease in the bacterial genes responsible for manufacturing riboflavin (vitamin B2) and biotin (vitamin B7) in patients diagnosed with Parkinson's disease.

Riboflavin and biotin, derived from microorganisms in food and the intestine, have anti-inflammatory properties, which may counteract the neuroinflammation seen in diseases such as Parkinson's disease.

B vitamins play critical roles in metabolic processes that affect the production and functions of short-chain fatty acids (SCFA) and polyamines, two factors that help maintain the integrity of the intestinal barrier and prevent toxins from entering the bloodstream.

Examination of fecal metabolites revealed a decrease in both in patients with Parkinson's disease.

The results suggest a possible explanation for the development of Parkinson's disease, as Nishiwaki explained: “Deficiency in polyamines and short-chain fatty acids can lead to thinning of the intestinal mucus layer and increased intestinal permeability, both of which are observed in Parkinson's disease. This high permeability exposes the nerves to toxins, which contributes to “Abnormal accumulation of alpha-synuclein, activation of immune cells in the brain, leads to long-term inflammation.”

He continued: "Complementary therapy targeting riboflavin and biotin holds promise as a potential therapeutic method to alleviate the symptoms of Parkinson's disease and slow the progression of the disease."