The disease is the fastest growing disorder.
Parkinson’s disease is rapidly becoming one of the most prevalent neurodegenerative disorders globally, according to the World Health Organization, which reported more than 8.5 million people living with the condition in 2019. Since 1990, the global prevalence of Parkinson’s has more than doubled.
The likelihood of developing Parkinson’s increases with age, with men being 50% more susceptible than women. Factors such as genetics, exposure to environmental toxins, and prior traumatic brain injury also play roles in its onset.
Symptoms manifest when nerve cells in the basal ganglia, a brain region controlling movement, degenerate and cease producing dopamine, a neurotransmitter crucial for movement control. This leads to tremors, muscle stiffness, slow movement, impaired balance, emotional changes, and gastrointestinal issues.
Recent studies suggest an association between imbalances in gut microbiota and Parkinson’s disease development.
A new study conducted across five countries examined the microbiota of individuals with and without Parkinson’s and found a significant decrease in bacterial genes responsible for producing riboflavin (vitamin B2) and biotin (vitamin B7) among those with the disease.
Led by scientists at Nagoya University Graduate School of Medicine, Japan, the research, published in npj Parkinson’s Disease, used fecal analysis to analyze gut bacteria genomes from 94 Parkinson’s patients and 73 controls in Japan. Employing shotgun sequencing, which studies all genetic material in a sample, they compared their findings with data from the USA, Germany, China, and Taiwan.
The study revealed variations in gut microbiota composition by country and between Parkinson’s patients and healthy individuals. Notably, regardless of bacterial species, Parkinson’s patients exhibited significantly reduced bacterial genes involved in riboflavin and biotin biosynthesis.
Riboflavin (B2) and biotin (B7) are essential for metabolizing nutrients into energy, supporting immune function, and possessing anti-inflammatory properties. Given that neuroinflammation is a hallmark of Parkinson’s, the researchers hypothesized that deficiencies in these vitamins might exacerbate such inflammation.
However, caution is warranted, as the study did not measure actual riboflavin or biotin levels in stool or circulation but rather predicted their synthesis based on bacterial genes.
The researchers also noted a correlation between reduced B2 and B7 genes and lower levels of short-chain fatty acids and polyamines in fecal samples from Parkinson’s patients. These substances contribute to intestinal mucus production, and their depletion could compromise the gut barrier, potentially allowing toxins to enter the bloodstream and worsen neuroinflammation.
Dr. Tim Sampson from Emory University School of Medicine highlighted the need for further research to clarify whether these microbial changes directly contribute to Parkinson’s symptoms through increased inflammation.
Understanding the intricate relationship between gut microbiota, vitamin production, and Parkinson’s disease could pave the way for novel therapeutic strategies targeting the gut-brain axis to alleviate symptoms and improve patient outcomes.
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