Health & body · 2020
Could gut microbes work differently in Parkinson’s disease?
A study found Parkinson’s-associated differences in the predicted secretion potential of nine microbial , including higher predicted secretion of methionine and cysteinylglycine. These were modelling predictions, not direct measurements of microbial secretion.
Details
Parkinson’s disease is a systemic disease clinically defined by degeneration of dopamine-producing neurons in the brain. Changes in gut microbiome composition have been reported in Parkinson’s disease, but their functional consequences remain unclear. To investigate, researchers analysed stool samples from the Luxembourg Parkinson’s Study: 147 people with typical Parkinson’s disease and 162 controls.
All participants received detailed clinical assessments, including neurological examinations and neuropsychological tests, followed by self-report questionnaires. The researchers first analysed stool samples using 16S rRNA gene sequencing. They then predicted the secretion potential of 129 microbial metabolites using personalised metabolic modelling based on microbiome data and genome-scale metabolic reconstructions of human gut microbes.
The key findings were as follows. The relative abundances of eight genera and seven species differed significantly between people with Parkinson’s disease and healthy controls. Parkinson’s-associated microbial patterns statistically depended on sex, age, BMI and constipation. In particular, the relative abundances of Bilophila and Paraprevotella were significantly associated with Hoehn and Yahr stage after controlling for disease duration.
The personalised metabolic modelling identified Parkinson’s-associated patterns in the predicted secretion potential of nine microbial metabolites, including increased predicted secretion of methionine and cysteinylglycine. Predicted microbial pantothenic acid production potential was linked to the presence of specific non-motor symptoms. The researchers suggest that Parkinson’s-associated gut microbiome changes could translate into substantial functional differences affecting host metabolism and disease phenotype.
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