Parkinson’s and the gut microbiota
Early research has suggested that the gut microbiota may play a role in the pathogenesis of Parkinson’s disease. To explore this further, we looked at a publication in the renowned journal PLoS One showing insights into the composition of the microbiota of Parkinson’s patients and their disease progression over a period of 2 years.
Researchers speculate that the gut microbiota might possibly be involved in the pathogenesis of the neurodegenerative disease Parkinson’s. The aggregated protein deposits that accumulate in Parkinson patient’s brains occur primarily in the central nervous system and can also be observed in the enteric nervous system. From there they might migrate to the brain via neuronal pathways. Whether the gut microbiota plays a role in this process is unclear. However, various studies have shown intestinal dysbiosis in Parkinson patients.
To investigate this further, Japanese researchers analysed the microbiota of patients with Parkinson’s disease over a period of 2 years to identify bacteria that might be associated with disease progression. Thirty-six patients were assigned to two groups using a clinical rating scale for Parkinson’s disease (UPDRS*), a stable group with 18 patients and a deteriorated group with 18 patients. Stool samples of both groups were analysed at baseline and after 2 years with the Yakult Intestinal Flora-SCAN test. Total faecal bacterial counts were decreased after 2 years in both the stable and deteriorated groups. The deteriorated group showed reduced numbers of L. gasseri subgroup, whereas the stable group had decreased counts of 7 bacterial groups: including the L. gasseri subgroup but also Bifidobacterium, Clostridium leptum, Bacteroides fragilis, Atopobium, Enterococcus and Lactobacillus reuteri. Using regression analysis, the researchers could predict a correlation of the counts of Bifidobacterium and Atopobium cluster at year 0 and a change of total UPDRS scores after 2 years (r=0.52, p<0.05), with increased hallucinations and delusions (for Bifidobacterium group, r=-0.56, p<0.01) and a worsening of motivation and initiative scores (for B. fragilis group, r=-0.38, p<0.05). Changes of serum Lipopolysaccharide-binding protein, as an indicator for gut barrier permeability, were positively correlated with the counts of L. brevis (r=0.92; p<0.0001) and L. plantarum subgroup (r=0.44; p<0.05) at baseline. Although this study provides some further insights, larger cohort with patients from different places worldwide are required to provide information as to whether changes of the microbial composition in the gut play a role in Parkinson’s disease or not.
* Unified Parkinson's disease rating scale