The nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behavior disorderOriginal paper
What was studied?
This study asked whether gut and nasal microbes differ in Parkinson's disease and in its prodrome, idiopathic REM sleep behavior disorder. Researchers compared the two body sites against healthy controls. They profiled flash-frozen stool and nasal wash samples using 16S and 18S ribosomal RNA amplicon sequencing. Metagenomic shotgun sequencing was used on selected samples. Seventy demographic, clinical, and processing variables were analyzed to control for confounders before differential abundance testing.
Who was studied?
The cohort included 76 Parkinson's disease patients, 21 people with idiopathic REM sleep behavior disorder, and 78 healthy controls from the German DeNoPa cohort. Groups were similar in age. Parkinson's patients averaged 68.0 years and 66 percent were male. Controls averaged 68.4 years. The REM sleep group averaged 66.1 years. Samples were collected at a single study center between 2012 and 2015 with deep clinical phenotyping of each participant.
What were the most important findings?
The gut microbiome differed by disease group, while the nasal microbiome showed no strong Parkinson's signature. Around 48 gut bacterial groups were differentially abundant in patients versus controls. Akkermansia was enriched in Parkinson's, alongside its parent Verrucomicrobia taxa. Constipation was more common in patients (62 percent) than controls (24 percent). About 80 percent of differential gut microbes in Parkinson's, including several Bacteroidetes, trended similarly in the prodromal REM sleep group, and some correlated with depression.
What are the greatest implications of this study?
The findings suggest gut microbial changes may appear before motor Parkinson's, since the prodromal REM sleep group shared many of the same shifts. This points to the gut as an early window on disease. The overlapping signatures raise the possibility of tracking microbial changes across disease progression. They do not prove the microbes cause Parkinson's. The authors stress that standardized sampling, metagenomics, and direct metabolite measurement in larger cohorts are needed to confirm any microbial role.