Really nice work showing similarities between the gut microbiome of patients with PD and idiopathic REM sleep behaviour disorder (RBD). This adds to the wealth of data that suggests significant overlap between these conditions... we know that 30-50% of patients with PD have confirmed RBD. We also know that PD is a common outcome in patients with iRBD (along with dementia with Lewy bodies and other synucleinopathies). However, the role of an altered gut microbiome is yet to be clarified... does it contribute to the development of these two related conditions (PD and RBD) or is it consequence of these conditions (reverse causality)?? It is clear that much more work needs to be done in this field, but the link between PD and the gut continues to strengthen...
Mov Disord. 2017 Aug 26. doi: 10.1002/mds.27105. [Epub ahead of print]
Heintz-Buschart A, Pandey U, Wicke T, Sixel-Döring F, Janzen A, Sittig-Wiegand E, Trenkwalder C, Oertel WH, Mollenhauer B, Wilmes P.
http://onlinelibrary.wiley.com/doi/10.1002/mds.27105/abstract;jsessionid=1F71A24EFF3A356871C32DAE7194B99C.f02t01
BACKGROUND:
Increasing evidence connects the gut microbiota and the onset and/or phenotype of Parkinson's disease (PD). Differences in the abundances of specific bacterial taxa have been reported in PD patients. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with idiopathic rapid eye movement sleep behavior disorder, a prodromal condition of α-synuclein aggregation disorders including PD.
OBJECTIVES:
To compare microbiota in carefully preserved nasal wash and stool samples of subjects with idiopathic rapid eye movement sleep behavior disorder, manifest PD, and healthy individuals.
METHODS:
Microbiota of flash-frozen stool and nasal wash samples from 76 PD patients, 21 idiopathic rapid eye movement sleep behavior disorder patients, and 78 healthy controls were assessed by 16S and 18S ribosomal RNA amplicon sequencing. Seventy variables, related to demographics, clinical parameters including nonmotor symptoms, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed.
RESULTS:
Differentially abundant gut microbes, such as Akkermansia, were observed in PD, but no strong differences in nasal microbiota. Eighty percent of the differential gut microbes in PD versus healthy controls showed similar trends in idiopathic rapid eye movement sleep behavior disorder, for example, Anaerotruncus and several Bacteroides spp., and correlated with nonmotor symptoms. Metagenomic sequencing of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms.
CONCLUSION:
Our study reveals differential abundances of gut microbial taxa in PD and its prodrome idiopathic rapid eye movement sleep behavior disorder in comparison to the healthy controls, and highlights the potential of metagenomics to identify and characterize microbial taxa, which are enriched or depleted in PD and/or idiopathic rapid eye movement sleep behavior disorder.
In view of the increasing evidence of gut microbiome involvement in PD is it feasible that it could be transferred from person to person in the presence of a 'suitable' genetic susceptibility? The immensely long incubation period of maybe 8 - 10 years might make a study of familial carers for PD patients worthy of consideration over an equally long term.
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