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Affecting approximately 145,000 people in the UK, Parkinson’s disease is one of the leading neurodegenerative conditions and is mainly characterised by tremors and stiffness of hands, arms, and legs, as well as slowness of movement [1]. The cause of these symptoms are depleted dopamine levels in the brain, although the main neuropathological hallmark is a build-up of alpha-synuclein (α-synuclein) [1] [2]. α-synuclein is a protein that exists in part as a monomer, but also as a folded tetramer [2]. Disruption in the balance of the monomer and tetramer causes amassing of pro-aggregating forms, such as Lewy bodies [2]. These aggregate forms are abundant in the brain and spinal cord of Parkinson’s disease patients and disrupt dopaminergic transmission [2].
Previous research has highlighted a link between the composition of the gut microbiota and Parkinson’s disease, so much so, that over recent years, more scientists are studying this topic area [3]. A recent paper has investigated the effects of gut microbes sampled from Parkinson’s disease patients on the accumulation of α-synuclein in Caenorhabditis elegans nematodes [4]. The α-synuclein in these worm models were tagged with yellow fluorescence protein to aid analysis [4]. The microbe isolated and processed for the study was Desulfovibrio spp., and using PCR, identification was achieved to a species level [4]. D. desulfuricans, D. fairfieldensis and D. piger were the chosen species isolated from faecal samples of Parkinson’s disease patients, which were processed in a Whitley Anaerobic Workstation and then fed to the worm models [4]. Using confocal microscopy, images of the heads of the worms were observed for aggregation of α-synuclein and it was found that the worms fed the Desulfovibrio diet had significantly more α-synuclein aggregates than the controls [3].
Desulfovibrio bacteria are an ideal microorganism to use in these studies as they are abundant in the human gut and colonise the colon [3]. Molecular research has shown that this bacterium influences α-synuclein, by producing hydrogen sulfide, which interferes with neuronal signalling [3]. More specifically, they can release cytochrome c into the cytosol and form α-synuclein radicals, which in turn causes α-synuclein aggregate formation [3]. It can therefore be concluded that there is a strong correlation between Desulfovibrio bacteria and Parkinson’s disease [3]. Knowledge of factors that exacerbate the disease are key to the development of treatment and care, as well as identifying those most at risk to give as earlier a diagnosis as possible [3].
Written by DWS Microbiologist, Kirsty McTear
References
- UK P. What is Parkinson’s? [Internet]. [cited 2023 Aug 09]. Available from: https://www.parkinsons.org.uk/information-and-support/what-parkinsons
- Calabresi P, Mechelli A, Natale G, Volpicelli-Daley L, Di Lazzaro G, Ghiglieri V. Alpha-synuclein in parkinson’s disease and other synucleinopathies: From overt neurodegeneration back to early synaptic dysfunction. Cell Death & Disease. 2023;14(3). doi:10.1038/s41419-023-05672-9
- Murros KE, Huynh VA, Takala TM, Saris PE. Desulfovibrio bacteria are associated with parkinson’s disease. Frontiers in Cellular and Infection Microbiology. 2021;11. doi:10.3389/fcimb.2021.652617
- Huynh VA, Takala TM, Murros KE, Diwedi B, Saris PE. Desulfovibrio bacteria enhance alpha-synuclein aggregation in a Caenorhabditis elegans model of parkinson’s disease. Frontiers in Cellular and Infection Microbiology. 2023;13. doi:10.3389/fcimb.2023.1181315
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