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P329 Faecal mycobiome disparities of individuals afflicted with parkinson’s diseases versus control
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  1. Luke Flain,
  2. Chris Probert,
  3. Alessandra Frau,
  4. Lauren Lett,
  5. Rachael Hough,
  6. Gerum Gebeyehu
  1. University Of Liverpool, Liverpool, UK

Abstract

Introduction Parkinson’s disease (PD) a complex neurodegenerative disorder mainly affecting the dopaminergic neurones of the substantia nigra. Numerous studies have examined the role of α-synuclein within PD pathogenesis, although as yet a causal factor has not been established.

The hibernating spore hypothesis was a theory originally delineated in 2002. It hypothesised the ability of an infectious agent, possibly fungal in origin to act as the casual factor in PD development .1 Recent literature has described varying levels of bacterial dysbiosis between individuals afflicted by PD, thus paving the way for research into the role of the mycobiome in PD pathogenesis.2

Methods Stool samples were obtained from 35 PD patients and 20 healthy controls. The samples were aliquoted and underwent DNA extraction utilising PSP and Qiagen kit protocols. Qubit analysis was performed with samples being diluted to 10 ng/µl to then undergo 18srRNA gene quantification for the PCR process. Once appropriate reagents had been added the PCR tube the constituents were entered into a Roche thermo-cycler 480 to undergo DNA replication. The amplified samples were then seeded at 5µl into a 1.6% agarose gel to undergo electrophoresis.

The trialled samples were refined to a total of 24 that proceeded to be inputted into the University of Liverpool CGR for sequencing. Generated data was analysed using MicrobiomeAnalyst. The data set was refined using a prevalence of 10% and variance filters employing inter-quartile ranges to remove fungal organisms with very low prevalence and reduce the number of sequencing errors. Data was then normalised using total sum scaling.

Results Comparison of the mycobiome of individuals with PD relative to healthy controls have presented an altered fungal composition of the gastro-intestinal tract. 8 OTU-level and 3 order-level specific fungal species have been identified to be differentially abundant by varying statistical tests (figure 1, depicts the relative species abundance change of fungal organisms between PD VS healthy controls)

Conclusion Overall this study provides evidence of alteration to the mycobiome of patients afflicted with PD relative to that of healthy controls. It reinforces data previously presented by the hibernating spore hypothesis on how a fungal organism may be involved in PD pathogenesis, and now paves the way for future studies examining specific fungal species and their possible pathological interaction with both the gastrointestinal system and the CNS.

References

  1. Broxmeyer L. ( 2002) Parkinson’s: another look. Medical Hypotheses. 59, 373–377

  2. Scheperjans F, Aho V, Pereira PAB, Koskinen K, Paulin L, Pekkonen E, Haapaniemi E, Kaakkola S, Eerola-Rautio J, Pohja M, Kinnunen E, Murros K and Auvinen P. Gut microbiota are related to Parkinson’s disease and clinical phenotype. Movement Disorders 2015;30:350–358.

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