Can your gut bugs show whether you will get Parkinson's?

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International researchers have looked into a genetic variant associated with a heightened risk of developing Parkinson's disease, and found changes to the composition of around a quarter of the gut bugs of people with this variant could indicate that those individuals are more likely to develop the disease. A variant of the GBA1 gene has previously been associated with a risk of Parkinson's, so the researchers looked into the gut bugs present in the poo of 271 people with Parkinson's, which included 43 carriers of the variant that had no clinical symptoms. When compared against the microbiome of 150 people without the disease, the team say they found 176 microbial species that differed between the groups. They say the abundance of the microbial species also changed between the two groups, and in GBA1 variant carriers who did not have any symptoms, their microbiomes looked more like a middle point between the two groups. While the authors note that their study cannot determine whether microbiome changes are predictive of future disease, they wish to perform more studies that can follow people over time to work out whether our gut bugs might be a direct indication of our likelihood of developing Parkinson's disease.

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From: Springer Nature

Gut microbiome changes may show progression towards Parkinson’s disease

Changes in the composition of about a quarter of the gut microbial species in people with a variant of the GBA1 gene — which is associated with an increased risk of Parkinson’s disease — may indicate that those individuals are more likely to develop the disease, according to a study in Nature Medicine. The findings suggest that certain biological changes linked to Parkinson’s disease may be present before the onset of clinical symptoms, and could potentially help identify individuals who are in the early stages of disease development.

Parkinson’s disease is a neurodegenerative condition marked by motor and non-motor symptoms, which often appear only after substantial neuron loss has occurred. Increasing evidence suggests that gut microbiome changes accompany both established Parkinson’s disease and the prodromal phase — the period during which subtle symptoms may precede diagnosis. Understanding these changes may offer new opportunities for early identification of individuals at heightened risk.

Anthony Schapira, Stanislav Dusko Ehrlich, and colleagues analysed clinical and faecal data from participants from the UK and Italy: 271 people with Parkinson’s disease, 43 carriers of the GBA1 variant (a genetic risk factor) with no clinical symptoms, and 150 healthy control participants. They found 176 microbial species that differed between healthy individuals and those with the disease, with over a quarter of the gut microbiome changing abundance between the two groups. Of these species, 142 changed consistently between healthy individuals and those who carry the GBA1 variant but do not have symptoms of Parkinson’s disease. In GBA1 variant carriers without the disease, this component of the microbiome resembled an intermediate pattern between that of healthy groups and that of affected groups, and its extent correlated with early symptoms. The authors observed similar microbial patterns in three external cohorts in the US, Korea, and Turkey, totalling an additional 638 cases of Parkinson’s disease and 319 healthy control participants.

These findings identify a distinct gut bacteria pattern in people who carry a GBA1 genetic variant but do not yet have symptoms, pointing to early biological changes linked to Parkinson’s disease. The authors note, however, that this was a cross-sectional study, and therefore cannot determine whether microbiome changes are predictive of future disease. Longitudinal studies following individuals over time will be necessary to establish whether the microbiome can reliably identify those most likely to develop Parkinson’s disease.

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Nature Medicine
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Organisation/s: UCL Queen Square Institute of Neurology, London, UK
Funder: This research was funded, in part, by Aligning Science Across Parkinson’s (grant ASAP-000420) through the Michael J. Fox Foundation for Parkinson’s Research (A.H.V.S. was funded as lead principal investigator (PI); S.D.E., F.B. and M. Almeida were co-PIs; and J.M. and H.B. were co-investigators) and by the EU Joint Programme-Neurodegenerative Research through MRC grant code MR/T046007/1 (A.H.V.S. was funded as lead PI, with F.B. as co-PI). Additional funding was provided from MetaGenoPolis grant ANR- 11-DPBS-0001 (M. Almeida). For the purpose of open access, the author has applied a CC BY 4.0 public copyright license to all author accepted manuscripts arising from this submission. R.M. and S.Y. are supported by a Royal Free Charity fellowship.
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