Literature Review

Common gut bacteria linked to Parkinson’s disease


 

FROM FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY

A common gut bacteria may play a role in the development of Parkinson’s disease (PD) by causing aggregation of the alpha-synuclein protein, a key feature in the pathology of PD, a small study suggests.

Environmental factors as well as genetics are also suspected to play a role in PD etiology, although the exact cause remains unknown.

“Our findings indicate that specific strains of Desulfovibrio bacteria are likely to cause Parkinson’s disease,” study investigator Per Erik Saris, PhD, from the University of Helsinki, Finland, says in a news release.

The study was published online in Frontiers in Cellular and Infection Microbiology.

Screen and treat?

It builds on earlier work by the researchers that showed that Desulfovibrio bacteria were more prevalent and more abundant in quantity in patients with PD, especially patients with more severe disease, than in healthy individuals.

Desulfovibrio is a genus of gram-negative bacteria commonly found in aquatic environments in which levels of organic material are elevated, as well as in waterlogged soils.

In their latest study, Dr. Saris and colleagues looked for Desulfovibrio species in fecal samples from 10 patients with PD and their healthy spouses. Isolated Desulfovibrio strains were fed to a strain of Caenorhabditis elegans roundworms that expressed human alpha-syn fused with yellow fluorescent protein.

They found that worms fed Desulfovibrio bacteria from patients with PD harbored significantly more (P < .001) and larger alpha-syn aggregates (P < .001) than worms fed Desulfovibrio bacteria from healthy individuals or worms fed Escherichia coli strains.

In addition, worms fed Desulfovibrio strains from patients with PD died in significantly higher quantities than worms fed E. coli bacteria (P < .01).

Desulfovibrio strains isolated from patients with PD and strains isolated from healthy individuals appear to have different traits. Comparative genomics studies are needed to identify genetic differences and pathogenic genes from Desulfovibrio strains from patients with PD, the researchers note.

“Taking into account that aggregation of alpha-syn is a hallmark of PD, the ability of Desulfovibrio bacteria to induce alpha-syn aggregation in large numbers and sizes, as demonstrated in the present study, provides further evidence for the pathogenic role of Desulfovibrio bacteria in PD, as previously suggested,” they add.

The findings highlight the potential for screening and targeted removal of harmful Desulfovibrio bacteria, Dr. Saris suggests in the news release.

No clinical implications

In a comment, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, cautioned that “this research is in a very early stage, uses a nonvertebrate animal model, and the number of participants is small.

“Understanding the role of the gut microbiome in influencing PD is in its infancy. These are important steps to determining what – if any – link may be between gut bacteria and PD,” Dr. Beck said.

“Right now, there are no implications for the screening/treatment of carriers,” Dr. Beck said.

“It seems that a lot of people, whether with PD or not, harbor Desulfovibrio bacteria in their gut. More research is needed to understand what is different between the Desulfovibrio bacteria of people with PD vs. those who do not have PD,” Dr. Beck added.

The study was supported by the Magnus Ehrnrooth Foundation and the Jane and Aatos Erkko Foundation. Dr. Saris and Dr. Beck have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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