It is believed that the gut microbiota influences the development of Parkinson’s disease by transporting pathogenic inducers via a neuronal route or blood circulation, but the exact mechanism is not known.
In our opinion, bacteria-produced EVs are a good candidate to provide such a mechanism, since they could cross the gut barrier, enter the bloodstream, travel to distant organs, and cross the blood-brain barrier.
Research into mammalian EVs has advanced rapidly over the past few decades, but the composition of EVs released by gut microbes has remained relatively unexplored, mostly due to the technical problems related to their isolation and characterization.
The most important insight, in my opinion, is the observation that the taxonomic origins of the bacterial EVs in Parkinson’s disease do not match the general composition of the gut microbiota.
This is confirmed by the fact that certain pathway differences were found only within the EVs—and not the gut microbiota—of Parkinson’s disease patients. This means that the brain-affecting bacteria in Parkinson’s disease might be different from the main bacteria found to be altered in the gut.
We indeed observed larger size and quantity of gut EVs in patients with Parkinson’s disease, along with a higher proportion of bacterial proteins, compared to healthy controls.
In general, larger EVs carry a greater diversity of proteins compared to their smaller counterparts. It is tempting to speculate that different EV characteristics could be related to dysbiotic conditions within the guts of patients with Parkinson’s disease.
