The study was published online December 1 in the journal Cell.
In the first of the experiments, the mice were divided into three groups: two with complete microbiomes of intestinal bacteria, mimicking the complexity in humans, and a third group that was bred to be germ-free.
In several tasks designed to measure motor skills that become dysfunctional in Parkinson's disease, including running on treadmills, descending from a pole, and crossing a beam, the mice who were germ-free performed substantially better than those with a complex microbiome and those with gut microbiota showed greater motor deficits.
The researchers further sought to determine whether imbalances in short-chain fatty acids (SCFAs), which can be related to intestinal bacteria, would be associated with activated immune responses in the brain, as has been suggested in previous research.
They found that germ-free mice who were treated with microbially produced SCFAs did show activation of microglia, indicating neuroinflammation that is linked to the malfunction of neurons.
"Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms," the authors said.
In a third experiment, the mice were transplanted with fecal samples from human patients with and without Parkinson's disease.
The germ-free mice who received transplants with the human gut microbiota from patients with Parkinson's disease remarkably displayed a significant worsening of the hallmarks of Parkinson's disease, whereas those receiving fecal transplants from healthy human donors did not show the symptoms.