By Nick Lavars
June 21, 2020

As a disease without a cure or means of prevention, there is a lot we don’t know about Parkinson’s and the way it takes hold in the human body. One school of thought is that it actually begins in the gut, and a new study has strengthened these ties by identifying a type of overabundant pathogen in the guts of Parkinson’s disease patients, a novel finding that opens up new lines of enquiry in understanding the root causes of the condition.

The idea that the onset of Parkinson’s disease is related to the gut dates back to the early 2000s, when German scientist Heiko Braak published a string of studies proposing that pathogens in gut make their way to the brain via the nervous system. The theory has since been gathering some steam, particularly of late, with a number of recent studies uncovering some interesting connections between the brains of sufferers and their bacteria in their bellies.

One animal study last year, for example, produced the best evidence to date of this gut-brain connection, demonstrating how misfolded proteins can travel to the brain through the vagus nerve. Another from earlier this year showed how some species of gut bacteria could inhibit the accumulation of these proteins, while another highlighted how altered neurons that regulate the digestive system may play a role in the early stages of Parkinson’s disease.

The latest discovery in this area comes from neurologists at the University of Alabama at Birmingham, who used advanced DNA sequencing and computational tools to re-analyze data from a 2017 study, along with an entirely new independent data set. Together, the research looked at 520 cases of Parkinson’s and more than 300 controls, making up what the authors describe as the largest microbiome-wide association study of the disease to date.

In doing so, the team found three clusters of bacteria in the guts of Parkinson’s patients that present in irregular concentrations. Two of these had been hinted at through previous research, with the new study confirming that a type of microbe that produces short-chain fatty acids was present in lower numbers, while another that metabolizes carbohydrates was present in higher numbers.

The novel finding, however, centers on what are known as opportunistic pathogens. These bacteria take advantage of holes in the body’s defenses, such as a compromised immune system, to drive infections, and the team’s research found an overabundance of these in the guts of Parkinson’s patients. While this presents as another interesting and useful finding in this particular arm of Parkinson’s research, the team cautions it is early days and their exact role in the disease is unknown.

“The exciting question is whether these are Braak’s pathogens capable of triggering PD, or are they irrelevant to PD but able to penetrate the gut and grow, because the gut lining is compromised in PD (Parkinson’s disease),” Payami said. “We emphasize that no claims can be made on function based solely on association. The identity of these microorganisms will enable experimental studies to determine whether and how they play a role in PD.”

The team hopes to learn more by expanding the scope of the research to include larger sample sizes and longer timeframes, enabling analysis of these types of pathogens at various stages of the disease using even more advanced tools.

The research was published in the journal Nature.