We have all become very interested in how gut bacteria relates to our health. I am particularly interested in how gut bacteria relates to Parkinson’s disease – which is the topic of my PhD. While it may initially seem farfetched that bacteria in our gut can affect physiological processes occurring within the brain in Parkinson’s, there is a very real bidirectional communication network between our gut and brain.
What we know about our gut bacteria and Parkinson’s disease so far
Through conducting a systematic review, we collated information from thirteen published studies about the abundance of gut bacteria in individuals with and without Parkinson’s. Most of the research (9/13 of the included studies) showed that bacteria capable of producing a particular short chain fatty acid, butyrate, were less abundant in the Parkinson’s groups compared to the groups without Parkinson’s. This difference in butyrate producing bacteria is relevant as butyrate has important health promoting functions, which include maintaining the health of our intestinal walls and also providing anti-inflammatory actions within the immune system. But how does this relate to Parkinson’s?
While the exact brain chemistry of Parkinson’s disease is unknown, it is thought to involve a build-up of abnormal proteins called alpha-synuclein. One hypothesis for how this protein initially misfolds, and becomes abnormal, is that a pathogen crosses the intestinal wall and causes the alpha-synuclein proteins found in the gut’s nervous system to misfold. The misfolded alpha-synuclein proteins are then thought to travel up the vagus nerve (a major sensory nerve connecting the gut and brain) where they spread to parts of the brain that are typically affected in Parkinson’s.
A reduction in butyrate and a compromised intestinal wall as a result, might mean it is easier for such a pathogen to cross the intestinal wall and cause the initial protein misfolding. In addition, inflammation around the body and brain have been implicated in progression of the disease, and a lack of anti-inflammatory compounds like butyrate, might further perpetuate this pathological process.
Where to from here?
It is great to have synthesised what the research shows so far, but there are of course important questions still to consider. For example, most of the studies did not measure lifestyle factors despite both diet and exercise being important for our gut bacteria. Knowing how gut bacteria is influenced by lifestyle factors, and what implications this has for Parkinson’s disease is crucial to further understand the role of our gut and its bacteria in this condition. Ultimately, there is the potential for earlier diagnoses and additional therapeutic treatment options.
Take part in research!
I am conducting a study looking to answer these very questions. Until September 2020, we are recruiting healthy younger and older adults, and people with a diagnosis of Parkinson’s disease in Melbourne and Geelong.
We’d love to hear from you: gutstudy@deakin.edu.au.
Read our systematic review article here.
This post is by Mr Nathan Nuzum, a PhD candidate in the School of Exercise and Nutrition Sciences at Deakin University. As part of his PhD Nathan is investigating the role of gut bacteria in Parkinson's disease, and how lifestyle factors like diet and exercise may affect gut bacteria in this population. To connect with Nathan, follow him on Twitter @nathnuz
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