Parkinson’s disease (PD) is a progressive neurodegenerative condition that results in the loss of brain cells responsible for secreting the neurotransmitter dopamine. Dopamine’s role in motor control is a key contributor to the characteristic symptoms of Parkinson’s, including tremors, reduced mobility and muscle stiffness.
Diagnosis is often centred around the loss of motor control, however, several studies have investigated the observed effects on the gut microbiome. This is due to the non-motor symptoms caused by PD expressed in the gastrointestinal tract such as inflammation and constipation, which have often been found to precede those symptoms affecting motor abilities. A meta-analysis recently carried out by researchers at the Quadram Institute with support from the Biotechnology and Biological Sciences Research Council (BBSRC) set out to establish a consensus on the effects of Parkinson’s on the gut microbiome.
The research involved analysing 1200 samples from 10 different studies involving both Parkinson’s patients and control groups. The key findings of the paper published in npj Parkinson’s Disease concluded a significant difference between the gut microbiome of PD patients and controls, with patients having an increased microbiome diversity but the lowered presence of the dominant bacterial species found in healthy human microbiota.
Why is this important? The many bacteria dwelling symbiotically within our gut play a large role in maintaining our homeostasis by synthesising important molecules such as enzymes, amino acids, and short-chain fatty acids, which our cells use to strengthen and maintain the intestinal lining. As a result, any significant alterations to an individual’s gut microbiome may lead to poor gut health as seen in patients with PD.
The Quadram researchers explore this through addressing a depletion of butyrate-producing bacteria in PD patients. Butyrate is a multifunctional short-chain fatty acid with anti-inflammatory properties and is used by epithelial cells in the gut as an energy source and reinforcer. The reduced levels of butyrate found in PD patients across the studies were found to correlate with increased gut permeability and inflammation, and pro-inflammatory proteins in the colon, suggesting systemic inflammation that could potentially activate neurons and drive the progression of disease.
The paper also goes on to highlight the similar correlation found in persons with inflammatory bowel disease such as Crohn’s disease or ulcerative colitis, who are at an increased risk (28% and 30% respectively) of developing Parkinson’s, further supporting their observations.
Despite the large variability between the studies, differences between gut microbiomes of PD patients and controls were consistent, and provide further evidence of an existing link with intestinal inflammation. Hence, future applications of this research could include using the gut microbiome as a therapeutic target in Parkinson’s treatment as well as a diagnostic tool in detecting the onset of disease.