Differences in the Composition of Gut Microbiota between Patients with Parkinson’s Disease and Healthy Controls: A Cohort Study

Abstract

Gut microbiome and colonic inflammation can be associated with the predisposition and progression of Parkinson’s disease (PD). The presented study aimed to compare gastrointestinal microbiota composition between patients diagnosed with PD and treated only with Levodopa to healthy controls. In this prospective study, patients were recruited in 1 academic hospital from July 2019 to July 2020. The detailed demographic data and medical history were collected using a set of questionnaires. Fecal samples were obtained from all participants. Next-Generation Sequencing was used to assess the microbiota composition. The endpoint was the difference in composition of the gut microbiota. In this study, we enrolled 27 hospitalized PD patients with well-controlled symptoms. The control group included 44 healthy subjects matched for age. Among PD patients, our results presented a higher abundance of Bacteroides phylum, class Corynebacteria among phylum Actinobacteria, class Deltaproteobacteria among phylum Proteobacteria, and genera such as Butyricimonas, Robinsoniella, and Flavonifractor. The species Akkermansia muciniphila, Eubacterium biforme, and Parabacteroides merdae were identified as more common in the gut microbiota of PD patients. In conclusion, the patients diagnosed with PD have significantly different gut microbiota profiles in comparison with healthy controls.

Oral ingestion of the environmental toxicant trichloroethylene in rats induces alterations in the gut microbiome: relevance to idiopathic Parkinson’s disease

“…In line with the many other published studies investigating gut microbiome and PD related neurodegeneration, the data collected from TCE treated rats partially conflicted with human PD microbiome and other animal model studies (Keshavarzian et al ., 2020). One of the major differences observed was the decrease in Akkermansia and Lactobacillus genera from TCE treated rats, compared to the relatively common increase found in human PD studies (Hill-Burns et al ., 2017b; Romano et al ., 2021; Wallen et al ., 2020; Zapała et al ., 2021), though at least one or more studies report decreases in either genus (Li et al ., 2019; Qian et al ., 2018). While the most obvious source of variation is likely rodent to human translation, MRL +/+ mice exposed to TCE in drinking water displayed a significant elevation in Akkermansia within the gut microbiome compared to control (Wang et al ., 2021b).…”

Microbiota: Not Just a Gut Feeling

“…For example, patients with PD have a higher abundance of the genera Butyricimonas , Robinsoniella , and Flavonifractor , compared with control subjects. The species Akkermansia muciniphila ( A. muciniphila ), Eubacterium biforme , and Parabacteroides merdae ( P. merdae ) are particularly abundant in patients with PD, whereas Faecalibacterium prausnitzii , Ruminococcus albus , and Blautia faecis are most abundant in healthy control subjects [ 3 ]. A. muciniphila and P. merdae are associated with the degradation of the mucus layer and intestinal mucins, the inflammation of the colon (found in over 80% of patients with PD), increased intestinal permeability, and the development of leaky gut.…”

“…A. muciniphila and P. merdae are associated with the degradation of the mucus layer and intestinal mucins, the inflammation of the colon (found in over 80% of patients with PD), increased intestinal permeability, and the development of leaky gut. These alterations lead to an increase in endotoxinemia and oxidative stress, which in turn result in an increase in the misfolding of alpha-synuclein (α-syn) in the brain of PD patients [ 3 ]. Another mechanism for intestinal mucosal damage is related to the decreased number of species producing the short-chain fatty acid (SCFA) butyrate, which is essential for intestinal mucosal integrity [ 1 , 2 , 3 ].…”

“…These alterations lead to an increase in endotoxinemia and oxidative stress, which in turn result in an increase in the misfolding of alpha-synuclein (α-syn) in the brain of PD patients [ 3 ]. Another mechanism for intestinal mucosal damage is related to the decreased number of species producing the short-chain fatty acid (SCFA) butyrate, which is essential for intestinal mucosal integrity [ 1 , 2 , 3 ]. The breakdown of mucins leads to increased water reabsorption, the production of dehydrated stool, and constipation.…”

“…The breakdown of mucins leads to increased water reabsorption, the production of dehydrated stool, and constipation. The latter typical symptom of PD could, therefore, be due not only to the motor changes typical of the disease, but also to intestinal dysbiosis [ 3 ]. There is also increasing evidence that PD may have an intestinal origin, and that α-Syn can travel from the ganglia of the enteric nervous system to the brain via the vagus nerve.…”