Gut microbiota in Parkinson’s disease patients: hospital-based study

Abstract

Background Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. There is accumulating evidence that link gut microbiota to symptomatology and pathophysiology of PD. The aim of this study was to describe the pattern of gut microbiota and its association with PD and identify the effect of environmental factors on gut microbiota. This case–control study included 46 patients diagnosed as Parkinson’s disease (PD) and 31 healthy volunteers age and sex matched. Detailed history including age of onset, duration of disease, environmental risk factors, diet data, treatment, Unified Parkinson’s Disease Rating Scale (UPDRS), and gastrointestinal tract (GIT) domain of Non‐Motor Symptoms Scale (NMSS) were assessed. After extraction of bacterial DNA from the fecal samples, bacterial abundance was quantified by qPCR using 16S rRNA group-specific primers. Results Significant high abundance of Clostridium cluster IV, Akkermansia, Bifidobacterium, and lactic acid bacteria were found in the PD group compared with the control group (P < 0.001, 0.04, 0.02 and < 0.001, respectively), while Firmicutes were significantly less abundant in the PD group (P < 0.001) compared with the control group. The naive PD patients had significant abundance of Bifidobacterium, and lactic acid compared with control group. Interestingly, Akkermansia was more abundant in treated than untreated patients. There were significant associations between pesticide exposure and Bifidobacterium (P = 0.002), while no significant correlations between different gut microbiota and demographic, environment data, different rating scores or dominant type of PD. There was a significant negative correlation between the Bifidobacterium with the duration of illness (P = 0.012). Conclusion The present study highlighted a significant connection between PD and levels of certain types of gut microbiota, in support of a possible link between gut microbiota and a neurodegenerative cascade of PD.

Microbiota Dysbiosis in Parkinson Disease—In Search of a Biomarker

“…Additionally, some studies generated contradictory outcomes. Akkermansia was found to be elevated in constipated PD patients in two studies [ 49 , 58 ].…”

“…It has been postulated that PD should be considered a syndrome rather than a homogeneous disease, due to its varied manifestation among PD patients [ 80 ]. Although it is possible that patients with different PD phenotypes share specific microbiome signatures, the results from the studies investigating distinct PD subtype pathogens are incompatible with one another [ 33 , 34 , 37 , 41 , 43 , 58 , 66 ].…”

Probiotic Supplementation in Parkinson’s Disease

“…These variations might contribute to the pathogenesis of PD by decreasing the production of short-chain fatty acids, the metabolism of lipids, immunoregulatory activity, and the permeability of the intestinal tract (Shen et al, 2021). A study conducted at an Egyptian hospital found that the PD group had considerably higher levels of lactic acid bacteria, Clostridium cluster IV, Akkermansia, Bifidobacterium, and a lower level of Firmicutes than the control group (Khedr et al, 2021) A previous meta-analysis found that probiotic intervention significantly improved motor symptoms, constipation, quality of life (QoL), anxiety, and depression parameters in PD patients (Park et al, 2023;Xie et al, 2023). Additionally, probiotic supplements boosted glutathione levels (GSH) in the serum of PD patients and decreased their reliance on laxatives.…”

Gut microbiome dysbiosis across early Parkinson’s disease, REM sleep behavior disorder and their first-degree relatives

“…The enrichment of lactate production pathway is consistent with the increase of lactic acid bacteria (LAB) in PD patients 9 . However, the role of lactate in the pathogenesis of PD remains unclear 49 , as it appears to conflict with the health-promoting effects of LAB. One possibility is that lactate might be further metabolized by other bacteria (e.g., non-butyrate-producing lactate-utilizing bacteria) and finally convert to the products that might be detrimental to gut health (e.g., disrupt gut barrier) 50 .…”