Minireview on the Relations between Gut Microflora and Parkinson’s Disease: Further Biochemical (Oxidative Stress), Inflammatory, and Neurological Particularities

Abstract

The aetiology of Parkinson’s disease (PD) is a highly debated topic. Despite the progressive increase in the number of patients diagnosed with PD over the last couple of decades, the causes remain largely unknown. This report is aimed at highlighting the main features of the microbial communities which have been termed “the second brain” that may be a major participant in the etiopathophysiology of PD. It is possible that dysbiosis could be caused by an overactivity of proinflammatory cytokines which act on the gastrointestinal tract as well as infections. The majority of patients who are diagnosed with PD display gastrointestinal symptoms as one of the earliest features. In addition, an unbalanced cycle of oxidative stress caused by dysbacteriosis may have the effect of gradually promoting PD’s specific phenotype. Thus, it seems that bacteria possess the ability to manipulate the brain by initiating specific responses, defining their capability to configure the human body, with oxidative stress playing a pivotal role in preventing infections but also in activating related signalling pathways.

Protein Deimination Signatures in Plasma and Plasma-EVs and Protein Deimination in the Brain Vasculature in a Rat Model of Pre-Motor Parkinson’s Disease

“…Deimination has previously been associated with bacterial immune evasion [71], as well as with bacterial membrane vesicle release and antibiotic resistance, highlighting roles for PAD-mediated mechanisms in host-pathogen interactions [6]. This may be of some interest as the brain-gut axis relationship between the gut microflora and PD has been a topic of investigation due to gastrointestinal symptoms being one of the earliest features of PD [72]. Roles for the gut microbiota in neuroinflammation has also been hypothesised and assessed for other neurodegenerative diseases, including AD and amyotrophic lateral sclerosis (ALS) [73].…”

Minireview Exploring the Biological Cycle of Vitamin B3 and Its Influence on Oxidative Stress: Further Molecular and Clinical Aspects

“…Alongside GPR41 and GPR43, HCA 2 mediates microbe-derived metabolites [ 20 , 21 , 22 , 23 ] in starvation. The receptor also regulates neuroimmune mediators of the gut–brain axis (GBA) via GPR109A [ 24 ] in neonates and adults that suffer from neurodevelopmental disorders [ 25 , 26 ].…”

“…Considering the myriad functions fulfilled by the gut microflora [ 131 ] and the close link between the brain [ 25 , 132 ] and digestive tract [ 33 , 133 ], there have been relatively few reports aiming to demonstrate how OS gradually induces dysbiosis. This section focuses on the studies and hypotheseses that clearly demonstrate how OS disrupts host eubiosis [ 134 ].…”

Mini-Review on the Possible Interconnections between the Gut-Brain Axis and the Infertility-Related Neuropsychiatric Comorbidities

“…A reduction in the host’s innate eubiosis triggers a pro-inflammatory cascade [ 62 ]. If this state is prolonged it may lead to gastrointestinal disorders [ 63 , 64 ], as well as neurodegenerative [ 65 ] or neuropsychiatric disorders [ 66 ].…”