Gut Dysbiosis

Role of gut microbiota in regulating gastrointestinal dysfunction and motor symptoms in a mouse model of Parkinson’s disease

Gut Dysbiosis, Gut Microbiota, Parkinson's Disease /

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized primarily by motor and non-motor gastrointestinal (GI) deficits. GI symptoms’ including compromised intestinal barrier function often accompanies altered gut microbiota composition and motor deficits in PD. Therefore, in this study, we set to investigate the role of gut microbiota and epithelial barrier dysfunction on motor symptom […]

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Impact of Contaminants on Microbiota: Linking the Gut–Brain
Axis with Neurotoxicity

Autonmic nervous system, Gut Dysbiosis, Gut Microbiota, Gut-Brain axis, Parkinson's Disease /

: Over the last years, research has focused on microbiota to establish a missing link betweenneuronal health and intestine imbalance. Many studies have considered microbiota as criticalregulators of the gut–brain axis. The crosstalk between microbiota and the central nervous system ismainly explained through three different pathways: the neural, endocrine, and immune pathways,intricately interconnected with each

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Axis with Neurotoxicity Read More »

Gut–Brain Axis: Role of Gut Microbiota in Neurodegenerative Disease

Gut Dysbiosis, Gut Microbiota, Gut-Brain axis, Parkinson's Disease /

The role of gut bacteria in neurodegenerative disease has long been speculated; however, the extent of influence and the exact composition of microflora that mechanistically alter outcomes are less understood. While aging was thought to be a major contributor to neurodegenerative disease, the role of the immune system started to become more appreciated bringing the

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Gastrointestinal Dysfunction in Parkinson’s Disease

Gut Dysbiosis, Vagal Nerve /

There has been exponential growth in the awareness and understanding of gastrointestinal (GI) dysfunction in Parkinson’s disease (PD) over the past 3 decades. The clinical features of GI dysfunction in PD have been clearly identified and innovative research has demonstrated the presence of pathology within the enteric nervous system (ENS) in individuals with PD, leading

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Are We What We Eat? Impact of Diet on the Gut–Brain Axis in Parkinson’s Disease

Butyrate, Diet and Exercise, Gut Dysbiosis, Gut Microbiota, Gut Permeability / Leaky Gut, Gut-Brain axis, Parkinson's Disease, Pre-PD, Probiotics, Prebiotics and Symbiotics /

Parkinson’s disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the development or exacerbation of this disorder. Dysbiosis of gut microbiota could have a crucial

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A Comprehensive Review on the Role of the Gut Microbiome in Human Neurological Disorders

Gut Dysbiosis, Gut Microbiota, Gut Permeability / Leaky Gut, Gut-Brain axis, Parkinson's Disease /

The human body is full of an extensive number of commensal microbes, consisting of bacteria, viruses, and fungi, collectively termed the human microbiome. The initial acquisition of microbiota occurs from both the external and maternal environments, and the vast majority of them colonize the gastrointestinal tract (GIT). These microbial communities play a central role in

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Clinical and imaging evidence of brain-first and body-first Parkinson’s disease

A-Synuclein, Autonmic nervous system, Constipation, ENS, Gut Dysbiosis, iRBD, Non-Motor Symptoms, Orthostatic Hypotension, Parkinson's Disease, Pre-PD /

Braak’s hypothesis has been extremely influential over the last two decades. However, neuropathological and clinical evidence suggest that the model does not conform to all patients with Parkinson’s disease (PD). To resolve this controversy, a new model was recently proposed; in brain-first PD, the initial α-synuclein pathology arise inside the central nervous system, likely rostral to

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Serum short-chain fatty acids and its correlation with motor and non-motor symptoms in Parkinson’s disease patients

Autonmic nervous system, Biomarkers, Butyrate, Gut Dysbiosis, Gut Permeability / Leaky Gut, Parkinson's Disease, Short Chain Fatty Acids /

Serum SCFAs are altered in PD patients, and the decrease of serum propionic acid level is correlated with motor symptoms, cognitive ability and non-depressed state. Thus, the gut microbial-derived SCFAs potentially affect Parkinson’s symptoms through the blood circulation. Propionic acid supplementation might ameliorate motor and non-motor symptoms of PD patients, although clinical trials are needed

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Parkinson’s Disease and the Metal–Microbiome–Gut–Brain Axis: A Systems Toxicology Approach

Detox, Gut Dysbiosis, Gut Microbiota, Gut-Brain axis, Parkinson's Disease, Pre-PD /

Parkinson’s Disease (PD) is a neurodegenerative disease, leading to motor and nonmotor complications. Autonomic alterations, including gastrointestinal symptoms, precede motordefects and act as early warning signs. Chronic exposure to dietary, environmental heavy metalsimpacts the gastrointestinal system and host-associated microbiome, eventually affecting the centralnervous system. The correlation between dysbiosis and PD suggests a functional and bidirectionalcommunication

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Porphyromonas gingivalis indirectly elicits intestinal inflammation by altering the gut microbiota and disrupting epithelial barrier function through IL9-producing CD4+ T cells

Gut Dysbiosis, Gut Microbiota, Oral Microbiome /

Background Recent epidemiological studies have shown that inflammatory bowel disease is associated with periodontal disease. The oral-gut microbiota axis is a potential mechanism intersecting the two diseases. Porphyromonas gingivalis is currently considered a keystone oral pathogen involved in periodontal disease pathogenesis and disease progression. Recent studies have shown that oral ingestion of P. gingivalis leads to intestinal inflammation. However,

Porphyromonas gingivalis indirectly elicits intestinal inflammation by altering the gut microbiota and disrupting epithelial barrier function through IL9-producing CD4+ T cells Read More »