The human gut microbiome dysbiosis plays an important role in the pathogenesis of Parkinson's disease (PD). The bidirectional relationship between the enteric nervous system (ENS) and central nervous system (CNS) under the mediation of the gut-brain axis control the gastrointestinal functioning. This review article discusses key mechanisms by which modifications in the composition and function of the gut microbiota (GM) influence PD progression and motor control loss. Increased intestinal permeability, chronic inflammation, oxidative stress, α-synuclein aggregation, and neurotransmitter imbalances are some key factors that govern gastrointestinal pathology and PD progression. The bacterial taxa of the gut associated with PD development are discussed with emphasis on the enteric nervous system (ENS), as well as the impact of gut bacteria on dopamine production and levodopa metabolism. The pathophysiology and course of the disease are associated with several inflammatory markers, including TNF-α, IL-1β, and IL-6. Emerging therapeutic strategies targeting the gut microbiome include probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT). The article explored how dietary changes may affect the gut microbiota (GM) and the ways that can affect Parkinson's disease (PD), with a focus on nutrition-based, Mediterranean, and ketogenic diets. This comprehensive review synthesizes current evidence on the role of the gut microbiome in PD pathogenesis and explores its potential as a therapeutic target. Understanding these complex interactions may assist in the development of novel diagnostic tools and treatment options for this neurodegenerative disorder.
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http://dx.doi.org/10.3389/fnut.2024.1496616 | DOI Listing |
Acad Radiol
December 2024
Mallinckrodt Institute of Radiology, Washington University in Saint Louis, St. Louis, MO (A.N.). Electronic address:
IUBMB Life
January 2025
Cheerland Watson Precision Medicine Ltd, Shenzhen, China.
Parkinson's disease (PD), characterized by progressive degeneration of dopaminergic neurons in substantia nigra, has no disease-modifying therapy. Mesenchymal stem cell (MSC) therapy has shown great promise as a disease-modifying solution for PD. Induced pluripotent stem cell-derived MSC (iMSC) not only has stronger neural repair function, but also helps solve the problem of MSC heterogeneity.
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January 2025
Department of Biomedical Engineering, Meybod University, Meybod, Iran.
Purpose: A debilitating and poorly understood symptom of Parkinson's disease (PD) is freezing of gait (FoG), which increases the risk of falling. Clinical evaluations of FoG, relying on patients' subjective reports and manual examinations by specialists, are unreliable, and most detection methods are influenced by subject-specific factors.
Method: To address this, we developed a novel algorithm for detecting FoG events based on movement signals.
Brain Behav
January 2025
Department of Neurology, Sichuan Taikang Hospital, Chengdu, Sichuan, China.
Background: Previous studies have confirmed the significant role of cathepsins in the development of neurodegenerative diseases. We aimed to determine whether genetically predicted 10 cathepsins may have a causal effect on Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS).
Methods: We conducted a two-sample bidirectional Mendelian randomization (MR) study using publicly available data from genome-wide association study (GWAS) to assess the causal associations between 10 cathepsins and three neurodegenerative diseases, including AD, PD, and ALS.
J Neurol Sci
December 2024
James J. and Joan A. Gardner Family Center for Parkinson's disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH, USA.
Introduction: Daytime sleepiness, reported in about 50 % of patients with Parkinson's disease (PD), is associated with high morbidity, poor quality of life and increased risk for accidents. While an association between dysautonomia and daytime sleepiness in early, de-novo PD has been reported, our understanding of the role of medications, cognitive status and co-morbidites on this relationship is inadequate.
Methods: Data were analyzed from the prospective Cincinnati Cohort Biomarkers Program.
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