The Gut‐Brain Axis in Parkinson disease: Emerging Concepts and Therapeutic Implications DOI Creative Commons
Elisa Menozzi, Anthony H.V. Schapira, Per Borghammer

et al.

Movement Disorders Clinical Practice, Journal Year: 2025, Volume and Issue: unknown

Published: March 13, 2025

Abstract Background The gut‐brain axis, i.e. the bidirectional communication system between gut and brain, has become of central importance in Parkinson disease (PD) research over past 20 years. Aims We aimed to describe milestones axis PD development theories proposing involvement gastrointestinal tract pathogenesis. Methods searched PubMed using terms ‘gut‐brain axis’ AND ‘Parkinson disease’, selected relevant articles provide foundation for reconstructing an historical overview PD. Results Mounting evidence from preclinical, clinical post‐mortem studies suggests that a subgroup patients present with range prodromal symptoms (e.g., autonomic dysfunction, rapid eye movement sleep behaviour disorder) which reflect initial accumulation later spread pathological α‐synuclein rostrally (“body‐first” PD). Through neural connections along may producing clinically manifest disease. Recently, two mechanisms involving have attracted increasing attention their role pathogenesis progression, namely perturbation composition microorganisms living (the microbiome), dysfunction enteroendocrine cells. Conclusion Treatments targeting especially microbiome cells pathway, could potentially slow progression or even prevent onset. Among these, pre/probiotics, faecal microbiota transplantation, glucagon‐like peptide‐1 receptor agonists, entered advanced stages trials humans shown potential symptomatic disease‐modifying effects.

Language: Английский

Lewy body diseases and the gut DOI Creative Commons
Timothy R. Sampson, Malú G. Tansey, Andrew B. West

et al.

Molecular Neurodegeneration, Journal Year: 2025, Volume and Issue: 20(1)

Published: Jan. 30, 2025

Abstract Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson. Recent experimental and human observational studies raise possibility that pathogenic alpha-synuclein (⍺-syn) might develop GI tract subsequently spread to susceptible brain regions. The cellular mechanistic origins ⍺-syn propagation disease are under intense investigation. Experimental LBD models have implicated important contributions from intrinsic gut microbiome, intestinal immune system, environmental toxicants, acting as triggers modifiers pathologies. Here, we review primary clinical observations link dysfunctions LBDs. We first provide an overview anatomy repertoire relevant for disease, with a focus on luminal-sensing cells epithelium including enteroendocrine express make direct contact nerves. describe interactions within resident microbes exogenous how these may directly contribute pathology along related metabolic immunological responses. Finally, critical knowledge gaps field highlighted, focusing pivotal questions remain some 200 years after dysfunction predict better understanding pathophysiologies influence risk progression will accelerate discoveries lead deeper overall potential therapeutic strategies targeting gut-brain axis delay, arrest, or prevent progression.

Language: Английский

Citations

1
The Gut‐Brain Axis in Parkinson disease: Emerging Concepts and Therapeutic Implications DOI Creative Commons
Elisa Menozzi, Anthony H.V. Schapira, Per Borghammer

et al.

Movement Disorders Clinical Practice, Journal Year: 2025, Volume and Issue: unknown

Published: March 13, 2025

Abstract Background The gut‐brain axis, i.e. the bidirectional communication system between gut and brain, has become of central importance in Parkinson disease (PD) research over past 20 years. Aims We aimed to describe milestones axis PD development theories proposing involvement gastrointestinal tract pathogenesis. Methods searched PubMed using terms ‘gut‐brain axis’ AND ‘Parkinson disease’, selected relevant articles provide foundation for reconstructing an historical overview PD. Results Mounting evidence from preclinical, clinical post‐mortem studies suggests that a subgroup patients present with range prodromal symptoms (e.g., autonomic dysfunction, rapid eye movement sleep behaviour disorder) which reflect initial accumulation later spread pathological α‐synuclein rostrally (“body‐first” PD). Through neural connections along may producing clinically manifest disease. Recently, two mechanisms involving have attracted increasing attention their role pathogenesis progression, namely perturbation composition microorganisms living (the microbiome), dysfunction enteroendocrine cells. Conclusion Treatments targeting especially microbiome cells pathway, could potentially slow progression or even prevent onset. Among these, pre/probiotics, faecal microbiota transplantation, glucagon‐like peptide‐1 receptor agonists, entered advanced stages trials humans shown potential symptomatic disease‐modifying effects.

Language: Английский

Citations

0