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RESEARCH PAPER ANALYSIS

Mechanisms of Exercise-Mediated Regulation of the Gut-Brain Axis in Parkinson's Disease.

AI interpretation is pending for this paper.

PMID42197098
JournalNutrients
Publication Date2026-05-21
Ingested2026-05-27 06:55 AM
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ABSTRACT

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Parkinson's disease (PD) is a progressive neurodegenerative disorder that is closely associated with dysfunction of the gut-brain axis. Exercise and diet exert neuroprotective effects on PD by regulating the gut-brain axis, yet the overall mechanisms underlying this regulation remain to be systematically elucidated. This article reviews the characteristic changes in gut microbiota during the progression of PD and the pathological mechanisms involving gut-brain axis dysfunction. It systematically outlines the intrinsic mechanisms by which gut microbiota modulate the onset and development of PD from the perspectives of metabolism, immunity and inflammation, neuroendocrinology, and the temporal and causal relationships between gut microbiota and PD. On this basis, the discussion focuses on the regulation of the gut-brain axis through exercise to improve PD, with emphasis on remodelling the composition and diversity of gut microbiota, enhancing gut barrier and blood-brain barrier (BBB) functions, regulating immune and inflammatory homeostasis, upregulating the expression of neurotrophic factors and promoting neuroplasticity, as well as the synergistic effects of exercise and diet. In parallel, the independent and synergistic effects of dietary interventions (e.g., high-fibre and Mediterranean diets) are discussed. In addition, the effects of different types of exercise on alleviating PD by regulating gut-brain axis are analysed. This review aims to provide new insights and a scientific basis for the prevention and intervention of PD.

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Central nervous system agents in medicinal chemistry 64.0 30 Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder. Signal transduction and targeted therapy 84.0 31 HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches. Inflammopharmacology 78.0 32 Beyond acid-base dyshomeostasis: Dynamic instability of neuronal lysosomal pH as a pathogenic mechanism and therapeutic target in neurological diseases. Biochemical pharmacology 88.0
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