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Recently, two mechanisms involved in the gut-brain axis have attracted increasing attention due to their role in the pathogenesis and progression of PD, namely, disruption of the composition of microorganisms living in the intestine (intestinal microbiome) and dysfunction of enteroendocrine cells, accompanied by impaired signaling through the GLP-1R [60]

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Charts and monitored markers in controlled settings reflect age-associated pathway response variability and duration of combined secretagogue activation