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Additionally, gut dysbiosis might promote alpha-synuclein expression and aggregation in neurons of the enteric plexuses and other intestinal cells [32,33,34,35], may result in increased exposure to various microbial or nonmicrobial xenobiotics with direct or indirect proinflammatory or neurotoxic effects [23,24,36], and may cause nutritional imbalances (e.g., malabsorption, altered production of vitamins by the microbiota) [23,24], all these mechanisms potentially causing neuronal injury or interfering with the neuronal susceptibility to injury and therefore with the onset and progression of PD [37]

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→ Dual-mechanism advantage: GLP-1s slow digestion and increase satiety via gut hormone pathways, while Cagrilintide adds a separate amylin-driven pathway, amplifying the effect