Figure 1: Underlying mechanisms of microbiota-gut-brain in Parkinson’s disease. Dysbiosis ...

Underlying mechanisms of microbiota-gut-brain in Parkinson’s disease. Dysbiosis of the gut microbiota, characterized by reduced levels of Prevotellaceae and increased abundance of Akkermansia in PD patients, leads to decreased expression of tight junction proteins such as ZO-1 and occludin, thereby impairing intestinal barrier function. Consequently, pro-inflammatory cytokines, including TNF-α and IL-1β, traverse from the gut to the brain via systemic circulation, promoting neuroinflammation and subsequent damage to dopaminergic neurons. Additionally, the gut microbiota regulates the release of metabolites such as SCFAs, bile acids, and amino acids, modulating the communication between the gut and the brain. Dysregulation of pro-inflammatory cytokine release and alterations in metabolite profiles are implicated in the misfolding and aggregation of α-synuclein in the gut, which is then transmitted to the brain via the vagus nerve. IL-1β: Interleukin-1 beta; PD: Parkinson’s disease; SCFA

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