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. 2022 Jan 12;8:9. doi: 10.1038/s41531-021-00263-x

Fig. 6. Schematic representation of pathophysiological intestinal paths in presymptomatic A53T PD mice.

Fig. 6

In the very early stages of PD before CNS pathology, the enteric α-syn accumulation 1 can promote the activation of immune/inflammatory signaling, including canonical caspase-1-dependent inflammasome pathways 2, with consequent massive release of IL-1β 3, which, in turn, impairs IEB 4, through the activation of IL-1 receptors on intestinal epithelial cells. In this setting, bowel inflammation and the impaired IEB can induce changes in SCFA levels 5, characterized by alterations of butyrate levels, that could contribute to IEB impairment 6, and, an increase in LPS concentration, which, translocating into the intestinal mucosa 7 could further contribute to the activation of immune/inflammatory pathways 8, thus generating a vicious circle that might lead to the chronicization of inflammatory processes and contribute both to intestinal symptoms and brain pathology 9.