Fig. 1.

Diagrammed representation of the gut-brain axis hypothesis for the development and progression of PD. An infection or exposure of the gut to toxins can cause preliminary intestinal inflammation and dysbiosis of the gut microbiome. As a result, there is an upregulation of α-synuclein expression and transport through the vagus nerve and into the brain. Increased permeability of the blood–brain barrier (BBB) facilitates the accumulation of α-synuclein within various brain regions, including the dorsal motor nucleus of the vagus nerve (DMV), leading to pro-inflammatory glial responses and the pathogenesis of neuroinflammation during PD