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. 2021 Nov 26;72(1):73–89. doi: 10.1136/gutjnl-2021-326023

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© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Schematic diagram of ‘Gut-first’ PD. Environmental microbial toxins lead to the erosion of segmented filamentous bacteria (SFB, green) in the ileum, which potentiates a Th17 proinflammatory response and the loss of intestinal barrier integrity. These events in the gut allow the progression of the disease into the brain either through the blood or the vagus nerve. Microbial toxins target mesencephalic mitochondria and activate neuronal innate immunity followed by aSyn expression, microglial activation and ultimately PD. aSyn, alpha-synuclein; BMAA, β-N-methylamino-L-alanine; IL, interleukin; PD, Parkinson’s disease; Th17, T helper 17. (This image was created at BioRender.com).