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. 2020 Aug 25;11:849. doi: 10.3389/fneur.2020.00849

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Copyright © 2020 Chao, Gulam, Chia, Feng, Rotzschke and Tan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Bi-directional interaction between gastrointestinal (GI) tract and central nervous system (CNS). Schematic representation summarizes Braak's model of Parkinson's disease (PD) progression initiated from the GI tract. Changes in GI mucosal immunity, environmental toxins, infection, sleep quality, diet, and genetics modify the gut microflora and induce inflammation, mitochondrial dysfunction, and abnormal protein accumulation. Accumulation of α-syn in the GI tract spread via the vagus nerve to the CNS and leads to dopaminergic neuron degeneration.