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In this work, we studied whether inflammatory bowel diseases (IBDs) in humans can progress with the emergence of pathogenic \u03b1\u2010synuclein (\u03b1\u2010syn) in the gastrointestinal tract and midbrain dopaminergic neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We have analysed the gut and the ventral midbrain from subjects previously diagnosed with IBD and form a DSS\u2010based rat model of gut inflammation in terms of \u03b1\u2010syn pathology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Our data support the existence of pathogenic \u03b1\u2010syn in both the gut and the brain, thus reinforcing the potential role of the ENS as a contributing factor in PD aetiology. Additionally, we have analysed the effect of a DSS\u2010based rat model of gut inflammation to demonstrate (i) the appearance of P\u2010\u03b1\u2010syn inclusions in both Auerbach's and Meissner's plexuses (gut), (ii) an increase in \u03b1\u2010syn expression in the ventral mesencephalon (brain) and (iii) the degeneration of nigral dopaminergic neurons, which all are considered classical hallmarks in PD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results strongly support the plausibility of Braak's hypothesis and emphasise the significance of peripheral inflammation and the gut\u2010brain axis in initiating \u03b1\u2010syn aggregation and transport to the substantia nigra, resulting in neurodegeneration.<\/jats:p>\n                  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