A study published in Neuropathology and Applied Neurobiology has now found evidence of α-synuclein aggregates — a key pathological hallmark of Parkinson disease (PD) — in the gut and brain in people and animals with inflammatory bowel disease (IBD). The findings lend support to a ‘body-first’ model of PD, in which α-synuclein pathology originates in the periphery and spreads to the brain through the vagus nerve.

The team used a rat model of IBD induced by oral administration of dextran sulfate sodium (DSS) to confirm their findings. Similar to humans with IBD, DSS-treated animals developed α-synuclein pathology in the gut and ventral midbrain, and they also showed degeneration of dopaminergic neurons in the substantia nigra — another important hallmark of PD.