Could Parkinson's disease start in the gut? -- ScienceDaily

 Parkinson's disease may start in the gut and spread to the brain via the vagus nerve, according to a study published in the April 26, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. The vagus nerve extends from the brainstem to the abdomen and controls unconscious body processes like heart rate and food digestion.

Here's the paper:

Vagotomy and Parkinson disease

A Swedish register–based matched-cohort study

Parkinson's disease may begin in the gut

New research indicates that Parkinson's disease may begin in the gastrointestinal tract and spread through the vagus nerve to the brain.

We have conducted a registry study of almost 15,000 patients
who have had the vagus nerve in their stomach severed. Between
approximately 1970-1995 this procedure was a very common method of ulcer
treatment. If it really is correct that Parkinson's starts in the gut
and spreads through the vagus nerve, then these vagotomy patients should
naturally be protected against developing Parkinson's disease,"
explains postdoc at Aarhus University Elisabeth Svensson on the
hypothesis behind the study.
"The study shows that patients who have had the the entire vagus
nerve severed were protected against Parkinson's disease. Their risk was
halved after 20 years. However, patients who had only had a small part
of the vagus nerve severed where not protected. This also fits the
hypothesis that the disease process is strongly dependent on a fully or
partially intact vagus nerve to be able to reach and affect the brain,"
she says.
The research project has just been published in the internationally recognised journal Annals of Neurology.

Direct evidence of Parkinson pathology spread from the gastrointestinal tract to the brain in rats -

The cellular hallmarks of Parkinson’s disease (PD) are the loss of
nigral dopaminergic neurons and the formation of α-synuclein-enriched
Lewy bodies and Lewy neurites in the remaining neurons. Based on the
topographic distribution of Lewy bodies established after autopsy of
brains from PD patients, Braak and coworkers hypothesized that Lewy
pathology primes in the enteric nervous system and spreads to the brain,
suggesting an active retrograde transport of α-synuclein (the key
protein component in Lewy bodies), via the vagal nerve. This hypothesis,
however, has not been tested experimentally thus far. Here, we use a
human PD brain lysate containing different forms of α-synuclein
(monomeric, oligomeric and fibrillar), and recombinant α-synuclein in an
in vivo animal model to test this hypothesis. We demonstrate that
α-synuclein present in the human PD brain lysate and distinct
recombinant α-synuclein forms are transported via the vagal nerve and
reach the dorsal motor nucleus of the vagus in the brainstem in a
time-dependent manner after injection into the intestinal wall. Using
live cell imaging in a differentiated neuroblastoma cell line, we
determine that both slow and fast components of axonal transport are
involved in the transport of aggregated α-synuclein. In conclusion, we
here provide the first experimental evidence that different α-synuclein
forms can propagate from the gut to the brain, and that
microtubule-associated transport is involved in the translocation of
aggregated α-synuclein in neurons.