According to a series of experiments performed on mice at Johns Hopkins Medicine suggests that the neuro-toxic protein alpha-synuclean (or α-syn), thought to be involved in the development of Parkinson’s disease, originates among cells in the gut and then makes its way to the brain via the vagus nerve.
“These findings provide further proof of the gut’s role in Parkinson’s disease and give us a model to study the disease’s progression from the start,” said leading co-author Ted Dawson from Johns Hopkins University School of Medicine. “This is an exciting discovery for the field and presents a target for early intervention in the disease.”
The study builds on the work conducted in the early 2000s by Heiko Braak of Germany’s Johann Wolfgang Goethe University and Michael J. Fox Foundation for Parkinson’s Research, showing that patients with the disease have an abnormally high concentration of α-syn in their nervous systems.
In line with Braak’s hypothesis, the study conducted on mice by Dawson and colleagues shows that α-syn proteins might, indeed, be reaching the brain through the gut-brain axis, i.e., by hitching a ride up the vagus nerve and into cerebral tissue.
Another piece of the puzzle was highlighted by another senior co-author – Han Seok Ko, also from Johns Hopkins University School of Medicine – namely that the initial appearance of alpha-synuclein proteins in the gut correlates with constipation, which is considered to be among the earliest symptoms of Parkinson’s.
If further studies bear this out, the authors speculate that performing a vagotomy could be a relatively simple and effective means of preventing, or at least reducing, the symptoms which otherwise occur as a result of alpha-synuclean-mediated death of cells in the brain.
Up next for the team will be to identify which specific parts of the vagus nerve can be blamed for acting as a ladder for α-syn to reach the brain, and what are the best ways of halting, or even reversing, this process in humans.