Research Provides New Evidence that Parkinson's Disease Originates in the Gut

The research of John Hopkins Medicine scientists lends further weight to an already existing theory.
Chris Young

Johns Hopkins Medicine researchers say they are finding mounting evidence to suggest that Parkinson's disease originates in the gut, before traveling up the body's neurons to the brain.

The study, published in Journal Neuron, provides a new and more accurate model for which to test future treatments for Parkinson's disease.


The gut's role in Parkinson's disease

"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," Ted Dawson, M.D., Ph.D., director of the Johns Hopkins Institute for Cell Engineering told Medical Xpress.

Parkinson's disease is caused by an accumulation of a misfolded protein called alpha-synuclein, in brain cells.

The buildup of these proteins causes nerve tissues to be damaged and die off. As the brain cells die, they impair the sufferer's ability to move, think and even feel emotions.

Research Provides New Evidence that Parkinson's Disease Originates in the Gut
Source: Ted Dawson, John Hopkins Medicine

New findings

The latest findings, based on studies in mice, lend even more weight to the already credible theory that misfolded alpha-synuclein may originate in the gut and then spread to the brain via the vagus nerve — a group of fibers that transports brain signals to many of the body's organs, including the gut.

The researchers say that the way the misfolded alpha-synuclein spreads in the brains of the mice greatly rembles the way the disease spreads in human beings.

The Johns Hopkins Medicine team firstly injected the misfolded alpha-synuclein into the gut of healthy mice and tracked the progress of the protein — after several months the protein was found to be in the mice's brains, giving them symptoms resembling Parkinson's disease in humans.

The team then repeated the injection of misfolded alpha-synuclein, but this time in mice with a severed vagus nerve, and another kind of mice that had been genetically engineered to be unable to produce normal alpha-synuclein. Both sets of mice showed no signs of having the misfolded alpha-synuclein in their brains.

Cause for optimism

Dr. Beckie Port, research manager at Parkinson’s UK, told the Guardian that the findings are a great cause for optimism:

“By identifying and halting these changes before they reach the brain, we may be able to prevent the majority of Parkinson’s symptoms ever appearing and improve the lives of people who will be affected.”

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