Parkinson’s disease may have originated in intestine cells according to a new study conducted by a group of researchers at the Johns Hopkins University medical school in the United States.
According to the researchers, the disease could then spread from the intestine to the brain.
The study, published in Neuron, provides “further evidence of the role of the intestine in Parkinson’s disease,” according to Ted Dawson, professor of neurology and one of the authors of the study.
To date, we know that Parkinson’s disease is caused by the accumulation of a particular protein, called alpha-synuclein, which occurs in brain cells. This accumulation causes the death of nerve tissues and this, in turn, causes the accumulation of dead brain matter, a matter called the “Lewy body.”
This new study is based on a discovery already made in 2003 when a German neuroanatomist realized that the accumulations of the alpha-synuclein protein occur in the parts of the central nervous system that are responsible for the intestine. Among other things, this would be consistent, according to the researchers, with the fact that one of the first symptoms of Parkinson’s disease is constipation. Already this anatomist, Heiko Braak, hypothesized that the disease could advance through the nerves from the intestine to the brain as if it were climbing up a ladder.
The researchers behind the study published in Neuron therefore wanted to understand how this spread could occur from the intestine to the brain and tried to understand if this protein responsible for accumulation traveled along the vagus nerve, a bundle of nerves that goes right from the stomach to the brain base. They therefore performed experiments on mice by injecting 25 µg of malformed synthetic alpha-synuclein into their bodies. The experiment, which lasted 10 months, actually showed that the alpha-synuclein began to accumulate precisely where the conjunction between the vagus nerve and the intestine is present and that it continued to spread reaching the brain.
The researchers then performed a second experiment on mice, similar to the first, but this time they cut the vagus nerve. After seven months, the researchers discovered that mice with vagus cut nerves did not show signs of cell death typical of Parkinson’s disease. The study therefore shows that blocking the transmission path via the vagus nerve could prove to be the key to at least prevent the signs of Parkinson’s disease, “an exciting discovery for the field,” says Dawson.
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