Wednesday , September 28 2022

The origin of Parkinson's disease may be in the gut



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The new study is based on the observations of the German neuroiatherapist Heiko Braac, who showed that people with Parkinson's disease also had accumulations of folded alpha-synuclein protein in the central nervous system parts that control the intestines.

John Hopkins' medical researchers have found evidence that Parkinson's disease originates from the gut cells and travels through the neurons in the body to the brain. iStock

John Hopkins' medical researchers have found evidence that Parkinson's disease originates from the gut cells and travels through the neurons in the body to the brain.

The mice study published in Neuron magazine offers a new and more accurate model for testing treatments that can prevent or stop the progression of Parkinson's disease.

"These findings provide further evidence of the role of the intestine in Parkinson's disease and provide us with a model to investigate the development of the disease from the very beginning," said Dr. Ted Dawson, director of the Johns Hopkins Institute of Cellular Technology and Professor. of neuroscience at Johns Hopkins Medical University.

Parkinson's disease is characterized by the accumulation of an incorrectly folded protein, called alpha-synuclein, in the brain cells. Since most of these proteins begin to cluster, they cause the death of the nerve tissue, leaving behind large portions of dead brain matter known as Levi's bodies. Since brain cells die, they affect the ability of a person to move, think or regulate emotions.

The new study is based on observations made in 2003 by German neuroanatomic heiko Braac who showed that people with Parkinson's disease also had accumulations of folded alpha-synuclein protein in parts of the central nervous system that control the intestines.

The appearance of these proteins, which are harmful to neurons, is consistent with some of the early symptoms of Parkinson's disease that include constipation, says Dr. Han Seok Co., associate professor of neurology at Johns Hopkins Medical University.

Braak assumed that Parkinson's disease progressed to the nerves that connect the intestines and the brain to climb as a ladder.

The increasing number of evidence is related to the cerebrovascular connection at the start of Parkinson's disease. Researchers were very curious to know whether the wrongly folded alpha-synuclein protein could move along the wandering nerve, which acts as an electrical cable from the stomach and the small intestine to the base of the brain.

To prove it, researchers injected 25 micrograms of improperly folded synthetic alpha-synuclein created in the lab into the intestines of dozens of healthy mice. They took samples and analyzed the brain tissue one, three, seven and 10 months after the injection. In the course of the 10-month experiment, scientists have seen evidence that alpha-synuclein begins to build up where the vagal nerve is connected to the intestine and continues to spread throughout the brain.

The researchers then performed a similar experiment, but this time they surgically cut the wandering nerve into a group of mice and injected their intestines with an incorrectly folded alpha-synuclein. After a seven month study, the researchers found that mice with cut vaginal nerves did not show any signs of cell death in mice with intact wandering nerves. The cut nerve seemed to stop the progress of improperly folded protein, Dawson says.

The researchers then wanted to know if these physical differences in the progression of the disease lead to behavioral changes. To test this, they assess the behavior of three groups: mice injected with mismatched alpha-synuclein, mice injected with folded alpha-synuclein with cut vaginal nerve and control mice without injection and intact wandering nerves. Researchers analyzed the tasks they used to distinguish the signs of Parkinson's disease in mice, such as nest construction and exploration of new environments.

Researchers have for the first time observed that mice build nests in their enclosure as a test of subtle motor skills that are commonly affected by Parkinson's disease in humans. Seven months after injection, mice receiving injectable mismatched alpha-synuclein were assessed consistently lower in the nest design.

Moreover, while most of the mice used all 2.5 grams of the supplied material, the group of mice that received an alpha-synuclein injection used less than half a gram of the suture material. "According to the symptoms of Parkinson's disease in humans, subtle motor control of mice has worsened as the disease progresses," says Co.

In another experiment that analyzes mice for symptoms similar to Parkinson's disease in humans, researchers measure anxiety levels by analyzing how they respond to new environments.

For this test, scientists put the mice in a large open box where the camera can track their research. Healthy mice are curious and will spend time exploring every part of a new environment. However, mice affected by cognitive decline are more anxious, making them more prone to stay on the edges of a box.

The research team found that control mice and mice whose wandering nerves were cut off to prevent Parkinson's disease spent between 20 and 30 minutes to examine the center of the box. Meanwhile, mice that received an incorrectly folded alpha-synuclein injection but had intact wandering nerves spent less than five minutes showing higher levels of anxiety consistent with the symptoms of Parkinson's disease.

Overall, the results of this study indicate that the misfolded alpha-synuclein can be transmitted from the intestine to the brain of mice on the vaginal nerve, and blocking the delivery pathway may be the key to preventing the physical and cognitive manifestations of Parkinson's disease.

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