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07/02/2018
12:10
Parkinson's disease is a neurodegenerative disease that affects the nervous system in a chronic and progressive manner. According to the Anti-Parkinson Foundation, this disease affects about one million people in the United States. EFE / Archivo (Photo: EFE )
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Miami, July 2 (EFE) .- A drug developed experimentally by researchers at Johns Hopkins University has slowed down both the progression of Parkinson's disease and its symptoms in mice, said the # 39, university today.
Researchers, who in experiments with human brain cell cultures and a preclinical model of Parkinson's disease in mice discovered that the so-called NLY01 stops "neuronal degeneration" project to test the drug in clinical trials this year.
"The drug protects the target cells of the nervous system in a truly incredible way," says Ted Dawson, director of the Institute of Cell Engineering and professor of neurology at the Johns Hopkins University School of Medicine, based in Baltimore , Maryland.
If clinical trials are successful, NLY01 would be one of the first pharmacological treatments whose action would not only aim to improve muscle rigidity, tremors and dementia, among other symptoms of Parkinson's disease, but especially to slow the progression of the disease, says Dawson.
The results of the study were published in the scientific journal Nature Medicine.
In a statement, Johns Hopkins University explains that NLY01 acts in the same way as compounds that are administered to increase glucose levels in the blood of people with diabetes mellitus.
Although the results of previous studies on animal models have made it possible to conjecture the neuroprotective potential of this type of diabetes medicine, it has not been demonstrated concretely how this mechanism worked in the brain.
To find out, Dawson and his team have tested the drug NLY01 using three types of brain cells of great relevance: astrocytes, microglia and neurons.
Astrocytes, star-shaped morphology cells that allow synaptic communication, when they become "reactive" because of a chemical signal sent by microglia, "rebel" and begin to "devour the points of contact of the cells." brain, which in turn produces neuronal death. "
In a preliminary experiment with human brain cells reproduced in vitro, the Dawson team administered NLY01 to human microglia and found that the activation signal did not occur and that astrocytes did not become destructive cells and retained their neuroprotective function.
They then tested the effectiveness of the drug in mice that, by genetic modification, carried a version of Parkinson's.
In a first experiment, the Dawson team injected the alpha-synuclein protein, which is thought to be the main cause of Parkinson's disease, into ten mice, which subsequently received NLY01.
In addition, the researchers injected alpha-synuclein into another group of similar mice, to whom the drug was not administered.
This second group of mice showed significant motor impairment in behavioral tests, whereas mice treated with NLY01 retained their normal physical functions and dopaminergic neurons, a clear indication of the protective effect of the drug in the development of the Parkinson disease. .
In a second experiment, the team of researchers studied a group of mice that, by genetic modification, naturally produced an alpha-synuclein protein more similar to the human.
Under normal conditions, the transgenic mice had to die in 387 days, but the Dawson team observed that treatment with NLY01 prolonged the survival of 20 mice treated with the drug in more than 120 days.
After conducting further analysis, the researchers cautioned that brains from mice treated with the drug NLY01 had little indication of the neurodegenerative features of Parkinson's disease.
Parkinson's disease is a neurodegenerative disease that affects the nervous system in a chronic and progressive way. According to the Anti-Parkinson Foundation, this disease affects about one million people in the United States.
EFE
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