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A drug developed experimentally by researchers at Johns Hopkins University managed to slow the progression of Parkinson's disease and its symptoms in mice, says the university center today. ; hui.
Researchers, only in experiments with human brain cell cultures and a preclinical model of Parkinson's disease discovered that the so-called NLY01 stops "neuronal degeneration", projected to test this year the drug in clinical trials .
"The drug protects the target cells of the nervous system in a truly incredible way," says Ted Dawson, director of the Institute of Cellular Engineering and professor of neurology at the Faculty of Medicine's Department of Medicine. Johns Hopkins University, Baltimore, Maryland.
If the 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 things. other symptoms párkinson but specifically 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 a similar manner to compounds that are administered to increase blood glucose levels in 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 drugs against diabetes, it has not been demonstrated concretely how this mechanism worked. in the brain.
To find out, Dawson and his team tested the drug NLY01 using three types of brain cells of great relevance: astrocytes, microglia and neurons.
Astrocytes, stellate 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 of the cell ". brain, which in turn produces neuronal death. "
In a preliminary experiment with human brain cells reproduced in vitro, Dawson's team administered NLY01 to human microglia and found that the activation signal did not take place and that astrocytes did not become destructive cells and were able to retain their neuroprotective function.
They then tested the efficacy of the drug in mice that, by genetic modification, wore a version of Parkinson's
In a first experiment, the Dawson team injected the alpha-synuclein protein, the folding of which would be the main cause of Parkinson's disease to ten mice, which then received NLY01. 19659003] 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 a motor impairmentsignificant in behavioral tests, while mice treated with NLY01 retained both their normal physical functions and dopaminergic neurons, a clear indication of the protective effect of the drug on the development of Parkinson's 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 analogous to humans.
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 warned that the brains of mice treated with the drug NLY01 had little indication of the neurodegenerative characteristics of párkinson .
Parkinson's Disease is a neurodegenerative disease that affects the nervous system in a chronic and progressive manner. According to the Foundation Against Parkinson this disease affects about one million people in the United States. EFE
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