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Scientists have discovered that the so-called NLY01 holds "neuronal degeneration" and intends to use this year's drug in clinical trials
Rats: animals treated with NLY01 retained their normal physical functions as neurons (AFP / AFP)
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Rats: animals treated with NLY01 retained their normal physical functions as neurons (AFP / AFP)
[Texte intégral – PDF] [Texte intégral – PDF] A drug developed experimentally by Johns Hopkins University researchers was able to slow the progression and the symptoms of Parkinson's disease according to the University Center reported Monday.
Human brain cells and a preclinical model of Parkinson's disease in rats have shown that the so-called NLY01 holds "neuronal degeneration", the intention to use this year's drug in clinical trials.
"The drug really protects amazing target cells from the nervous system," said Ted Dawson, director of the Institute of Cell Engineering and professor of neurology at the University's Faculty of Medicine (19659008). If clinical trials prove conclusive, NLY01 would be one of the first pharmacological treatments whose action would not only aim to improve muscle rigidity, tremors and dementia, the results of the study. study was published in the digital journal Nature Medique
In a statement, the Johns Hopkins University explained that NLY01 acts similar to the compounds used to increase glycemic levels in people with diabetes.
the results of previous animal studies have allowed us to conjecture the neuroprotective potential of this type of diabetes medicine, it has not been possible to This mechanism has worked in the brain.
To find out, Dawson and his team tested the drug NLY01 in three
Astrocytes, cells that allow synaptic communication, when they become "reactive" because of a chemical signal sent by microglia , are "rebellious" "And begin to" devour the points of contact of brain cells, which, in turn, causes neuronal death. "
In a preliminary experiment with human brain cells reproduced in vitro, the Dawson team used the NLY01 in human microglia and found that the activation signal was not occurring and that the astrocytes did not become destructive cells and could retain their neuroprotective function.
Then they tested the efficacy of the drug in rats a version of Parkinson
In a first experiment, Dawson's team injected alpha-synuclein protein, which is considered the leading cause of Parkinson's disease, in 10 mice that subsequently received NLY01.
In addition, the researchers injected alpha-synuclein into another group of similar mice, who did not receive the drug.
This second group of mice had a significant deterioration of the motor behavioral tests, whereas the N treated rats LY01 retained their normal physical functions and dopaminergic neurons, a clear indication of the protective effect of the drug compared to the development of Parkinson's disease.
In a second experiment, scientists studied a group of mice that, by genetic modification, naturally produced an alpha-synuclein protein more badogous to human
Under normal conditions, transgenic mice would die in 387 days, but the Dawson team observed that treatment with NLY01 prolonged the survival of the 20 drug-treated rats in more than 120 days.
After conducting a more comprehensive review, the researchers warned that the brains of the rats treated with the drug NLY01 had little evidence of the neurodegenerative features of Parkinson's.
Parkinson's disease is a neurodegenerative disorder that affects the nervous system in a chronic and progressive manner. According to the Parkinson's Foundation, this disease affects an estimated one million people in the United States. (Js = d.getElementById (id)) {var js = d.createElement ("script"), ref = d.getElementsByTagName ("script" ") [0]; js.id = id, js.async = true, js.src = "https: / / connect.facebook.net / pt_BR /all.js", ref.parentNode.insertBefore (js, ref)}}) (document)
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