Director of the CIB U. Mayor participates in research that created a method that successfully slows the progress of Parkinson's
09-24-2019
09-24-2019
A new strategy to stop Parkinson's disease at an early stage is the result of three years of collaborative research between Dr. Felipe Court, director of the Center for Integrative Biology (CIB) of the Universidad Mayor and Claudio Hetz, director of the Millennium Institute of Biomedical Neuroscience (BNI) of the Faculty of Medicine of the Universidad de Chile.
The technique consists in blocking the destruction of the axon with a drug, a segment of the neuron similar to an extension or branching that allows communication between different brain cells.
Parkinson's disease that causes loss of motor control, occurs when dopaminergic neurons stop functioning or die. These cells are located in the brain and secrete dopamine, a chemical that coordinates movement. Court's team, a doctor of neurosciences, discovered in previous research that before the first symptoms manifested "as tremor, stiffness and balance problems" something crucial happened in these neurons.
The director of the CIB explains it: "In the dopaminergic neurons necroptosis occurs, a mechanism that produces the destruction of the axons before the neuron dies. We demonstrated that the necroptosis was responsible for the degeneration of the axons and we concluded that this could be a therapeutic target in Parkinson's; if we were able to block this mechanism, we could stop the degeneration of axons, the death of neurons and delay the loss of motor function. "
If there is necroptosis, there are fewer dopaminergic neurons that secrete dopamine, which affects the motor function of the human body. The scientists then set out to devise a strategy to stop the destruction of axons.
Necrostatin
The team, which is also integrated by Dr. Maritza Oñate, worked in the laboratory with a model that simulated the early stages of Parkinson's in two groups of 25 mice each.
Court explains that both groups of diseased mice were injected; one with the drug necrostatin and one with a placebo. "The importance is that this drug acts only on the axons of the neurons that are dying from necroptosis. It does not produce any negative effects on the axons of the nervous system that are healthy."
Necrostatin, Court adds, "has as its target a specific axon protein called RIPKI, which is part of a protein complex that is formed to activate necroptosis. Then the drug inhibits RIPKI and prevents this protein complex from conforming. that triggers the destruction of the axon. "
Before and after injecting the diseased mice, the researchers measured their locomotor parameters with motor, strength and coordination tests. The idea was to check if the group that was treated with the drug showed some improvement over the other where the placebo acted.
About the results Hetz, a doctor of biomedical sciences, comments that "we observed that aspects such as coordination and motor capacity that diminished in the Parkinson's model used were attenuated in animals with the treatment that inhibits necroptosis."
Court adds that "the animals that were injected with the drug had more axons and more neurons and manifested a locomotive loss less than the other group."
