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Researchers at the University of Coimbra in Portugal, have identified a new mechanism responsible for the origin of Parkinson's disease.
The finding contradicts some scientific theories about the causes of one of the most common neurodegenerative disorders affecting, according to the latest data, more than four million people worldwide.
The results, published in the journal Human Molecular Genetics, show that the dysfunction of mitochondria, responsible for energy production in cells, is largely responsible for the onset of the disease.
Portuguese researchers demonstrated for the first time in studies of patients with Parkinson's disease cells, the intracellular traffic deficiency is caused by mitochondrial dysfunction patients.
"Means any cell analyzed and found that, in Parkinson's disease, mitochondrial dysfunction is the event which is the basis of a deficient autophagy, the mechanism by which the degradation is dysfunctional and organelles of damaged proteins, ie the accumulation of biological waste during the aging process and that if not eliminated leads to cell death, "explains lead researcher, Sandra Morais Cardoso.
According to the authors, the discovery provides new clues to the future development of drugs capable of preventing the traffic disruption and thus ensure the normal intracellular transport, which takes place throughout the neuron from the core to the terminals synaptic.
"We note that autophagy itself may not be used as a therapeutic target after diagnosis of the disease and it is necessary to develop therapeutic approaches that simultaneously promotes autophagy and restore the cellular traffic," said Cardoso.
Whereas the process autophagic has two separate components, taking on the one hand, the paper quality control of cells and, secondly, transforming during prolonged fasting, the elements of cell nutrients to prolong the preservation of the organism, Researchers studied the entire autophagic process and found that, in Parkinson's disease, its activation may be harmful.
The team's next step is to study and discover how the dysfunction of mitochondria leads to destabilization of cellular highways.