The origins of this neurodegenerative disorder are not entirely understood, it is understood that numerous of its signs are triggered by the death of nerve cells that create dopamine.A research study conducted in mice by a research study team at the University of Cordoba has actually uncovered one of the causes of this neuronal loss: the crucial lives in the protein called DJ1, whose association with Parkinsons illness has formerly been established, but its specific role was unidentified until now.This research took things a step further by exposing one of the proteins action mechanisms. To accomplish this, the researchers carried out a comparative research study of nerve cells in the brains of mice with and without this active gene, with the goal of “comparing the distinctions between the two protein patterns and, therefore, studying the mechanisms that may be modified,” discusses Raquel Requejo, the research studys lead scientist and a member of the BIO126 group at the University of Cordoba.Image of the team that brought out the examination Credit: University of CórdobaWhen dividing is not an optionAccording to the results of the study, the absence or dysfunction of the gene revealing the DJ1 protein causes the activation of what is known as the cell cycle, the process by which cells divide; in other words, the equipment utilized by cells to change others that have passed away, as occurs, for example, when a wound heals.What is the genuine problem here? As an outcome, when a gene is altered, its nerve cells are forced into a division procedure that they are not able to complete and end up passing away, thus producing many particular symptoms of Parkinsons disease.This is what is known in the scientific literature as an “aberrant cell cycle” and its relationship “with this neurodegenerative illness and the lack of the DJ1 protein has actually been explained for the first time in this research study,” said Requejo.To date, Parkinsons illness has no remedy, per se, and present treatments consist of externally providing the dopamine that the passing away nerve cells stop producing naturally, discussed the studys lead author.
