Parkinson's disease affects about 7 million people worldwide, according to data provided by the World Health Organization (WHO). This neurodegenerative disorder affects the central nervous system and, although its causes are not yet fully understood, it is known that many of its symptoms are due to the loss of neurons that produce dopamine.
A study carried out by a research team at the University of Cordoba has revealed, in mice, one of the reasons for this neuronal loss: the key lies in the protein called DJ1, whose relationship with Parkinson's disease had already been demonstrated, although until now its exact function was unclear.
This study went a step further in this area, revealingone of this protein's action mechanisms. To do this, the research team carried out a comparative study of neurons in the brains of mice that have this active gene, and others that lack it, with the aim of "comparing the differences between the two protein patterns and, thus, studying the mechanisms that may be altered," explains Raquel Requejo, principal investigator of the study and a member of the BIO126 group at the University of Cordoba.
When dividing is not an option
According to the results of the study, the absence or dysfunction of the gene expressing the DJ1 protein causes the activation of what is known as the cell cycle, the process by which cells divide; in other words, the machinery used by cells to replace others that have died, as occurs, for example, when a wound heals.
What is the real problem here? The answer is that neurons do not have the capacity to divide,yet they 'receive instructions' to do so through the triggering of a cell cycle that, under normal conditions, should not occur. As a result, when a gene is altered, its neurons are forced into a division processthat they are unable to complete and end up dying, thus producing many characteristic symptoms of Parkinson's disease.
This is what is known in the scientific literature as an "aberrant cell cycle" and its relationship "with this neurodegenerative disease and the absence of the DJ1 protein has been described for the first time in this study," said Requejo.
To date, Parkinson's disease has no cure,per se, and current treatments consist of externally supplying the dopamine that the dying neurons stop producing naturally, explained the study's lead author. In the future, this finding could favor the development of new therapeutic approaches that not only combat the symptoms but also prevent their cause, also behind other neurodegenerative diseases: neuronal death.
Cellular and Molecular Neurobiology
Deficiency of Parkinson's Related Protein DJ-1 Alters Cdk5 Signaling and Induces Neuronal Death by Aberrant Cell Cycle Re-entry
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