Gene that might prevent Parkinson’s disease has been identified by scientists

A crucial protein found in flies and mice that protects against Parkinson’s disease might be a new therapeutic target, according to researchers at the University of Geneva.
The results of the study were published in the journal ‘Nature Communication.’ Parkinson’s disease is a neurodegenerative condition in which a specific group of dopaminergic neurons is destroyed.
Except in rare cases involving a single gene, most Parkinson’s cases are caused by a combination of genetic and environmental risk factors. However, mitochondrial failure in dopaminergic neurons is a frequent feature of the disease’s beginning. When a cell is injured, these little factories within it are responsible for energy generation as well as initiating the cell’s self-destruct mechanisms.

The fruit fly, or Drosophila, is used in the laboratory of Emi Nagoshi, Professor in the Department of Genetics and Evolution at the UNIGE Faculty of Science, to explore the causes of dopaminergic neuron degeneration. Her research group is particularly interested in the Fer2 gene, whose human equivalent encodes a protein that regulates the expression of many other genes and whose mutation may cause Parkinson’s disease through unknown pathways.
This research team previously established that a mutation in the Fer2 gene induces Parkinson’s-like symptoms in flies, including a delay in movement beginning. They also noticed anomalies in the structure of dopaminergic neurons’ mitochondria, which were comparable to those seen in Parkinson’s patients.

Because a lack of Fer2 induces Parkinson’s disease-like symptoms, the researchers wondered whether, on the other hand, increasing Fer2 levels in the cells may protect the cells. When flies are exposed to free radicals, their cells experience oxidative stress, which causes dopaminergic neurons to degrade. The scientists were able to see that when the flies overproduce Fer2, oxidative stress has no negative effect on them, corroborating the concept of its protective role. Fer2 regulates a number of genes, the majority of which are involved in mitochondrial function.

As a result, this key protein appears to play a critical role in preventing dopaminergic neuron degeneration in flies by controlling not only the structure but also the functions of mitochondria,” said Federico Miozzo, a researcher in the Department of Genetics and Evolution and the study’s first author.
The researchers produced mutations of the Fer2homolog in mouse dopaminergic neurons to see if Fer2 has the similar role in mammals. They found abnormalities in the mitochondria of these neurons, as well as motility impairments, in elderly mice, much as they did in the fly.

“We are currently testing the protective role of the Fer2 homolog in mice and results similar to those observed in flies would allow us to consider a new therapeutic target for Parkinson’s disease patients,” concluded Emi Nagoshi.