Parkinson’s is a neurodegenerative disorder caused by the destruction of neurons known as dopaminergic neurons.
During this study, the team from the University of Geneva looked at these neurons with the fruit fly as a model of study. They pinpointed a major protein, in the flies and in mice, that has a protective effect from this illness and may become a new therapeutic tool.
This gene is the Fer2gene-its human homolog encodes a protein that controls the expression of other genes and its mutation is associated with the onset of Parkinson’s.
The Role of the Fer2gene in Parkinson’s Disease
Apart from rare forms with a single gene, most cases of Parkinson’s are a consequence of the interaction between various genetic and environmental risk factors.
But, a common element in the disease’s onset is the mitochondria dysfunction in the dopaminergic neurons. These “factories” in the cells produce energy, but also activate the cells’ mechanisms for self-destruction when they’re damaged.
In a study done before, the team showed that a mutation of this gene led to deficiencies associated with Parkinson’s, but also found defects in the mitochondria’s shape of the dopaminergic neurons, similar to the ones seen in patients with this disease.
What Did the Researchers Do for the New Study?
As the absence of Fer2 leads to Parkinson’s-like conditions, the team wanted to discover if the increase of this gene’s presence in the cells may have a beneficial influence.
When the flies were exposed to free radicals, their cells experienced oxidative stress and this caused the dopaminergic neurons to degrade.
But, the team noticed that oxidative stress doesn’t have a negative impact on the flies which overproduced Fer2, and thus, they confirmed their study’s hypothesis.
According to Federico Miozzo, one of the researchers and first author of the study, they’ve identified the genes that Fer2 regulates and they’re mostly included in the mitochondrial functions.
This protein seems to have a major role in preventing dopaminergic neurons’ degeneration by controlling the mitochondria’s structure and its functions.
In order to discover if Fer2 will have the same effect in mammals, the team made mutants of the Fer2 in mice dopaminergic neurons.
Same as in the flies, the team found abnormalities in the mitochondria of the neurons as well as defects in locomotion in the aged mice.
If the final results are similar to that gotten from the flies, the team notes that they will have a new therapeutic target for Parkinson’s.
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