Parkinson’s disease (PD) is a multifactorial disorder caused by a combination of genetic and environmental factors. Evidence suggests that PD risk factors lead to common pathological processes, including excessive production of reactive oxygen species, axonal pathology, neuroinflammation, and mitochondrial dysfunction.
Most PD cases result from an interaction between genetic and environmental risk factors. However, a common element in the onset of the disease is a dysfunction of mitochondria in dopaminergic neurons .
In a recently published study, researchers from the University of Geneva have investigated the destruction of these dopaminergic neurons using the fruit fly as study model. The scientist identified key protein in flies and mice that play a protective role against PD. The study was published in the journal Nature Communications.
In a previous study, the same team demonstrated that a mutation in the gene Fer2 causes Parkinson’s-like deficiencies in flies, including a delay in the initiation of movement.
The team tested whether an increase in the amount of Fer2 in the cells could have a protective effect. They found that oxidative stress no longer had a deleterious effect on the flies if they overproduced Fer2.
The protein seems to play a crucial role against the degeneration of dopaminergic neurons by controlling not only the structure of mitochondria but also other functions. The research team is also testing their hypothesis in a mouse model and if the results are similar to those observed in flies would allow them to consider a new therapeutic effect in PD patients.
Federico Miozzo, et al. Maintenance of mitochondrial integrity in midbrain dopaminergic neurons governed by a conserved developmental transcription factor. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-29075-0
Université de Genève. (2022, March 17). A gene could prevent Parkinson’s disease. ScienceDaily. Retrieved March 18, 2022 from: