Researchers have identified a genetic ‘switch’ that may help prevent or delay the symptoms of Parkinson’s disease.
The study showed that a gene called ATF4 plays a key role in Parkinson’s disease, acting as a ‘switch’ for genes that control mitochondrial metabolism for neuron health.
When the expression of ATF4 is reduced in flies, expression of these mitochondrial genes drops.
This drop results in dramatic locomotor defects, decreased lifespan, and dysfunctional mitochondria in the brain.
“Interestingly, when we overexpressed these mitochondrial genes in fly models of Parkinson’s, mitochondrial function was re-established, and neuron loss was avoided,” said Miguel Martins from the University of Leicester in London.
By discovering the gene networks that orchestrate this process, the researchers have singled out new therapeutic targets that could prevent neuron loss.
Some forms of Parkinson’s are caused by mutations in the genes PINK1 and PARKIN.
Fruit flies with mutations in these genes accumulate defective mitochondria and exhibit Parkinson’s-like changes, including loss of neurons, the researchers said.
For the study, published in the journal Cell Death and Differentiation, the team used PINK1 and PARKIN mutant flies to search for other critical Parkinson’s genes and using a bioinformatics approach discovered that the ATF4 gene plays a key role.
“Studying the roles of these genes in human neurons could lead to tailored interventions that could one day prevent or delay the neuronal loss seen in Parkinson’s,” Martins added.
Previous studies have showed several genes that protect neurons in Parkinson’s disease, creating possibilities for new treatment options.—IANS