Parkinson's disease could be prevented after scientists discovered what actually causes it at a cellular level.
It had been thought some inherited forms of early-onset Parkinson's disease have typically been blamed on poorly functioning mitochondria.
These are the powerhouses of cells and without reliable sources of energy, neurons wither and die.
But Medical Research Council researchers at University of Leicester found this may not be the complete picture of what is happening within cells affected by Parkinson's.
Instead neurodegeneration was the result of stress on the endoplasmic reticulum (ER) - part of the outer skin of the cell - rather than failure of the mitochondria as previously thought.
The death of neurons associated with the disease was prevented when chemicals that block the effects of endoplasmic reticulum stress were used.
Dr Miguel Martins said: "This research challenges the current held belief the Parkinson's disease is a result of malfunctioning mitochondria.
"By identifying and preventing ER stress in a model of the disease it was possible for us to prevent neurodegeneration. Lab experiments, like this, allow us to see what effect ER stress has on Parkinson's disease.
"While the finding so far only applies to fruit flies, we believe further research could find that a similar intervention in people might help treat certain forms of Parkinson's."
The study by Leicester's MRC Toxicology Unit used a "mutant" common fruit fly to investigate this further as they provide a good genetic model for humans.
It was found that the bulk of the damage to neurons with damaged mitochondria stems from a related but different source - the neighbouring maze-like endoplasmic reticulum (ER).
The ER has the important job of folding proteins so that they can do the vast majority of work within cells.
Misfolded proteins are recognised by the cell as being dangerous.
Cells halt protein production if there are too many of these harmful proteins present.
While this system is protective, it also stalls the manufacture of vital proteins, and this eventually results in the death of neurons.
The study was published in the journal Cell Death and Disease.