Researchers from the University of Leicester have offered new insight into how Parkinson's disease develops.
According to the findings, the condition is triggered by stress in a specific part of the cell, rather than the failure of the cell's mitochondria as previously thought.
The study, which was carried out in fruit flies, found that death of neurons inside the brain associated with Parkinson's could be prevented by releasing chemicals to stop this stress having an impact on the cell.
Poorly functioning areas of the cell - called the mitochondria - have been blamed for the progression of some inherited forms of early-onset Parkinson's disease. However, the findings from the new study suggest this may not be the entire picture.
A team from the Medical Research Council (MRC) Toxicology Unit at the University of Leicester looked at fruit flies with mutant forms of the pink1 or parkin genes, which is known to prevent the body from getting rid of defective mitochondria. These are also the genes that lead to the hereditary versions of the disease.
The researchers found that most of the damage to neurons were caused by stress in the endoplasmic reticulum (ER), which is needed to allow proteins to perform tasks within the cell.
Proteins that are prevented from doing this become misfolded, and the cell recognises them as being dangerous and stops further proteins from being released. Although this is designed to protect the body, it also causes the death of neurons as none of the vital proteins are being produced.
Compared to normal flies, the team found that the genetic mutation caused a large amount of ER stress.
Dr Miguel Martins, who led the study, said: "This research challenges the current held belief the Parkinson's disease is a result of malfunctioning mitochondria."
"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," he explained.
The study was published in the journal Cell Death and Disease.
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