Parkinson’s disease affects approximately 7-10 million people worldwide and is characterised by progressive loss of motor function, psychiatric symptoms and cognitive impairment.
Current treatments for Parkinson’s only treat symptoms of the disease rather than its underlying causes, so these new findings in fruit flies could lead to novel preventative treatments if replicated in humans.
Previous research suggests that defects in mitochondria, which are tiny ‘batteries’ in cells that provide energy, play an important role in a number of diseases that affect the nervous system, including Parkinson’s. However, until now the neuronal processes underlying the development of these conditions were unknown.
The study, published in PNAS, discovered that damaged mitochondria in fruit flies produce a signal which stops nerve cells from working. A gene called HIFalpha was found to regulate the nerve signals from damaged mitochondria and, when this gene was ‘switched off’ by the research team, nerve function in flies with Parkinson’s disease was restored. By deactivating the HIFalpha gene, the early failure of nerve cells caused by mitochondrial damage was prevented.
An identical effect was observed in flies with Leigh syndrome, a rare neurological disorder caused by a severe mitochondrial defect, which typically arises in the first year of life in humans.
As the HIFalpha gene is also found in humans, this new finding could pave the way for new treatments in the future, according to the study authors.