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. (Representational Image)
Washington:
British researchers said they have identified a new gene linked to nerve function, that could hold the key to treating neurodegenerative diseases such as Parkinson's disease.
Parkinson's disease affects about 7 million to 10 million people worldwide and is characterised by progressive loss of motor function, psychiatric symptoms and cognitive impairment.
Current treatments for Parkinson's disease 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, the researchers concluded in the study published in the US journal Proceedings of the National Academy of Sciences.
Previous research suggested 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 disease. However, until now the neuronal processes underlying the development of these conditions were unknown.
The new study, conducted by researchers at the King's College London, discovered that damaged mitochondria in fruit flies produce a signal which stops nerve cells from working, Xinhua reported on Monday.
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. As a result, 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 researchers.
"Like their human counterparts flies with Parkinson's disease progressively lose motor function, that includes a negative impact on their ability to climb. Remarkably, we found that switching off a particular gene dramatically improved their motor function and climbing ability," said study author Joseph Bateman from the Institute of Psychiatry, Psychology & Neuroscience at King's College London.
"The biggest surprise from our work is that damaged mitochondria produce a signal that actively prevents nerve cells from working properly. Thanks to this study we now have a much better understanding of how nerve cells' function, that could transform the way in which neurological diseases such as Parkinson's are understood and treated."
Parkinson's disease affects about 7 million to 10 million people worldwide and is characterised by progressive loss of motor function, psychiatric symptoms and cognitive impairment.
Current treatments for Parkinson's disease 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, the researchers concluded in the study published in the US journal Proceedings of the National Academy of Sciences.
Previous research suggested 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 disease. However, until now the neuronal processes underlying the development of these conditions were unknown.
The new study, conducted by researchers at the King's College London, discovered that damaged mitochondria in fruit flies produce a signal which stops nerve cells from working, Xinhua reported on Monday.
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. As a result, 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 researchers.
"Like their human counterparts flies with Parkinson's disease progressively lose motor function, that includes a negative impact on their ability to climb. Remarkably, we found that switching off a particular gene dramatically improved their motor function and climbing ability," said study author Joseph Bateman from the Institute of Psychiatry, Psychology & Neuroscience at King's College London.
"The biggest surprise from our work is that damaged mitochondria produce a signal that actively prevents nerve cells from working properly. Thanks to this study we now have a much better understanding of how nerve cells' function, that could transform the way in which neurological diseases such as Parkinson's are understood and treated."
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