Los Angeles:
Scientists, including an Indian-origin researcher, have discovered a 'Dorian Gray' gene that may extend lifespan and delay the onset of ageing.
Researchers from the University of California, Los Angeles found that the gene, which has previously been implicated in Parkinson's disease, extended the healthy lifespan of fruit flies by more than 25 per cent.
The research, they say, could have important implications for ageing and disease in humans.
The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.
"Ageing is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.
"We think that our findings shed light on the molecular mechanisms that connect these processes," said Mr Walker.
Mr Walker and his colleagues show that parkin can modulate the ageing process in fruit flies, which typically live less than two months.
The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 per cent, compared with a control group that did not receive additional parkin.
"In the control group, the flies are all dead by Day 50," Mr Walker said.
"In the group with parkin over-expressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound," he said.
"Just by increasing the levels of parkin, they live substantially longer while remaining healthy, active and fertile," said Anil Rana, a postdoctoral scholar in Mr Walker's laboratory and lead author of the research.
Treatments to increase parkin expression may delay the onset and progression of Parkinson's disease and other age-related diseases, the biologists believe.
"Our research may be telling us that parkin could be an important therapeutic target for neurodegenerative diseases and perhaps other diseases of ageing," Mr Walker said.
As we age, our cells accumulate damaged or misfolded proteins. When proteins fold incorrectly, the cellular machinery can sometimes repair them. When it cannot, parkin enables cells to discard the damaged proteins, said Mr Walker.
While the researchers found that increased parkin can extend the life of fruit flies, Mr Rana also discovered that too much parkin can have the opposite effect.
When he quadrupled the normal amount of parkin, the fruit flies lived substantially longer, but when he increased the amount by a factor of 30, the flies died sooner.
Researchers from the University of California, Los Angeles found that the gene, which has previously been implicated in Parkinson's disease, extended the healthy lifespan of fruit flies by more than 25 per cent.
The research, they say, could have important implications for ageing and disease in humans.
The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.
"Ageing is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.
"We think that our findings shed light on the molecular mechanisms that connect these processes," said Mr Walker.
Mr Walker and his colleagues show that parkin can modulate the ageing process in fruit flies, which typically live less than two months.
The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 per cent, compared with a control group that did not receive additional parkin.
"In the control group, the flies are all dead by Day 50," Mr Walker said.
"In the group with parkin over-expressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound," he said.
"Just by increasing the levels of parkin, they live substantially longer while remaining healthy, active and fertile," said Anil Rana, a postdoctoral scholar in Mr Walker's laboratory and lead author of the research.
Treatments to increase parkin expression may delay the onset and progression of Parkinson's disease and other age-related diseases, the biologists believe.
"Our research may be telling us that parkin could be an important therapeutic target for neurodegenerative diseases and perhaps other diseases of ageing," Mr Walker said.
As we age, our cells accumulate damaged or misfolded proteins. When proteins fold incorrectly, the cellular machinery can sometimes repair them. When it cannot, parkin enables cells to discard the damaged proteins, said Mr Walker.
While the researchers found that increased parkin can extend the life of fruit flies, Mr Rana also discovered that too much parkin can have the opposite effect.
When he quadrupled the normal amount of parkin, the fruit flies lived substantially longer, but when he increased the amount by a factor of 30, the flies died sooner.
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