Scientists have increased the lifespan of fruit flies by genetically manipulating microscopic structures in their cells, a technique that might help researchers find the key to longer life in humans.
It’s all down to mitochondria - the microscopic structures in the cells that turn food into energy - and a compound called NAD+, which is used to transfer electrons during the cell’s metabolic reactions.
By changing the DNA of fruit flies, a team led by Dr Alberto Sanz of the University of Newcastle-upon-Tyne, in the UK, replaced the enzyme normally used by the flies to metabolise food with another. This switch caused the levels of NAD+ in the cell to rise.
At high concentrations, NAD+ can strengthen the cell’s chances of survival, meaning the fly lives longer.
‘A higher concentration of NAD+ would be expected to extend the lifespan of the host organism,’ said Dr Sanz, who is conducting the research as part of the EU-funded COMPLEXI&AGING project.
These results are very significant because the enzyme normally used by fruit fly mitochondria is the same as that used in people, meaning this research could help us find a way to tackle ageing in humans.
‘The only thing the mitochondria care about is their own survival. Still, their callous ways allowed life to develop as we know it.’
Professor Luca Scorrano, University of Padua, Italy
Parkinson’s and Alzheimer’s
Mitochondria could also play a central role in identifying the causes of currently incurable age-related diseases. Professors Elena Ziviani and Luca Scorrano at the University of Padua in Italy are looking into what mitochondria can teach about the causes of Parkinson’s disease.
Professor Ziviani, whose work is part of the MITOFUSIN-PD project, is examining the role of a protein called parkin, which is defective in people with Parkinson’s disease. By attaching fluorescent molecules to mitochondria she can use a special high-resolution microscope to examine how parkin regulates the behaviour of mitochondria within a cell.
She has found that parkin helps mitochondria to tether and communicate with other structures in cells. Professor Ziviani believes this communication helps the cells to survive. ‘Impaired communication could cause premature death in brain cells, leading to Parkinson’s disease,’ she said.
Exactly how mitochondria tether with other cell structures is now being researched by Professor Scorrano in the framework of the European Research Council project ERMITO. The research, which is due to finish in 2016, is aimed at finding out more about the anatomy of the tethering mechanism and how it impacts upon the lifespan of cells.
Mitochondria are also being investigated in efforts to beat other degenerative diseases. The European MitoMyelin project has been awarded EUR 2 million to study the role of mitochondria in a group of diseases that includes nerve damage caused by diabetes.
Dysfunctional mitochondria have been identified as one of the causes of these diseases and researchers are testing whether altering the mitochondria could lead to a prevention or cure. The results of this work will also be relevant for the treatment of brain diseases such as Alzheimer’s and multiple sclerosis.
When asked why mitochondria are involved in so many life-threatening conditions, Professor Scorrano points to their origins. ‘The mitochondrion is a parasite that colonised the primordial cell billions of years ago,’ he said. ‘The union may remain to our advantage, but the only thing the mitochondria care about is their own survival. Still, their callous ways allowed life to develop as we know it.’
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