Researchers at Karolinska Institutet, Sweden and the Max Planck Institute for Biology of Ageing, Germany, found that ageing is determined not only by the accumulation of changes during our lifetime but also by the genes we acquire from our mothers.
The findings on mice may lead to new methods that target mitochondrial functions to slow down ageing in humans.
There are many causes of ageing that are determined by an accumulation of various kinds of changes that impair the function of bodily organs.
This structure is located in the cell and generates most of the cell's supply of Adenosine triphosphate (ATP) which is used as a source of chemical energy.
"The mitochondria contains their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the ageing process," said Nils-Goran Larsson, professor at the Karolinska Institutet and principal investigator at the Max Planck Institute for Biology of Ageing, and co-leader of the current study.
"Many mutations in the mitochondria gradually disable the cell's energy production," said Larsson.
"Surprisingly, we also show that our mother's mitochondrial DNA seems to influence our own ageing. If we inherit mDNA with mutations from our mother, we age more quickly," Larsson said.
"The study also shows that low levels of mutated mDNA can have developmental effects and cause deformities of the brain," said lead author Jaime Ross, at the Karolinska Institutet.
"Our findings can shed more light on the ageing process and prove that the mitochondria play a key part in ageing; they also show that it's important to reduce the number of mutations," said Larsson.
The study was published in the journal Nature.
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