There are many causes of ageing, a process that is determined by an accumulation of various kinds of cell damage that impair the function of bodily organs. Of particular importance to ageing, however, seems to be the damage that occurs in the cell’s power plant – the mitochondrion.
“The mitochondrion contains its own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the ageing process,” says Nils-Göran Larsson, professor at Karolinska Institutet and principal investigator at the Max Planck Institute for Biology of Aging, and leader of the current study alongside Professor Lars Olson at Karolinska Institutet. “Many mutations in the mitochondria gradually disable the cells energy production.”
Now, however, the researchers have shown that the ageing process is attributable not only to the accumulation of mitochondrial DNA damage during a person’s lifetime, but also to their maternally inherited DNA.
“Surprisingly, we also show that our mothers mitochondrial DNA seems to influence our own ageing,” says Professor Larsson. “If we inherit mDNA with mutations from our mother, we age more quickly.”
Normal and damaged DNA is passed down from generation to generation. However, the question of whether it is possible to affect the degree of mDNA damage through, for example, lifestyle intervention is yet to be investigated; all that the researchers know now is that mild DNA damage is transferred from the mother and contributes to the ageing process.
“The study also shows that low levels of mutated mDNA may have developmental effects and help to cause deformities of the brain”, says Lars Olson, professor, Department of neuroscience.
“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,” says Professor Larsson.
The data published in the paper come from experiments on mice. The researchers now intend to continue their work on mice, and on fruit flies, to investigate whether reducing the number of mutations can extend their lifespan.
Jaime M. Ross, James B. Stewart, Erik Hagström, Stefan Brene, Arnaud Mourier, Giuseppe Coppotelli, Christoph Freyer, Marie Lagouge, Barry J. Hoffer, Lars Olson & Nils-Göran Larsson
Nature, online 21 August 2013, doi:10.1038/nature12474