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Ageing process determined by mum's DNA

27 August 2013

By Matthew Thomas

Appeared in BioNews 719

Genetic mutations passed on from mothers may speed up the ageing process and shorten life expectancy, according to a study on mice.

Damage to the DNA in mitochondria – the chemical power sources of a cell – builds up over time and influences ageing. The study, published in Nature, shows that mutations in mitochondrial DNA (mtDNA) passed from mothers to children can lead to premature ageing.

Mice that did not inherit mutated mtDNA aged at a slower rate. Offspring inheriting mutations lived for 42.7 weeks on average, while the offspring of unaffected mothers lived an average of 7.5 weeks longer.

'In essence we studied ageing and ageing is caused by the multiple types of accumulated damage', senior author Professor Nils-Göran Larsson of Karolinska Institutet in Sweden and the Max Planck Institute for Biology of Ageing in Germany told the Independent.

'When we age, we accumulate damage to the mitochondrial DNA and we've shown that some of this damage is actually inherited from the mother', said Professor Larsson.

The researchers artificially introduced mtDNA mutations into families of mice. Offspring would inherit these mutations from their mother. Some families of mice in the experiment were also bred with a gene causing high levels of mtDNA mutations over the course of life. Other mouse families lacked this high rate of so-called somatic mtDNA mutations.

Mice with both the inherited and somatic mtDNA mutations not only aged prematurely and lived shorter lives but also grew enlarged hearts and deformed brains.

Mitochondria are vital for providing energy to cells. Mitochondrial DNA mutates faster than the DNA in the nucleus of a cell. Over time, mtDNA is liable to become damaged, which may cause the mitochondria to malfunction, contributing to the ageing process.

The researchers said it remains unclear whether lifestyle choices such as diet or medication can lessen the damage to mtDNA.

'There are various dietary manipulations and drugs that can up-regulate mitochondrial function or reduce mitochondrial toxicity. An example would be antioxidants', said co-author Dr Barry Hoffer from Case Western Reserve University School of Medicine, USA.

'This mouse model would be a platform to test these drugs or diets'.

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