Our Aging Process Is Hastened Due To Maternal Genetics
August 22, 2013

Our Aging Process Is Hastened Due To Maternal Genetics

April Flowers for redOrbit.com - Your Universe Online

There are many reasons our bodies age. The process is determined by an accumulation of various kinds of cell damage that impair the function of bodily organs.

A new study from the Karolinska Institutet and the Max Planck Institute for Biology of Aging shows the damage occurring in the cell’s power plant – the mitochondrion – is of particular importance in the aging process and is determined by the genes we inherit from our mothers as much as the accumulated damage. The findings of the study were published in a recent issue of Nature.

"The mitochondrion contains its own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process," says Nils-Göran Larsson, professor at Karolinska Institutet and principal investigator at the Max Planck Institute for Biology of Aging. "Many mutations in the mitochondria gradually disable the cell's energy production."

The mitochondrion is located in the cell and generates most of the cell’s supply of ATP, which is used as a source of chemical energy.

This study represents the first time researchers have shown the aging process is influenced by DNA inherited from an individual’s mother, as well as the accumulation of mitochondrial DNA damage during a person’s lifetime.

"Surprisingly, we also show that our mother's mitochondrial DNA seems to influence our own aging," said Larsson. "If we inherit mDNA with mutations from our mother, we age more quickly."

DNA, whether normal or damaged, is passed down between generations. The question of whether it is possible to affect the degree of mDNA damage through lifestyle intervention, however, is yet to be investigated. For now, all the researchers know is mild mDNA damage transferred from the mother contributes to the aging process.

"The study also shows that low levels of mutated mDNA can have developmental effects and cause deformities of the brain," said Jaime Ross, PhD, at the Karolinska Institutet.

"Our findings can shed more light on the aging process and prove that the mitochondria play a key part in aging; they also show that it's important to reduce the number of mutations," said Larsson.

"These findings also suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging," said Barry Hoffer, MD, PhD, from the Department of Neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine. Hoffer is also a visiting professor at the Karolinska Institutet.

"There are various dietary manipulations and drugs that can up-regulate mitochondrial function and/or reduce mitochondrial toxicity. An example would be antioxidants. This mouse model would be a 'platform' to test these drugs/diets," said Dr. Hoffer.

The team plans to continue their research on mice, and expand to using fruit flies, to investigate whether reducing the number of mutations can extend their lifespan.