Scientists at the Karolinska Institute and the Max Planck Institute for Biology of Aging report that aging is determined not only by the accumulation of cellular changes during our lifetime but also by the genes we acquire from our mothers. They published the results of the study in this week’s issue of Nature.

There are many causes of aging that are determined by an accumulation of various kinds of changes that impair the function of bodily organs. Of particular importance in aging, however, seems to be the changes that occur in the mitochondria.

“The mitochondria contain their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process,” explained Nils-Göran Larsson, Ph.D., professor at the Karolinska Institute and principal investigator at Max Planck. He led the current study along with Lars Olson, Ph.D., professor in the department of neuroscience at Karolinska. “Many mutations in the mitochondria gradually disable the cell’s energy production.”

The team’s work indicates that aging is influenced not only by the accumulation of mitochondrial DNA damage during a person’s lifetime, but also by the inherited DNA from their mothers.

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

The question, however, of whether it is possible to affect the degree of mDNA damage through lifestyle intervention is yet to be investigated. All that the researchers know now is that mild DNA 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,” added lead author Jaime Ross, Ph.D., at the Karolinska Institute.

“Our findings…also show that it’s important to reduce the number of mutations,” pointed out Dr. Larsson.

In addition, noted Barry Hoffer, M.D., Ph.D., a co-author of the study from the department of neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine, the findings suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging.

“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, who also serves as a visiting professor at Karolinska.

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.

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