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Mom's genes may play part in how children age

Updated: Aug 22, 2013 03:06 PM
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THURSDAY, Aug. 22 (HealthDay News) -- A mother's genes can affect the aging process in her children, a new study in mice suggests.

One of the major factors in aging is the accumulation of various kinds of changes that occur in mitochondria, which are the so-called power plants of cells.

Mitochondria have their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process. Many mutations in the mitochondria gradually disable the cell's energy production, the researchers explained.

Their experiments with mice showed that the aging process is influenced not only by the accumulation of mitochondrial DNA damage during an individual's lifetime, but also by the mitochondrial DNA inherited from their mothers. The findings suggest that people who inherit mitochondrial DNA with mutations from their mother may age more quickly.

However, experts note that research involving animals often fails to produce similar results in humans.

The study by the researchers at the Karolinska Institute in Sweden and the Max Planck Institute for Biology of Aging in Germany appears in the Aug. 22 issue of the journal Nature.

The study findings improve understanding of the aging process, prove that mitochondria play an important role in aging and show that it's important to reduce the number of mitochondrial mutations, according to study co-leader Nils-Goran Larsson, a professor at the Karolinska Institute and a principal investigator at the Max Planck Institute for Biology of Aging.

Study co-author Dr. Barry Hoffer noted that the "findings also suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging." Hoffer is from the department of neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine.

"There are various dietary manipulations and drugs that can up-regulate mitochondrial function and/or reduce mitochondrial toxicity," he said in a Case Western news release. "An example would be antioxidants. This mouse model would be a 'platform' to test these drugs/diets," explained Hoffer, who is also a visiting professor at the Karolinska Institute.

More information

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