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Academic Journal
Main Category: Genetics
Also Included In: Biology / Biochemistry
Article Date: 24 Aug 2013 - 1:00 PDT

Scientists say that the process through which we age is determined not only by the changes we go through in our lifetime, but also by the genes we get from our mothers, according to a study published in the journal Nature.

Researchers from Karolinska Institute and the Max Planck Institute for Biology of Aging, say that the aging process appears to be very dependent on the power plant of each cell in the body - the mitochondrion.

The mitochondrion is located within the cell and is responsible for producing the cell's supply of Adenosine 5'-triphosphate (ATP) - a source of chemical energy.

Nils-Göran Larsson, professor at the Karolinska Institute and principal investigator at the Max Planck Institute for Biology of Aging, explains:

"The mitochondria contains their own DNA, which changes more than the DNA in the nucleus, and this has a significant impact on the aging process."

He adds: "Many mutations in the mitochondria gradually disable the cell's energy production."

The researchers generated a series of inbred mice in order to study the role of mitochondrial mutations in aging. They add that mice tend to transmit low levels of DNA mutations through a germ line.

Mitochondrial DNA (mDNA) damage can build up over a person's lifetime, according to the researchers. But this latest study has found that mitochondrial DNA damage can actually be passed on from our mothers.

Mutated DNA 'speeds up aging process'

Using MRI scanning, the scientists were able to detect levels of mutated DNA in the mitochondria of the inbred mice, which sped up their aging process.

Prof. Larsson says:

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

The researchers say they are, as of yet, unaware of a way mitochondria DNA damage can be affected through lifestyle intervention.

But they add that the study also showed how even low levels of passed on mutated mitochondria DNA can have developmental effects and lead to brain deformities.

"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 is important to reduce the number of mutations," adds Prof. Larsson.

Dr. Barry Hoffer, of the Department of Neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine, notes that the findings also call for the development of potential treatments that target mitochondrial function influencing 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 or diets," he adds.

The study authors say that further research will be conducted on mice, as well as fruit flies, to determine whether lifespan can be increased by reducing the number of mutations.

Written by Honor Whiteman

Copyright: Medical News Today
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