Your mother's DNA affects how fast you age
How well we age depends in part on the genes we inherit from our mothers, according to a new study published in the journal Nature.
While stress and other life challenges can influence the pace at which we age, the study found that the aging process appears to be very dependent on the power plant of each cell in the body – specifically, the mitochondrion, which is located within the cell and is responsible for producing the cell's supply of Adenosine 5'-triphosphate (ATP), a source of chemical energy.
Researchers from Karolinska Institute and the Max Planck Institute for Biology of Aging conducted the study.
"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," explained Nils-Göran Larsson, a professor at the Karolinska Institute and principal investigator at the Max Planck Institute for Biology of Aging.
"Many mutations in the mitochondria gradually disable the cell's energy production," he added.
For the study, the researchers reported producing a succession of inbred mice in an effort to study how mitochondrial mutations influence the aging process, and they added that mice have a tendency to transmit low levels of DNA mutations through a germ line.
As the researchers explained, mitochondrial DNA (mDNA) damage can accumulate over time, but their study also discovered that mitochondrial DNA damage can be inherited from our mothers.
Using MRI scanning on the inbred mice in the study, the researchers were able to detect levels of mutated DNA in their mitochondria, which accelerated the rate at which they aged.
"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," said Larsson.
As of now, however, the research team admits to not knowing how mitochondria DNA damage can be affected through lifestyle intervention, although they noted that the study demonstrated how even low levels of inherited mDNA can affect development and result in 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," Larsson added.
As pointed out by Dr. Barry Hoffer of the Department of Neurosurgery at University Hospitals Case Medical Center and Case Western Reserve University School of Medicine, the results of the study also sheds light on the need to develop possible treatments for targeting mitochondrial function as it pertains to the aging process.
"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," said Dr. Hoffer.
According to the study authors, additional research will be conducted on both mice and fruit flies to find out if lifespan can be increased by reducing the number of mutations.
SOURCE: Journal Nature, "Germline mitochondrial DNA mutations aggravate aging and can impair brain development," August 2013 (doi:10.1038/nature12474).