Researchers of a new study found that a person's aging process is affected not only by how quickly his or her cells change and degenerate but also by the genes acquired from the mother.
Aging occurs when the cells in our body begin changing and slowly degenerating. It is an accumulation of the various kinds of changes our body undergoes during our lifetime. However, researchers of a new study found that this degeneration of body cells is not the only thing that impacts a person's aging process.
The most important changes in the body that contribute to aging are the ones that take place in the mitochondrion, known as the cell's power plant. It is responsible for generating most of the cell's supply of ATP, which is used as a source of chemical energy.
"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," said Nils-Göran Larsson, Ph.D., professor at the Karolinska Institutet, in a press release. "Many mutations in the mitochondria gradually dis-able the cell's energy production."
This is the first study, which found that aging is not only impacted by the accumulation of mitochondrial DNA damage during a person's lifetime, but also by the DNA a person inherits from his mother. People inherit both normal and damaged DNAs from their mother. Researchers found that mild DNA damage transferred from the mother contributes to the aging process of a person.
Further studies need to be conducted on whether it is possible to affect the degree of mDNA damage through lifestyle intervention. Findings of this study confirm that mitochondria play an important role in the aging process and the need to reduce the number of mutations.
"These findings also suggest that therapeutic interventions that target mitochondrial function may influence the time course of aging," said Barry Hoffer, M.D., Ph.D., a co-author of the study from the Department of Neurosurgery. "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."
