Mitochondria remain important throughout our lives. People with higher mitochondria function age 'better.'
Yet how mitochondrial defects lead to disease and aging has not been well understood. A paper published today in Aging Cell links mitochondrial dysfunction to the shortening of telomeres, specialized DNA sequences that act as caps that stabilize the ends of chromosomes, and premature aging.
The experiments were done with a type of mouse model called the Polg “mutator” in which the mice carry a specific genetic defect that accelerates the rate of mitochondrial DNA mutations.
“We also were able to show in humans how a single nucleotide change in mitochondrial DNA that’s specifically associated with poor function of mitochondria and causing pediatric mitochondrial disorders can accelerate aging,” said Taosheng Huang, MD, PhD, professor and chief of the Division of Genetics at University at Buffalo. “We found that reactive oxygen species due to poor function of mitochondria leads to increased DNA damage over time.”
The paper is the first to show that the mitochondrial DNA mutations in this model produce more rapid aging as demonstrated by the DNA clock, which estimates an individual’s biological age according to particular chemical markers in the DNA.
In a Nature Communications paper, the researchers also describe how a new technique they developed based on optogenetics can help restore normal function to abnormal mitochondrial interactions.
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