Why do we lose muscle mass with age? Scientists find one factor Premium

Understanding how deletion mutations in mitochondrial DNA contribute to aging can help delay age-related decline in mitochondrial function.

As we age, we lose bits of our genome in tissues such as the skeletal muscle and the brain. These losses, called deletion mutations, gradually erode the function of a cell component called the mitochondrion.

Muscle cells lacking a sufficient number of functional mitochondria to support their contractile function die and this causes a loss of muscle mass.

Gaining a better understanding of the process that causes deletion mutations might help us to prevent or at least delay it.

The overwhelmingly large fraction of our genome (DNA) resides in the cell’s nucleus. The rest, a mere five-millionth of the nuclear genome, is located in the mitochondrion. The age-related deletion mutations accumulate in the mitochondrial genome (mtDNA).

On November 27, researchers from the University of California Los Angeles and the University of Alberta, Canada, reported in the journal Genome Research that — together with the deletions — many mitochondrial genes also became aberrantly expressed.  Both deletion mutations and aberrant expression of mtDNA correlated with biological aging in humans and in rodents.

So although mtDNA represents only a small fraction of our genome, its deletion mutations appear to be a major trigger of the decrepitude that comes with old age.

Mitochondria are the powerhouses of the cell. They are where most synthesis of the compound adenosine triphosphate (ATP) happens. ATP is the energy source for all functions of a cell.