Vanderbilt University Medical Center researchers beleive that the discovery, which they are referring to as a 'biomarker' could help cosmetics companies develop more efficacious treatments for wrinkles, according to a new report in this month's Journal of Investigative Dermatology.
"There's a lot of interest in the pharmaceutical and cosmetic industries in developing products that will minimise or reduce certain signs of ageing," said James Sligh M.D., Ph.D., assistant professor of Medicine and Cell & Developmental Biology.
"The quantifiable biomarkers we've characterised could be useful for monitoring laboratory-simulated aging as well as potential drugs or therapies that alter the ageing process."
According to the research, the newly discovered biomarkers are changes to the DNA of cellular organelles called mitochondria. Mitochondria, which have their own DNA that is distinct from the DNA in the cell's nucleus, serve as the 'power plants' of the cell.
In turn they manufacture energy in the form of the molecule ATP and this energy generation includes a byproduct, which can damage the DNA present in mitochondria, Sligh said.
Scientists have been researching the part mitochondrial plays in skin cell ageing for years, centering on the decreased energy capacity as the mitochondrial mutates. In turn these mutations lead to conditions often associated with ageing, such as tumor development.
"We initiated this project with the idea that perhaps there was a specific mitochondrial DNA deletion signature that would be associated with tumor development in the skin," Sligh said.
The investigations then began to centre on patients with non-melanoma skin cancer. While studying samples the scientists discovered a panel of mitochondrial DNA deletions that was adjacent to the tumors, but not in the tumors themselves.
In turn the tumor samples were more likely to have full-length mitochondrial DNA, with point mutations rather than significant deletions, Sligh said. He also added that the mitochondrial DNA mutations in the tumor-free skin correlated with the ageing process.
The scientistific team will new place the newly identified deletion mutations into 'Mitomap,' a database of all known human mitochondrial genome changes.
"Unraveling the molecular clues as to why ageing cells function differently than young cells requires that we have molecular markers that we can track," Sligh said.
The Tennessee-based University team says that ultimately the newly identified biomarkers will provide another tool for studying mitochondrial damage that contributes to aging and cancer, and for screening compounds that prevent or reverse the process, a process that will inevitably impact approaches to anti-ageing treatments.