We would all be lucky to live to 105 years old. Anyone who’s been alive for a full century (plus five years) certainly has a lot of stories to tell. Now, a fascinating new study has discovered that people who live to see such advanced ages show a “unique genetic background” that appears to make their bodies more adept at repairing DNA. Did modern science just discover the genetic secret to a long life?
Why do some people live longer than others?
Participants aged 105-110 years old, dubbed individuals with “extreme longevity,” allowed researchers to decode and analyze their genomes. Study authors say this is the first research project of its kind.
“Aging is a common risk factor for several chronic diseases and conditions,” explains first study author Paolo Garagnani, Associate Professor at the Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Italy. “We chose to study the genetics of a group of people who lived beyond 105 years old and compare them with a group of younger adults from the same area in Italy, as people in this younger age group tend to avoid many age-related diseases and therefore represent the best example of healthy aging.”
More specifically, the genes of 81 semi-supercentenarians (ages 105+) and supercentenarians (those aged 110 years+) were compared to the genes of a group of 36 healthy people with an average age of 67. All participants were Italian.
That process led to the identification of five common genetic changes occurring between two genes called COA1 and STK17A. Many of the genetic fluctuations among long-living participants were linked to increased activity within the STK17A gene, which is integral to three distinct areas of cell life. Those are coordinating the cell’s response to DNA damage, encouraging damaged cells to initiate programmed cell death, and managing the amount of dangerous reactive oxygen species within a cell. This is quite notable because all three of those processes play a part in the development of various diseases, such as cancer.
Meanwhile, the COA1 gene helps facilitate “crosstalk” between the cell nucleus and mitochondria. Importantly, malfunctions within the mitochondria are considered a key element of aging.
“Previous studies showed that DNA repair is one of the mechanisms allowing an extended lifespan across species,” says senior study author Cristina Giuliani, Senior Assistant Professor at the Laboratory of Molecular Anthropology, Department of Biological, Geological and Environmental Sciences, University of Bologna. “We showed that this is true also within humans, and data suggest that the natural diversity in people reaching the last decades of life are, in part, linked to genetic variability that gives semi-supercentenarians the peculiar capability of efficiently managing cellular damage during their life course.”
It’s also important to mention that long-living participants had far fewer gene mutations than others. Usually, as we grow older our cells deal with more pesky mutations, which can lead to various problems, illnesses, and diseases. Individuals with these longevity genes, though, don’t appear to experience the usual mutation rate.
“This study constitutes the first whole-genome sequencing of extreme longevity at high coverage that allowed us to look at both inherited and naturally occurring genetic changes in older people,” says first study author Massimo Delledonne, Full Professor at the University of Verona.
“Our results suggest that DNA repair mechanisms and a low burden of mutations in specific genes are two central mechanisms that have protected people who have reached extreme longevity from age-related diseases,” concludes senior author Claudio Franceschi, Professor Emeritus of Immunology at the University of Bologna.
These discoveries are no doubt headline-worthy, but the mind races with possibilities moving forward as well. These findings are preliminary, but could they open the door toward a better understanding of human longevity in general? If so, would it be possible to extend these genetic advantages to the rest of us?
The full study can be found here, published in eLife.