Marking the first time that people with so-called extreme longevity have had their genomes so highly decoded, this offers insight into why they live so long. It also offers hints as to how they manage to avoid age-related diseases.
“Aging is a common risk factor for several chronic diseases and conditions,” first author Paolo Garagnani, associate professor at the Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Italy, said in a press release. “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.”
The research team gathered 81 participants ages 105 years or older — referred to as semi-supercentenarians — and participants 110 years old or older — called supercentenarians. The participants were from various places in the Italian peninsula. Researchers compared them with 36 healthy people who were on average 68 years old and from the same region.
Blood samples were obtained from all the participants. Researchers searched for differences in the genes in the older and younger group. To do so, they conducted whole-genome sequencing before cross-checking their new results with genetic data from another previously published study. That prior study examined 333 Italian people over 100 years old and 358 people who were around 60 years old.
In the 105 and 110-plus age groups, five common genetic changes were found to occur more frequently. The same variants were found in people over 100 in the cross-checked data.
The genetic changes that occurred most often were found in a gene involved in three areas important to cell health. They include stimulating damaged cells to undergo programmed cell death, regulating the cell’s response to DNA damage and managing how many dangerous reactive oxygen species are inside a cell. Such processes are involved in initiating and growing many diseases, including cancer.
“Previous studies showed that DNA repair is one of the mechanisms allowing an extended lifespan across species,” said 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.”
In studying various naturally occurring mutations that people in the age groups experience, researchers discovered people 105 or 110 and older had a much lower burden of mutations in six of the seven genes tested.
“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,” senior author Claudio Franceschi, Professor Emeritus of Immunology at the University of Bologna concluded.
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