From Kurzweil AI:
Why is it that within a homogeneous population of the same species, some individuals live three times as long as others? EPFL researchers investigated this question and found the mechanism responsible for aging hidden deep within mitochondria. The were able to dramatically slow aging down in worms by administering antibiotics to the young, achieving a lifespan extension of 60 percent. The aging process identified by EPFL scientists takes place within organelles called mitochondria, known as the cellular powerhouses because they transform nutrients into proteins including adenosine triphosphate (ATP), used by muscles as energy. Several studies have shown that mitochondria are also involved in aging. The new EPFL research, done in collaboration with partners in the Netherlands and the U.S., pinpoints the exact genes involved and measures the consequences to longevity when the amount of protein they encode for is varied: less protein, longer life.
Laboratory mice in the BXD reference population typically live from 365 to 900 days. This population, which reflects genetic variations that occur naturally within a species, is used by many researchers in an approach known as “real-world genetics.” The benefit of working with this population in particular is that their genome is almost completely decoded. The team led by professor Auwerx, head of EPFL’s Laboratory of Integrative and Systemic Physiology, analyzed mice genomes as a function of longevity and found a group of three genes situated on chromosome number two that, up to this point, had not been suspected of playing any role in aging. But the numbers didn’t lie: a 50 percent reduction in the expression of these genes — and therefore a reduction in the proteins they code for — increased mouse life span by about 250 days.