Slowing the aging process using only antibiotics! By kurzweilai

“This research gives us hope not only for increasing longevity, but also for lengthening the period of adult vitality, and doing this with simple drugs such as antibiotics,” concludes Auwerx.

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.

Mitochondia: biological timekeepers

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.

Natural variations in mice

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.

Extending life in worms

Next, the team reproduced the protein variations in a species of nematode, Caenorhabidtis elegans. “By reducing the production of these proteins during the worms’ growth phase, we significantly increased their longevity”, says Auwerx.

The average life span of a worm manipulated in this way went from 19 to more than 30 days, an increase of 60 percent. The scientists then conducted tests to isolate the common property and determined that the presence of mitochondrial ribosomal proteins (MRPs) is inversely proportional to longevity.

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Posted By F. Sheikh

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