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   Slowing the aging process -- only with antibiotics    
   Date:    
   May 22, 2013    
   Source:    
   Ecole Polytechnique Fédérale de Lausanne    
   Summary:    
   Scientists reveal the mechanism responsible for aging hidden deep within   
   mitochondria -- and dramatically slow it down in worms by administering   
   antibiotics to the young.    
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   FULL STORY    
      
   Johan Auwerx, Nestlé Chair in metabolism at EPFL, head of the Laboratory of   
   Integrative Systems Physiology (LISP), identified a group of genes whose   
   expression have an essential impact on longevity.    
   Credit: EPFL / Alain Herzog    
   Why is it that within a homogeneous population of the same species, some   
   individuals live three times as long as others? This question has stumped   
   scientists for centuries.    
      
      
   Now, EPFL researchers led by Johan Auwerx report in the journal Nature how a   
   mechanism in mice plays a determining role in longevity. And they go a step   
   further: by disrupting this mechanism using simple antibiotics in a population   
   of nematodes, or    
   roundworms, they can multiply lifespan by a factor of 1.6.    
      
   Mitochondia: biological timekeepers    
      
   The 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.    
      
   But that's not all they do. 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 US, 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.    
      
   Life-prolonging stress    
      
   The researchers concluded that a lack of MRP at certain key moments in   
   development created a specific stress reaction known as an "unfolded protein   
   response" within the mitochondria. "The strength of this response was found to   
   be directly proportional to    
   the life span," says Auwerx. "However, we noted that it was more pronounced if   
   the protein imbalance -- the reduction in MRP -- occurred at a young age. A   
   similar stimulation in an adult did not affect the worms' longevity."    
      
   What's more, the effect can be induced without genetically manipulating the   
   worms. "Exposure to certain readily available drugs inhibits ribosomal   
   function and thus causes the desired reaction," says Auwerx. In other words,   
   mitochondria are sensitive to    
   certain antibiotics, and the drugs can be used to prolong life.    
      
   Weary youngsters, vigorous old folks    
      
   Worms given antibiotics don't just live to ripe old age. At maturity, which is   
   13 days, they also moved twice as much as the others, according to Laurent   
   Mouchiroud, co-author of the study. "Around 20 days of age, the difference was   
   even more pronounced    
   because the 'control' individuals were often already in bad shape," he adds.    
      
   Using a software program modified by colleagues in EPFL's School of Computer   
   and Communications Sciences, Mouchiroud was able to follow, measure and   
   qualify the movements of many worms during their entire life, and he observed   
   that those who had    
   undergone drug treatment had superior endurance and energy. "In addition,   
   their muscles were in better shape," he reports.    
      
   However, individuals who were given the antibiotics early in life -- for   
   example in the larval stage -- also presented several less favorable   
   characteristics. Their development was slightly slower, they laid fewer eggs   
   and they had less energy at about    
   three days old, the outset of adult development. "This reminded us of the   
   vaguely flu-like state one gets right after the administration of a vaccine,"   
   says Monchiroud. "But the stress reaction in the mitochondria, and thus the   
   potential for increased    
   longevity, remained after the treatment phase."    
      
   All indications are that the observed and proven mechanisms in worms should be   
   similar to those in mice, and therefore possibly in other mammals. Further   
   studies are necessary, of course, to confirm that aging and its deleterious   
   effects could be slowed    
   down in mammals using antibiotics at precise moments in development.    
      
   "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.    
      
      
   Story Source:    
      
   The above post is reprinted from materials provided by Ecole Polytechnique   
   Fédérale de Lausanne. Note: Materials may be edited for content and length.    
      
   Journal Reference:    
      
   Riekelt H. Houtkooper, Laurent Mouchiroud, Dongryeol Ryu, Norman Moullan,   
   Elena Katsyuba, Graham Knott, Robert W. Williams, Johan Auwerx. Mitonuclear   
   protein imbalance as a conserved longevity mechanism. Nature, 2013; 497   
   (7450): 451 DOI: 10.1038/   
   nature12188    
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