Rethinking aging

Aging may not be caused by the accumulation of cellular damage, as a linkurl:prominent theory; suggests. Instead, the process may result from the deterioration of crucial developmental pathways, according to a study published tomorrow in Cell. "What we found is, I think, a different way to think about aging,"

By | July 24, 2008

Aging may not be caused by the accumulation of cellular damage, as a linkurl:prominent theory; suggests. Instead, the process may result from the deterioration of crucial developmental pathways, according to a study published tomorrow in Cell. "What we found is, I think, a different way to think about aging," linkurl:Stuart Kim; of Stanford University, main author of the study, told The Scientist. Kim and his colleagues used microarray gene chips to compare the genes being expressed in old and young C. elegans worms. They found 1254 genes that had different expression levels between the two groups. Almost all of these genes were developmental genes, necessary for proper intestinal and skin development in young worms. Kim's team also found a set of three transcription factors that had different expression levels in old worms. Two of the transcription factors -- called ELT-5 and ELT-6 -- were overexpressed in old worms. In turn, those two suppressed the expression of the third transcription factor -- called ELT-3. When ELT-3 was suppressed by the other two, the 1254 developmental genes were turned off. When the researchers blocked ELT-5 and ELT-6 in RNA interference experiments, ELT-3 expression went up, expression of the 1254 genes went up, and the worms lived 50% longer. This suggests that ELT-3 controls the continued expression of the developmental genes and might be the crucial link between aging and development. The researchers don't yet know what is pushing the transcription factors off balance, but their results suggest the culprit is not environmental factors of cellular damage such as oxidative stress. Exposing young worms to extreme oxidative stress didn't induce overexpression of ELT-5 and ELT-6. Kim's team is now looking into what unbalances the transcription factors in the first place. "People have been looking for gene expression changes in aging for a while," linkurl:Brian Kennedy,; from the University of Washington, told The Scientist. "To have it linked to a specific set of transcription factors is definitely a step forward; now there's a potential mechanism by which those changes in gene expression occur." According to Kim's theory, oxidative damage to cells still occurs over the course of an organism's lifetime, but it's not the only cause of aging. Oxidative damage is like rust accumulating on a car, said Kim. In this new model of aging, the rusting still happens, but internal mechanisms in the car -- like the gas or break pedals -- start breaking down. The proportion of aging attributed to environmental factors versus this internal mechanism is still a mystery, said Kim. "I think Dr. Kim is right to raise this hypothesis," Kennedy said. "A lot of linkurl:previous studies; were done at the organism level. Now people are trying to ask what specific tissues are these genes having their effect in that causes increased lifespan. So looking at tissue specificity [like intestine and skin development] is very informative." Kim added that an internal aging mechanism might explain why some organisms live for two weeks (C. elegans), some 80 years (humans), and some 200 (sea turtles). Under Kim's theory, different organisms' developmental pathways degrade at different rates. Depending on natural selection, degradation might set in much earlier for some organisms than others, he said. "That could be contributing to why some animals live to 40, and others to 80."


Avatar of: JOHN DUNNE


Posts: 6

July 24, 2008

Exactly what The Scientist blog ought to do...tease a broad audience about an upcoming specialized publication. Who cares about aging? All us mortals. Who is otherwise likely to miss one more C. elegans transcription factor regulation paper? Me.\n\nand one other opinion, it pleases me to think that regulation of aging is an active, selectable process. Organisms evolving their generational strategies is much more satisfying (at least to this organism) than the prospect of simply burning out at some inevitable rate. Making room for younger, brighter, more environmentally appropriate progeny is something I hope to continue to celebrate, even as my own demise looms.\n
Avatar of: anonymous poster

anonymous poster

Posts: 1

July 25, 2008

Since the Dr. Sinclair study on resveratrol's ability to switch on the anti-aging gene Sirt-1 was published in Nature a flood of somewhat dubious companies have sprung up selling resveratrol. Most of the dodgy ones have some variation of resveratrol in their name and sell only one or two products. One even makes his capsules in a rented house in Florida. Consumer Lab, an independent testing authority, evaluated the major brands and found many lacking in content and quality. The high potency ones that passed their evaluation were Transmax and Bioforte by www.biotivia. A product by Life Extension Co. failed badly with only 26% of the claimed resveratrol. Another brand, Revatrol, had virtually no trans-resveratrol in its supplement. The problem with some of the ones that did pass is that they contain less than 250mg of actual resveratrol which does not conform to the studies and is very expensive on a relative mg basis. The ConsumerLab test results are available on their web site.
Avatar of: null null

null null

Posts: 97

July 25, 2008

Genes Age, Too...They Are Organisms...\n\nYeast, worms and people may age by similar mechanisms\n\n(posted also in\n\n\nBecause genes are organisms and age too...\n\n\nA. Yeast, worms and people may age by similar mechanisms...\n\n\n\n"Nearly all organisms experience aging".\n\n\nB. And the organisms genes do not "experience aging"?\n\nRight you are. "Nearly all organisms experience aging". But why "nearly"?\n\nNot only yeast, worms and people. Also genes and the interdependent-genes-communes, genomes. These are organisms, too. It is their "lifehood" that makes us and all life forms "alive".\n\nBy plain common sense, my favorite scientific approach, they should also be "experiencing aging"...\n\n\nC. The aging of genes should be contributing to aging of organisms...\n\nSince genomes are cooperative communes of interdependent genes there are many genes that "modulate aging" to smaller or larger extent at various time-rates depending on circumstances and environment and.... various things happen to them or affect them and impair their functionalities and ....\n\nSuggesting,\n\nDov Henis\n
Avatar of: Milos Djekic

Milos Djekic

Posts: 1

July 25, 2008

Old hen comes from young egg, but we must not forget that young egg comes from old hen.\nOur cells are old not a few decades, but many generations, millions of years.\nFree radicals forget that young egg comes from old hen.\nThis article begins to touch this problem.
Avatar of: Stephen Levy

Stephen Levy

Posts: 1

July 25, 2008

Let's not forget that aging and death is integral and intrinsic to the evolution of life on this planet and that an organism's 'living' is a means for genes to complete their cycle of replication with progressive changes to fill every exploitable energy niche on the planet. As with most other systems of importance, there is likely redundancy so it strikes me as remarkable that interfering with only one such pathway can make a significant difference in life expenctancy. I would speculate that all up or down regulation of pathways that result in life extension, both current and to be discovered, are expressions of environmental impacts that would be interpreted by the organism as interfering with reproductive success- ie lack of energy or the cofactors to make use of that energy. To go beyond what could be a reasonable extension of life to ensure reproduction will require more than interference with pathways. In any case, such interference will have other impacts that would foster organism survival until the stress is resolved- both those we would desire and not.
Avatar of: BILL SPARKS


Posts: 4

July 25, 2008

for those who found the article informative you need to get a copy of sang-kyu park's alpha and gamma tocopherol study just published in the journal of nutrition..he used a similar assay method , high density olignucleotide arrays to observe changes in the aging brain and heart of mice. he found that 8523 of 45,037 transcripts changed significantly with aging brain . there was a 13.2 % inhibtion effect on the changed transciption factors by alpha tocopherol (500mg/kg) and 31.6 % inhibition by alpha + gamma tocopherol. gamma tocopherol is becoming a very hot topic in nutrtional is dominate isomer in foods . alpha is used in most dietary supplements. alpha has a higher unit of activity based upon USP in vivo assay methods .. the use of genetic methods to look at thousands of genes in one experiment and observe relationships opens a whole new world of sciences

Popular Now

  1. Opinion: Why I Published in a Predatory Journal
    News & Opinion Opinion: Why I Published in a Predatory Journal

    My “colleagues” and I at the fictitious Arthur Vandelay Urological Research Institute were surprised to find our bogus “uromycitisis” case report swiftly accepted, with only minor revisions requested.

  2. Consilience, Episode 3: Cancer, Obscured
  3. A History of Screening for Natural Products to Fight Cancer
  4. March for Science: Dispatches from Washington, DC