The following is an extract from an article, The Genetics of Ageing, which was written by Cynthia Kenyon and originally appeared in Nature in March 2010.
“For many years, molecular biologists interested in regulatory mechanisms did not study ageing, as the tissue decline associated with ageing suggested a passive, entropic process of deterioration that occurred in a haphazard way. We know now, however, that the ageing process, like so many other biological processes, is subject to regulation by classical signalling pathways and transcription factors. Many of these pathways were first discovered in small, short-lived organisms such as yeast, worms and flies, but a remarkable fraction turn out to extend lifespan in mammals as well. In this article, I describe these pathways and their regulation by environmental and physiological signals. I also discuss unsolved mysteries in the field and, finally, the outlook for drugs that could slow ageing in humans.
Many people assume that extending lifespan by slowing ageing would mean certain death from, say, Alzheimer’s disease. Instead, we are finding that mutations that slow ageing also postpone age-related disease. This link raises the possibility of combating many diseases all at once by targeting ageing, their greatest risk factor. Fascinating as this topic is, age-related disease is not the focus of this article. Rather, its focus is ageing itself.”
The article goes on to discuss pathways that regulate ageing.
“We now know that the longevity response to dietary restriction is actively regulated by nutrient-sensing pathways involving the kinase target of rapamycin (TOR), AMP kinase, sirtuins and insulin/insulin-like growth factor (IGF-1) signalling. Unexpectedly, which nutrient sensor is most important in extending lifespan in response to dietary restriction depends on the way that dietary restriction is imposed. In C. elegans, for example, one nutrient sensor extends lifespan in response to life-long food limitation, another in response to every-other-day feeding and a third if dietary restriction begins in middle age.”
and notes
“Slowing ageing might seem like an overwhelming challenge, as the decline is so pervasive. So it is noteworthy that when we extend the lifespans of laboratory animals, we do not have to combat individually all the problems of age, such as the declining muscles, the wrinkled skin and the mutant mitochondria. Instead, we just tweak a regulatory gene, and the animal does the rest. In other words, animals have the latent potential to live much longer than they normally do.”
For the full text of the article, which is well worth reading, click here.
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