A thousand seemingly insignificant things change as an organism ages. Beyond the obvious signs like graying hair and memory problems are myriad shifts both subtler and more consequential: Metabolic processes run less smoothly; neurons respond less swiftly; the replication of DNA grows faultier.
But while bodies may seem to just gradually wear out, many researchers believe instead that aging is controlled at the cellular and biochemical level. They find evidence for this in the throng of biological mechanisms that are linked to aging but also conserved across species as distantly related as roundworms and humans. Whole subfields of research have grown up around biologists’ attempts to understand the relationships among the core genes involved in aging, which seem to connect highly disparate biological functions, like metabolism and perception. If scientists can pinpoint which of the changes in these processes induce aging, rather than result from it, it may be possible to intervene and extend the human life span.
So far, research has suggested that severely limiting calorie intake can have a beneficial effect, as can manipulating certain genes in laboratory animals. But recently in Nature, Bruce Yankner, a professor of genetics and neurology at Harvard Medical School, and his colleagues reported on a previously overlooked controller of life span: the activity level of neurons in the brain. In a series of experiments on roundworms, mice and human brain tissue, they found that a protein called REST, which controls the expression of many genes related to neural firing, also controls life span. They also showed that boosting the levels of the equivalent of REST in worms lengthens their lives by making their neurons fire more quietly and with more control. How exactly overexcitation of neurons might shorten life span remains to be seen, but the effect is real and its discovery suggests new avenues for understanding the aging process.
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