考研阅读精选：可以永葆青春？
Forever young?可以永葆青春？
Nov 5th 2011 | from The Economist
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BIOLOGISTS have made a lot of progress in understanding ageing. Theyhave not, however, been able to do much about slowing it down. A pieceof work reported in this week’s Nature by Darren Baker of the MayoClinic, in Minnesota, though, describes an extraordinary result thatpoints to a way the process might be ameliorated. Dr Baker has shown—inmice, at least—that ageing body cells not only suffer themselves, butalso have adverse effects on otherwise healthy cells around them. Ifsuch ageing cells are selectively destroyed, these adverse effects goaway.
The story starts with an observation that senescentcells often produce a molecule called P16INK4A. Dr Baker geneticallyengineered a group of mice that were already quite unusual. They had acondition called progeria, meaning that they aged much more rapidly thannormal mice. The extra tweak he added to the DNA of these mice was away of killing cells that produce P16INK4A. He did this by insertinginto the animals’ DNA, near the gene for P16INK4A, a second gene thatwas, because of this proximity, controlled by the same genetic switch.This second gene, activated whenever the gene for P16INK4A was active,produced a protein that was harmless in itself, but which could be madedeadly by the presence of a particular drug.
The resultswere spectacular. Mice given the drug every three days from birthsuffered far less age-related body-wasting than those which were not.Their muscles remained plump and effective. And they did not suffercataracts of the eye. They did, though, continue to experienceage-related problems in tissues that do not produce P16INK4A as they getold. In particular, their hearts and blood vessels aged normally. Forthat reason, since heart failure is the main cause of death in suchmice, their lifespans were not extended.
Regardless of thebiochemical details, the most intriguing thing Dr Baker’s resultprovides is a new way of thinking about how to slow the process ofageing—and one that works with the grain of nature, rather than againstit. Existing lines of inquiry into prolonging lifespan are based eitheron removing the Hayflick limit（an anticancer mechanism, it provides abackstop that prevents a runaway cell line from reproducingindefinitely, and thus becoming a tumour）, which would have all sorts ofuntoward consequences, or suppressing production of the oxidativechemicals that are believed to cause much of the cellular damage whichis bracketed together and labelled as senescence. But these chemicalsare a by-product of the metabolic activity that powers the body. If 4billion years of natural selection have not dealt with them it suggeststhat suppressing them may have worse consequences than not suppressingthem.
By contrast, actually eliminating senescent cellsmay be a logical extension of the process of shutting them down, andthus may not have adverse consequences. It is not an elixir of life, foreventually the body will run out of cells, as more and more of themreach their Hayflick limits. But it could be a way of providing ahealthier and more robust old age than people currently enjoy.
Genetically engineering people in the way that Dr Baker engineered hismice is obviously out of the question for the foreseeable future. But ifsome other means of clearing cells rich in P16INK4A from the body couldbe found, it might have the desired effect. The wasting and weakeningof the tissues that accompanies senescence would be a thing of the past,and old age could then truly become ripe.（596 words）
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