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In 1984, University of California, Berkeley biology professor Elizabeth Blackburn and then grad student Carol Greider made the discovery that a quarter century later would win them the Nobel Pnze: They identified telomerase as the enzyme that protects the DNA in our chromosomes, in effect keeping our cells-and, to some degree, us-young. But telomerase is naturally produced only minimally and intermittently in some of our cells-just enough to grt. disposable us a maximum life span of around 120 years. Unless, that is, someone figures out how to increase the telomerase inside our bodies. Such tinkering with the basic machinery of life has been a theoretical possibility since the 1990s, when scientists
at the Bay Area biotech firm Geron and elsewhere identified the human telomerase gene.

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WALL STREET JOURNAL | By SHIRLEY S. WANG

It’s not quite the Fountain of Youth, but scientists have found a way to induce some of our cells to live forever.

The purpose isn’t to make people immortal, but rather to create therapies that might one day treat or delay the onset of disease, such as progressive eye disease, gastrointestinal disorders and cancer.

The research is focused on so-called telomeres, small bits of DNA that serve as protective coverings at the end of our chromosomes. These caps keep our chromosomes from unraveling, much like the plastic tips at the ends of shoelaces. When our telomeres are healthy, our cells remain healthy. But each time the cells divide, telomeres get shorter. When they reach a critically short length, as they do with age or the onset of certain diseases, cells lose the ability to divide and eventually die.

http://online.wsj.com/article/SB10001424052702304370304575151711477702710.html?KEYWORDS=telomeres

Inside chromosomes are telomeres that age as we age, and may serve as indicators of how long we’ll live.

L.A. Times |Cathryn Delude

Wrinkles may betray our age externally, but our cells divulge their age — and chronicle life’s toll — at the tips of our chromosomes. These tips, called telomeres, may also foretell our risk of early death.

Telomeres are the protective caps made of repetitive chunks of DNA that keep the rest of the gene-laden chromosome from disastrously unraveling. But they lose bits of themselves with each cell division, so over a lifetime, like a counter, telomeres shorten. Eventually, shortened telomeres send cells into senescence, a retirement-like state in which they no longer divide or remain active but do not die.

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NewScientist | Linda Geddes

COULD artificially raising levels of a key enzyme hold back the effects of ageing? It has long been a hope but now two lab experiments – one with human cells and one in animals – are providing the first evidence that this may actually be possible.

The enzyme in question is telomerase, which is present naturally in some mammalian cells. Its function is to maintain the protective caps called telomeres at the ends of our chromosomes, which unravel with each cell division as we get older. It has been suggested that this shortening triggers some of the negative effects of ageing at a cellular level. As a result, telomerase has been hailed by some as a potential elixir of life.

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SAUSALITO, Calif., Sept. 17 (UPI) — Shorter telomeres — DNA-protein complexes at the end of chromosomes — increase disease risk, but this may be reversed via lifestyle, a U.S. researcher says.

Dr. Dean Ornish of the Preventive Medicine Research Institute in Sausalito, Calif., and colleagues at the University of California, San Francisco, say telomere shortness in human beings is emerging as a prognostic marker of disease risk, progression and premature mortality.

Severe stress such as caring for a spouse or parent with dementia has been shown to shorten telomeres of the caregiver, but Ornish says that telomere shortening
is counteracted by the cellular enzyme telomerase — via lifestyle changes.

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The Oprah Winfrey Show

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