Telomere enzyme a likely key to longevity

Study gives mice a longevity boost without high cancer risk

A new experiment suggests that the enzyme telomerase can extend the lifespan of mice by about 26 percent.

Some cells can keep dividing forever, essentially becoming immortal thanks in part to telomerase. But evidence for whether this enzyme affects aging and longevity in larger organisms such as people has been muddled and contradictory.

While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control — that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors.

Reporting in the Nov. 14 Cell, researchers in Spain engineered mice to have not only an extra copy of the gene for telomerase, but also extra antitumor genes to combat the enzyme’s cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes, the team reports.

“These observations demonstrate the anti-aging effects of telomerase in … living organisms,” Maria Blasco of the Molecular Oncology Program at the Spanish National Cancer Research Center in Madrid and her colleagues write in the report.

Telomerase lengthens telomeres — the “caps” on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. After a certain number of divisions, the telomeres in the daughter cells become too short and the chromosomes start to degrade, thus preventing the cells from dividing any further. So this shortening of telomeres places a limit on the number of times that most body cells can divide, the so-called Hayflick limit.

Telomerase enables the cell to divide indefinitely by adding back the bit of telomere lost during each cell division, essentially keeping the fuse from burning. Previous research has shown that adding an active copy of the telomerase gene to human cells causes those cells to surpass the Hayflick limit and apparently divide without end. But people with longer telomeres don’t necessarily live any longer than people with short telomeres do, so evidence for a link with lifespan has been fuzzy.

Leonard Hayflick, the biogerontologist who in 1961 discovered the limit on cell division that bears his name, says he agrees that the new research shows that telomerase can affect longevity in mice. But he doubts the scientists’ claim that the enzyme affects the actual rate of aging.

The problem, Hayflick says, is how to measure that rate. Blasco’s team tested a series of traits that might be thought of as associated with aging: whether the mice had enough coordination to walk across a rope, the health of the mice’s skin and small intestines, the mice’s sensitivity to insulin and glucose, concentrations of insulinlike growth factor-1 in the blood and, of course, average telomere length. In each of these cases, mice with the extra telomerase gene performed more like youthful mice than those with only the anti-tumor genes. But these tests may or may not reflect the actual rate of aging, Hayflick says.

“They’re about as bad as looking at gray hair,” says Hayflick, who is a professor of anatomy at the University of California, San Francisco School of Medicine. “Look at me. I’m 80 years old and my hair’s still black.”

A lack of reliable, agreed-upon ways to measure the rate of aging is a problem for the whole field of aging research, Hayflick says, not just for this study.

Longevity — how long an animal lives — is less ambiguous. While the question still is not settled, Hayflick says, “A strengthening case has been made on the role of telomeres in affecting longevity.”

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