Academic journal article Generations

Hype, Hope, and Reality: Telomere Length, Telomerase, and Aging

Academic journal article Generations

Hype, Hope, and Reality: Telomere Length, Telomerase, and Aging

Article excerpt

Telomeres are the ends of chromosomes. Repetitive DNA sequences at telomeres help conserve chromosome tips, and telomerase is an enzyme that induces this activity. These genetic factors have been at the center of much current discussion about "anti-aging" possibilities. In this article we quote from popular and scientific writing to illustrate the hype (the first two quotations) and the hope (the third) surrounding this issue. The purpose of the discussion that follows is to illuminate the reality.

THE HYPE

If we're willing to spend enough money on research, and if we spend it intelligently, I believe in 25 years we could see the creation of the first products that can postpone human aging significantly This would be only the beginning of a long process of technological development in which human lifespan would be aggressively extended. The only practical limit to human lifespan is the limit of human technology.

-October 1992, LIFE

Scientists for the first time have used a natural chemical (i.e. telomerase) to dramatically increase the lifespans of human cells in laboratory dishes and perhaps make them immortal, prompting a flood of speculation about the potential for slowing aging and extending human life.

The work provides long-awaited proof that an unusual chemical found in young cells provides key protection against cellular aging. The chemical is not normally present in adult cells. But when the scientists provided it to aging cells, the cells regained-and have continued to maintain-their youthful vigor.

-April 14, 1998, WASHINGTON POST

THE HOPE

It also seems clear that escape from replicative senescence and cell immortalization allows tumors to survive long enough to accumulate the many mutations seen in lethal cancers. Thus, measurements of telomere length and telomerase activity may be diagnostic markers of normal aging and cancer, respectively More importantly, if it is possible to delay telomere loss by transiently reactivating telomerase or by slowing the rate of telomere loss, we might be able to extend cell lifespan and delay the onset of replicative senescence, whereas inhibition of telomerase might provide a safe, universal, and effective anti-cancer therapy.

-C. B. Harley, 1995

THE REALITY

One of the first questions to be asked in the area of molecular gerontology was, Why do human fibroblast cells have a limited lifespan when grown in culture? The limited lifespan of these cells was discovered by Leonard Hayflick (i965) in the early ig6os, and once this concept was accepted, Hayflick and other cell biologists began to wonder whether this "cell senescence" could be used as a cellular model of aging. If so, cellular senescence could provide a powerful tool for understanding the molecular mechanisms of aging.

Although we still don't know exactly how the proliferative capacity of cells is limited, and the value of using cultured cells to model the aging of whole organisms remains controversial, some promising clues have been discovered. It is dear that the counting mechanism is an event counter, rather than a time clock. It is also clear that the characteristic of limited proliferative capacity is dominant over unlimited proliferative capacity (Pereira-Smith and Smith, 1998). The most plausible counting mechanism to have emerged since r965 consistent with these facts is based on a recently discovered phenomenon called telomere shortening (Harley et al., 1990). The remainder of this chapter summarizes what we currently know about the role of telomere length in aging and in cancer.

TELOMERES AND WHY THEY SHORTEN

The telomere shortening model is based on our biochemical knowledge about how a linear piece of Dim (a chromosome) is replicated. This knowledge predicts that each time cell division occurs, a little bit of DNA is lost from each end of the chromosome, thus shortening the DNa with each cell division. …

Search by... Author
Show... All Results Primary Sources Peer-reviewed

Oops!

An unknown error has occurred. Please click the button below to reload the page. If the problem persists, please try again in a little while.