A microarray of genes involved in replicative senescence. Red represents increased expression of a gene in senescent cells compared to early passage proliferating cells; green represents decreased expression.

Laboratory of Dr. Stanley N. Cohen, Stanford University

Cells that were once vital and capable of dividing repeatedly to supply healthy new tissues lose that ability.

Replicative Senescence

Among all the biomedical riddles almost everyone would like to overcome, there’s the enigma of aging. We spend years struggling to grow up, enduring teenage angst, learning a trade, raising a family, coping with parenthood, only to reach the Golden Years burdened with declining energy, chronic ailments, failing vision, and finally dark oblivion. For this reason, improving end of life health has to be a major objective of gerontological research.

We humans, of course, are not alone. Nature has arranged life to emphasize successful reproduction, not successful aging. Discovering how and why we age is the challenge for basic biomedical research.

What’s clear is that for some reason, or various reasons, a phenomenon called replicative senescence occurs along with advancing age. Cells that were once vital and capable of dividing repeatedly to supply healthy new tissues lose that ability. They go into senescence (as if asleep), remaining alive but no longer rebuilding their assigned body parts. How and why this happens – and how to restart cellular growth – are under intense study.

There’s also strong focus on telomeres, the end-caps on chromosomes that keep the double helix from unraveling, and naked chromosome tips from binding to each other. And there’s the fascinating p53 gene – the guardian of the genome – which sits in every cell ready to repair damaged DNA, or if that fails, kill its host cell to prevent unrestrained growth from becoming cancer. Paradoxically, p53 – while it’s guarding the genome – also seems to play some unexplained role in premature aging.

Most anxiously awaited, of course, are useful treatments that lessen or eliminate the chronic diseases that make old age such a chore. Parkinson’s disease, Alzheimer’s disease and other neurodegenerative disorders – and the big one, cancer – are all on the list of major research targets that are linked to aging.


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