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Aging as a way of survival

New discovery by CECAD Cologne: Persistent DNA damage induces longevity assurance program

A German-Dutch research team led by a scientist of the Excellence Cluster on aging and aging associated diseases of the University of Cologne (CECAD Cologne), Björn Schumacher reports in this week online publication of "Nature Cell Biology" that damage in the genetic material induces a longevity assurance program.

These findings have led to a new concept of aging as a way to survive: genetic programs that antagonize cancer formation keep the body alive despite accumulating damage in aging.

The genetic material (DNA) in every cell of the body is constantly under attack from extrinsic sources, such as for instance ultraviolet irradiation from the sun, or intrinsic sources, such as metabolic by-products. To fend off those damages cells have developed sophisticated DNA repair mechanisms. Incorrect repair, however, can lead to mutations and consequently to cancer.

But when damages are left unrepaired, they contribute to aging. The causal effect of DNA damage in aging is particularly apparent when damages accumulate already early in life as a result of congenital repair defects. These patients develop signs of premature aging already very early in life. Studying those diseases Dr. Schumacher's group has investigated why certain DNA repair defects lead to premature aging while other give rise to cancer development.

During the past two decades of aging research it has become apparent that aging is not only a result of accumulating damages that compromise the functioning of the body but also that there are genetic programs that regulate aging. Those programs regulate body growth but were also found to have a profound effect on longevity. Dr. Schumacher's team now found that specifically damage that persisted in expressed and thereby active genes induced the longevity assurance program. In cells of premature aging patients this program was already activated upon extremely low doses of damage. However, damages that persisted outside of active genes failed to induce longevity assurance mechanisms.

Interestingly, these observations precisely reflect the syndromes that are associated with defects in specific DNA repair systems. Patient who cannot repair damage in active genes age prematurely, whereas patients that cannot fix damages outside of active genes develop cancer but do not age prematurely. The scientists concluded that this program suppresses cancer development and thus keeps the body alive amid accumulating damage during aging. Dr. Schumacher's research group at the excellence cluster CECAD Cologne now aims at understanding how this "survival program" is activated to then develop novel therapeutic strategies that are aimed at preventing age-related diseases including cancer.

For further information, please contact:
Inge de Vries
PR-Manager, CECAD Cologne
Tel: 0221 - 470 4962

Merle Hettesheimer | idw
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