Now some scientists are going even further and asking whether cellular aging in any way relates to physiological aging. Some recent studies suggest that, at least in some tissues, the two might be connected. As early as the 1930s Barbara McClintock and Hermann J. Muller proposed independently that something at the ends of chromosomes protected them from degradation and so helped maintain their integrity. When telomeres were first described in the late 1970s by Elizabeth Blackburn, now of the University of California at San Francisco, it became apparent that they were also necessary for the complete replication of the chromosome-with implications for aging. In 1991, Blackburn observed that the telomeres of most human cells become progressively shorter with each round of cell division.
Telomeres shorten progressively with each cell division, leading to cellular senescence.
Follow-up studies confirmed Blackburn's prediction. With successive cell divisions, the telomeres ultimately become so short that chromosomal replication can no longer proceed. And if their chromosomes cannot replicate, cells become senescent and can no longer divide. This explains why most noncancerous human cells can only divide a finite number of times. Establishing a relationship between telomeric shortening and cellular senescence is one thing.