The award of this year’s Nobel Prize in Physiology or Medicine to Elizabeth H. Blackburn, Carol W. Greider, and Jack W. Szostak certainly came as no surprise. It was more a question of when, rather than whether, these three American scientists would win the coveted prize as their seminal collaborative research solved one of the greatest mysteries of our time — how chromosomes are protected from degradation as they divide continuously. The trio discovered that telomeres, the protective caps found at both ends of the chromosome, prevent it from degradation. While Dr. Blackburn and Dr. Szostak discovered that a unique DNA sequence in the telomeres, found in all organisms from amoeba to humans, protects the chromosomes, Dr. Blackburn and Dr. Greider found that the enzyme telomerase is responsible for restoring the length of the telomeres as they get worn out. But as humans grow older, the activity of the enzyme decreases, and hence its ability to maintain the length of the telomeres is compromised. This leads to a shortening of the telomeres, and ultimately to cellular senescence. While enzyme activity is high in the cells of newborns and stem cells, and is at a detectable level in many normal adult cell types, it is highly active in nearly 90 per cent of human tumours. Ironically, the higher activity in many malignancies seems responsible for maintaining the telomeres’ length and for delaying cellular senescence.
Apart from providing a powerful insight into the cellular mechanism, this scientific breakthrough has opened up a vast field of research aimed at finding ways to fight cancer. Several studies are in progress to find therapies and vaccines that would reduce the enzyme activity of cancer cells. Contrary to the earlier assumption that maintaining the level of telomerase activity in normal cells would delay the cellular aging process, and by extension, the aging of an organism, research has shown that the aging process is far more complex. One of Dr. Blackburn areas of collaborative research with interdisciplinary features reveals the effects of an external factor in telomere shortening. A landmark study found otherwise perfectly healthy pre-menopausal mothers of critically ill children who were more stressed, objectively and subjectively, than a control group had shorter telomeres. As a reviewer points out, the finding that prolonged and major stress, in and of itself, predicts worsening of some key cellular biomarkers of aging is of tremendous significance. Can meditation and other lifestyle interventions turn the clock back on telomere shortening of a morbid kind? We don’t know yet but there is an obvious advantage in exploring such interventions as they cost little in terms of money and time.
