Mystery of getting old and dying in new light

HAVE you ever thought why we die? This apparent naive question has a bearing with this year's Nobel Prize in Medicine. Of course you have thought of the question, and had the answers of heart attack, bronchitis, excessive bleeding, brain injury, etc. But how about a healthy person dying of old age? Smart you are with the answer, lack of hayat! What is hayat any way, in scientific term? In a sense, it is the number of times our cells, past the stem cell stage, undergo division. After I started growing from a fertilized egg in my mother's womb, I became two, four, eight, sixteen,…so on, identical cells, in successive divisions untill I reached a stage called stem cell (still present in my bone marrow). While growing up, the stem cells gave rise to all other types of cells making my limbs, skin, blood, brain, everything. And many of these cells keep on dividing fast at the early stages and more slowly as I am getting older. When vital cells become damaged and cannot be replaced by new ones, we die.
What happens when a cell divides? Cells have chromosomes made of two long threads (called strands) of DNA, intertwined like a rope, and then coiled onto itself like a spool of rope. 23 pairs of chromosomes of our cell, that contain all the information and instructions (called genes, largely dictating an individual's metabolism, build up behaviour, personality and most other charaters), get copied into two by a process called replication. Replication however fails to copy the total length of the DNA (or chromosome). So, after replication, the newly formed DNA is shorter than the original one. Now, this shorter DNA becomes part of a new cell. As the process of cell division continues, so does shortening of the new DNA. That means, the chromosomes in a new cell will have less DNA information than the original, causing a havoc leading to the cell's death.
To protect cells from information (or gene) erosion, nature has added many copies of a small stretch of DNA (sequence with no apparent information), one after another, at the end of chromosomes. Such ends are called telomeres. One copy of this telomeric DNA is lost in one cell division, but the cell remains healthy. In cancer, cells do not stop dividing because, among many factors, telomeres do not get shorter, for an enzyme called telomerase keeps on lengthening the telomere. While teaching "Fundamentals of Biology" at a local college recently, this beautiful telomere-telomerase business caught my attention. I am sure many molecular biologists in Bangladesh know a lot more about it. By killing telomerase, it may be possible to stop cancerous growth. On the contrary, by making telomerase stronger (or active), one may think of increasing the number of cell division and our longevity.
The Nobel Assembly in Sweden noted "Elizabeth Blackburn (UCSF) and Jack Szostak (Massachusetts General Hospital) discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation. Carol Greider (Johns Hopkins U) and Elizabeth Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase." Apparently, this is the first time that two women were awarded the prize together.

The writer is a well-known scientist and is currenty residing in the USA.