THE SCIENCE
The Biologic Importance of Telomerase Activation

There are trillions of cells in our body - about ten trillion (10,000,000,000,000) to be more exact - and at any given time a great number are dividing furiously to keep us alive and well. The process is directed by genes sitting on the 23 pairs of chromosomes found in the nucleus of each and every cell. The chromosomes are long sequences of deoxyribonucleic acid (DNA) that contain all our genetic material. Each Chromosome consists of two matched strands of DNA twisted around each other to form a structure called the double helix. Most of us are familiar with this famous double helix from our Biology schoolbooks. It was first described by James Watson and Francis Crick more than a half a century ago. They were awarded the Nobel Prize in 1962 for their discovery.
Of particular interest to the scientists at T.A. Sciences are the ends of each chromosome known as telomeres. Telomeres have no genetic function; they are simply stretches of DNA that protect the rest of the chromosome. These little bits of DNA are critical to healthy cell function and have been likened to the plastic tips on shoe laces because they prevent the chromosome from fraying.
Shortened Telomeres Lead To Cellular Aging
However, telomeres become progressively shorter each time the cell divides. When they get too short, the result can be the various conditions associated with old age.
Scientists have only recently begun to understand the critical importance of shortened telomeres. Research has shown that people over sixty who have long telomeres experience greater heart and immune system health than their age-matched counterparts with shorter telomeres. Further proof of the drastic consequences of having degraded telomeres is exemplified by people born with unusually short telomeres that shorten at an accelerated pace. These unfortunate individuals prematurely suffer the effects of old age.
Clearly, there is a cause and effect relationship between shortened telomeres and the ravages of aging. The phenomenon of cellular aging was first noted by Professor Lenhard Hayflick in 1961. He discovered that cells cannot divide beyond a specific number of times. This is called the Hayflick Limit. Cells reaching this limit become old. Although Professor Hayflick discovered this important scientific principle, he had no idea what caused it.
It took almost thirty more years before the role telomeres play in cellular aging was finally understood. In 1990, Calvin Harley at McMaster University in Canada and Carol Greider at Cold Spring Harbor Laboratory in the U.S. (where James Watson is Chancellor) discovered that telomere shortening goes hand-in-hand with the aging process.
Telomerase Regenerates Shortened Telomeres
Concurrent with the study of telomeres there is a growing focus on telomerase, the human enzyme directly related to telomere length. When the telomerase enzyme is present it causes regeneration and restoration of shortened telomeres.
The presence of telomerase and the effects of telomere shortening are so basic to human aging and the maladies of old age that an entirely new branch of biology (Telomere Biology) has sprung up in the last two decades. Studying telomeres and telomerase is attracting some of the brightest scientific minds in the academic world.
In 1985, cell biologists Elizabeth Blackburn, now at the University of California in San Francisco, and her colleague Carol Greider, now at the Johns Hopkins University School of Medicine, discovered telomerase.
In 2006, Drs. Blackburn and Greider won the prestigious Lasker Basic Research Award "For the prediction and discovery of telomerase, a remarkable RNA-containing enzyme that synthesizes the ends of chromosomes, protecting them and maintaining the integrity of the genome." (http://www.laskerfoundation.org/) Notably, since 1962, 71 Lasker Award recipients have gone on to win a Nobel Prize, most within two years of receiving the Lasker Award.
Telomerase And Chromosome Ends
Telomerase is controlled by a gene called hTERT. The problem is that in almost all adult cells, the hTERT gene is turned off and the telomerase enzyme is substantially reduced or absent. Such cells have no way to regain lost telomere length. If only there were a way to turn on the hTERT gene and keep cells dividing and healthy.
Fortunately nature has produced a natural molecule that supports the maintenance of telomere length. This molecule, TA-65 comes from the Chinese herb Astragalus which has been used traditionally in China for over a thousand years. When TA-65 is introduced into a cell, it has the extraordinary ability to support the continued function of the hTERT gene and activate telomerase.
Think about it: If shortened telomeres are the common denominator in many of the problems associated with aging, then making telomeres long again should be able to slow the signs of aging. Scientific evidence suggests that promoting telomere length helps to restore youthful cells.
References
- Ridley M. Genome: The Autobiography of a Species in 23 Chapters. New York City: HarperCollins, 1999.
- Siegel LJ. Are Telomeres the Key to Aging and Cancer? The Univeristy of Utah, Genetic Science Learning Center . 2006.
Ref Type: Electronic Citation
- Chan SR, Blackburn EH. Telomeres and telomerase. Philos Trans R Soc Lond B Biol Sci 2004; 359((1441)):109-121.
- Blackburn EH, Greider CW, Szostak JW. Telomeres and telomerase: the path from maize, Tetrahymena and yeast to human cancer and aging. Nature Medicine 2006; 12((10)):1133-1138.
- Dollemore D. Cech To Discuss 'Life at the End of the Chromosome'. National Institutes of Health. 2006.
Ref Type: Electronic Citation
- Zucchero T, Ahmed S. Genetics of proliferative aging. Exp Gerontol 2006; [Epub ahead of print].
- Cawthon RM, Smith KR, O'Brien E, Sivatchenko A, Kerber RA. Association between telomere length in blood and mortality in people aged 60 years or older. Lancet 2003; 361(9355):393-395.
- Fossel M. Telomerase and the aging cell: implications for human health. JAMA 1998; 279((21)):1732-1735.


