Today it seems that nearly every industry has a product claiming to combat aging: supplements, skin creams, workouts, foods, juice, yoga and even pillowcases (which claim to prevent the skin from losing moisture). But many of these inventions leave much to be desired once their claims are evaluated in an unbiased way, and they produce results that are often far from optimal.
In all of the claims that these products make, they often fail to include one important word: telomeres. As it turns out, telomeres are the most important word when it comes to the aging process because it is the shortening of their length that causes aging at the molecular level.
A recent discovery has shown that the enzyme that helps to rebuild telomeres has an “on-off” switch that controls whether telomeres are rebuilt or whether they deteriorate, promoting aging.
Timothy Tucey, a graduate student at the Salk Institute, and Vicki Lundblad, a professor in the molecular and cellular biology laboratory at the Institute, completed the research. Their finding is based on the fact that we depend upon our cells constantly dividing in order to keep organs such as the skin and liver functioning.
At each division, there is a profound change that takes place at the telomeres. The telomere is a region of repetitive nucleotide sequences located at both ends of a chromosome that serve as a buffer and protection during cell division. When DNA is replicated in preparation for the cell to divide, inevitably, the ends of the chromosomes are not preserved as well, and pieces may be lost. Telomeres allow the other genes on the chromatid to remain intact while the repeating region of the telomere itself is shortened. During the regular lifetime of a cell, the enzyme telomerase restore telomeres to their original lengths so that cells can continue to divide without any problems. This enzyme is so integral to the process that even a small change in the amount of telomerase can have a major impact on health. Telomerase activity decreases with age, allowing the ends of the chromosomes to be shortened and causing deterioration of DNA that holds necessary genes.
The finding at the Salk Institute concerns the activity of telomerase. They found that telomerase can be turned off and can disassemble, in contrast to the prior thinking that when telomerase is present, it is always working. This is a powerful realization, because this “on-off” switch controls the aging process, and if scientists can learn how to better work with it, they may be able to create treatments for the diseases typically associated with aging in many organs of the body.
The research was done on the same yeast used to make wine and bread, the fungus Saccharomyces cerevisiae. The species is an ideal organism for experimentation because it is single-celled and simple enough that it can manipulated easily, but it’s cellular processes are similar enough to mammals’ that the results can be used to understand human biology.
The scientists observed every stage of cell growth and division at an extremely high resolution so that it was apparent how the cell acts at different times in its life cycle. Specifically, they found that during cell replication, telomerase sits as an incomplete “preassembly” complex. After replication, it can return to the subunit and begin to rebuild deteriorating telomeres. After this process is finished, it disassembles until it is ready to be used again.
Though it may seem beneficial to have as much telomerase as possible in the body so that aging would never occur, cancer cells have shown that this is undesirable — they have recognized the benefit of telomeres that do not deteriorate, thriving on high telomerase levels.
If scientists can harness the power of the telomerase “on-off” switch, they may be able to help the body maintain an optimal telomerase level to keep the body healthier for longer.
