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Can we become younger
One of the biggest puzzles in biology – how and why living cells age – continues to be a subject of investigation and research. An international team based at Newcastle University in NE England, along with researchers at the University of Ulm in Germany, has added some new evidence to the discussion.
The answer to the secret of aging is complex, and will not produce a magic anti-aging elixir in the foreseeable future. However, we can certainly expect better treatments to be created to fight age-related illnesses, such as diabetes and heart disease, not to mention things like wrinkle treatments, as a result of these new insights into the biochemical pathways involved in the aging process.
The research teams used a comprehensive systems biology approach, involving computer modeling, experiments using cell cultures and genetically modified mice to investigate why and how our cells age. They learned that old cells either stop dividing or self-destruct. Those cells that continue to divide, and the tissues they make up, show physical signs of deterioration, from wrinkling skin to a weakening cardiovascular system.
The research, which was recently published by the journal Molecular Systems Biology, shows that when an ageing cell discover serious damage to its DNA (caused by the wear and tear of life) the cell transmits specific distress signals that trigger the cell’s energy-producing power packs, the mitochondria, to manufacture free radical molecules, which in turn give the directions to the cell either to destroy itself or to stop dividing. The cells likely are programmed to do this to avoid allowing the damaged DNA to exist, as that causes cancer.
This study identifies additional major causative factors in addition to the role of telomeres, the protective tips on the ends of human chromosomes, which gradually become shorter as we grow older. This new information does not deny the importance of telomere shortening, but it illustrates that there are additional, vital factors, and the biology is very complicated.
These new findings indicate that we have a much better chance of making a successful attack on age-related diseases while at the same time avoiding the risk of unwanted side-effects such as cancer. We need to be very careful in researching new ways to prevent cellular aging, however, because the last thing we want to do is to help age-damaged cells to become malignant ones.
