Amrita, Aab-i-Hayat, Maha Ras, Aab-Haiwan, Dancing Water, Chasma-i-Kausar, Mansarover or the Pool of Nectar, Philosopher's stone and Soma Ras. These are all different names for the elixir of life, which is to give people a long life, keep them forever young and grant them immortality. From medieval times onward, people from all civilizations have been looking for such an elixir. Many in the past have claimed to have found that magic potion, but as we know now for sure no one has really achieved the desired results, at least not in the recorded history. As the hunt for the elusive substance continues, U.S. researchers may have found the answer to the “Elixir of Eternal Youth” in a breakthrough study that has managed to reverse the degeneration in mice, including brain damage and infertility, which could benefit people with signs of premature aging.
Image:
White Hare on the moon is making elixir of immortality
During a
recent research, Scientists from Havard University claim to have partially reversed age-related degeneration in mice, resulting in new growth of the brain and testes, improved fertility, and the return of a lost cognitive function for the first time in history. The research was led by Ronald dePinho who stated that they had achieved the milestone in aging science by engineering mice with a controllable telomerase gene.
Exactly how the telomerase gene helps in the degenerative process is something that needs to be understood in order to fully comprehend the importance of this study and its future implications for humans.
What are Telomeres?
A telomere can be found at the end of a chromosome, which acts like a cap or a bookend. Telomeres are protective DNA-protein complexes that prevent the chromosomes from fusing into rings or binding with other DNA. They play an important role in cell division. When the cell divides, it copies the exact DNA sequence from the chromosomes of the parent cell and in the process, a part of the telomere is clipped off (shortened) and donated to the DNA sequence at the end of the chromosome so that the copying is complete and accurate. Therefore, the telomeres get shortened each time a cell divides.
The Process of Aging
The length of the telomeres can get shorter and the essential parts of the DNA can get damaged in the replication process. The scientists have noted that cells stop replicating when telomeres are shorter. Normally in humans, it is found that a cell replicates about 50 times before the telomeres become too short. This limit is called the
Hayflick limit. Thus, the length of a cell’s telomeres can be used to determine the age of the cell and also how many more times it will replicate. Therefore, we can understand that longer telomeres will lead to longer life.
So, what can be done counteract the shortening of the telomeres, or even slow down the process? Well, there are two possibilities: encouraging less frequent cell division and the enzyme telomerase. Less frequent cell division can be accomplished by calorie-restricted diets, and by avoiding inflammation and injury. The enzyme “telomerase” adds chemical components to the ends of the telomere, which slows their erosion.
Scientists have been examining this enzyme “telomerase” as a possible “
Fountain of youth” substance. However, too much of telomerase can increase the risk of cancer, as there is no slowing down of cell division.
The U.S. researchers studied this telomerase enzyme by “creating mice with a telomerase switch by which they were able to generate prematurely aged mice. The switch allowed them to find out whether reactivating telomerase would restore telomeres and mitigate the symptoms of aging. The results showed a dramatic reversal of many aspects of aging, including reversal of brain disease and infertility.”
The human applications of this study still remain in the distant future, but the implications are tremendous. “We may be able to treat conditions like rare genetic premature aging syndromes in which the shortened telomeres play an important role, said DePinho, senior author of the report posted by the journal
Nature.
Original article posted at
Xomba.