Progeria is an extremely rare genetic disorder (fewer than 1000 US cases occur per year) in which symptoms resembling aspects of aging are manifested at a very early age. Often present in humans and publically exposed by documentaries and charities like the Progeria Research Foundation many are fighting to find a way to reverse this disease’s progress. As such, this article demonstrates a study concerning research being done on Progeria through xenografts derived from mice. This new study suggests that, “four proteins can transform adult cells into embryonic-like ones” which effectively results in an ability to turn back the aging clock. According to researchers as of December 15, “partial reprogramming of cells within prematurely aging mice’s bodies extended the rodent’s average life span from 18 weeks to 24 weeks.” Even normal mice, without progeria-like symptoms of premature aging, seemed to benefit as well. Muscles and pancreas cells healed better in middle-aged mice who got these rejuvenation treatments in comparison to those that did not. This experiment demonstrates possible evidence that epigenetic marks (chemical tags on DNA and proteins that change with age, experience, disease and environmental exposures) are a driving factor of aging. A biologist at the Mayo Clinic in Rochester, Minnesota, Jan van Deursen, who studies diseases of aging, stated “It’s an inspiring paper.” Although he gave the paper an “A” for sparking imagination, he allotted lower marks for the practical applications of the study to human aging because it would involve gene therapy and could be risky. Furthermore, stating “It’s all cool, but I don’t see that it could ever be applied in medicine. We could be terribly wrong. Hopefully we are.” Clearly a bit of a pessimist, but always a realist, Jan van Deursen states the obvious. Just because the technique works in mice, further toxicity studies and research must be done before any experiments involving human patients take place. In regards to the specific molecular makeup of the genetic engineering it is as follows. The researchers reset the mice’s aging clock by genetically engineering the animals to make four proteins when the rodents were treated with the antibiotic doxycycline. These four proteins, Oct4, Sox2, Klf4 and c-Myc, are known as “Yamanaka factors” after Shinya Yamanaka. The article provided detail that Yamanaka is “The Nobel Prize‒winning scientist demonstrated in 2006 that the proteins could turn an adult cell into an embryonic-like cell known as an induced pluripotent stem cell, or iPS cell” in order to demonstrate his significance and therefore the validity of this new research.
This new research into Progeria-like conditions in mice is extremely influential on our society. Although a rare disease, those affected by Progeria have their lives, and lifespans, defined by it. By performing this incredible research there is a hope that those with the debilitating conditions may someday be “normal.” It is terrible to think that children as young as eight have arthritis and other old age-related problems in the first decade of their life. And, to make it even worse, many of these children have extremely short lifespans, living an average of just 13 years old. This is incredibly impactful, especially to us in high school. Most of us are 16, 17, or 18 and we often forget how fortunate we are that we are healthy. Science can be a wonderful thing and hopefully this study proves to be a step closer to a cure of medication to slow the process of aging caused by Progeria.
The author of this article, Tina Hesman Saey, overall wrote a wonderful piece. I particularly enjoyed her use of quotes as well as her evident in-depth research about the topic. She included key details such as listing the “Yamanaka factors” and giving a little background on Shinya Yamanaka, whom they were named after. In addition, Saey used a great graph that displayed the increased survival rate for mice treated with the cell reprogramming. This graph allowed any reader to understand the study even without advanced biological knowledge. However, there are a few areas upon which Saey could improve. Primarily, I felt there could have been more background on Progeria. I, for example, in the beginning of this review, wrote about the significance of the study in regards to the rare disease. Saey however just jumped right into the science. I believe her article would have been for effective had she appealed to the aristotelian appeal of “pathos” or emotion. Additionally, I felt Saey could have added more about the details of the experiment. This is because besides stating and analyzing the proteins in depth, I felt I did not know the procedure. Of course, Saey is not expected to go incredibly in depth, but a few sentences about how the cell reprogramming would have been appreciated. By simply researching how the study occurred procedurally and adding some information about progeria, Saey’s article would have been more effective and therefore more comprehensible for the reader.
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