The researchers note that using these techniques in humans would involve gene therapy, which raises ethical concerns. So, does this study showcase the next great leap forward in human longevity? Probably not. However, it’s not clear whether the treatment actually increased the longevity of the normally-aging mice.
Additionally, when the researchers applied the treatment to normal 1-year old mice, they found that it increased the capability for self-repair in muscle cells and pancreatic cells. The researchers found that this treatment, while unable to completely reverse the aging process, did allow the mice to survive longer: 24 weeks instead of 18 (the normal life expectancy of lab mice is 2-3 years). The trigger that they used was the antibiotic doxycycline: when the mice were dosed with the antibiotic (twice a week for this study), they produced the OSKM proteins which acted on the epigenetic marks. That’s why these researchers wanted to have a controllable trigger on the expression of the OSKM proteins in this study: they only wanted to use the proteins to strip some epigenetic marks from the cells, not go all the way to creating an iPS cell. These OKSM proteins have been used in the past to reprogram mouse cells into iPS cells, but that approach created tumors in the mice. IPS cells are extremely flexible embryonic-like cells that can become almost any other type of cell. These proteins – Oct4, Sox2, Klf4, and c-Myc – or OSKM for short, are also known as “Yamanaka factors” after the Nobel prize-winning Shinya Yamanaka, who discovered that these proteins could turn adult cells into induced pluripotent stem cells (iPS cells). The second required trait was the ability for the mice to produce four specific proteins when given an externally-controllable trigger. The first trait necessary was to show the same premature aging patterns as mice used as models to study Hutchinson Gilford Progeria Syndrome. The research took mice that had been genetically engineered to express two important characteristics. What if there was a way to strip these epigenetic marks from cells? Would that allow us to effectively reset the aging clock? A recent article in Science News talks about how researchers are working on answering that question through experiments on genetically engineered mice. The buildup of these epigenetic marks in our cells has been suspected as a driving factor of the aging process. These epigenetic marks are not governed by the genetic code, but are nevertheless capable of influencing the way genes are expressed. Epigenetic marks are cellular features that are made up of various amino acid and protein groups that can modify proteins within a cell. However, DNA is not the sole tool for implementing genetic instructions. DNA is fundamental for carrying genetic instructions for the growth and development of all known living organisms.
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