New findings from the Mayo clinic may lead to the ability to one day extend human life span’s by up to 30%.
Is there a way that a human’s lifespan could be extended? This seems to be a gigantic question that many scientists have been trying to unearth. Even though this has been quite a challenge for scientists, it seems like there is a glimmer of hope. This is after researchers at Mayo Clinic came up with an intelligent genetic engineering that can expand the lifespan of mice by 35 percent, and could possibly offer significant clues to extending the lifespan of human beings and potentially fight aging.
Led by cell biologists, Darren Baker and Jan Van Deursen, the researchers at Mayo Clinic College of Medicine have probably made the biggest advance in unlocking the complex issues involved in aging. According to the journal Nature, the scientists uncovered that a methodical removal of a particular category of living cells that are stagnant and cannot reproduce anymore can extend the lives of mice by 35 percent.
The researchers also noted that the removal of these unproductive cells will not only slow the process of aging in mice, but will also make the stay healthier for very long periods by discarding numerous age-related illnesses such as tumor formations and deteriorations that are related to the heart and kidney. Known as cellular senescence, this one-of-its-kind biological mechanism perfectly works as an ‘emergency brake’ that can stop damaged and non-productive cells that cause aging from dividing.
By eliminating the senescence cells, which are otherwise normal cells that have just stopped reproducing and dividing, the scientists were able to prevent the cells’ hyper-stress effects and possibly their unfettered reproduction and cancerous fears. Before unearthing the effects of senescence cells on the body, it had been a mystery what their actual effects on the body were.
However, thanks to the modern techniques of genetic engineering and the dedication of the Mayo Clinic towards this study, Baker, Deursen and their colleagues were able to set up an incisive experiment that categorically proved that the presence of senescence cells in the body had very negative consequences on the body in relation to aging.
Even though the results of the study have been positive on the mice, it has taken the scientists ultimately painstaking 7 years of highly careful experiments to reach this current level. Baker and his colleagues noted that senescence cells progressively produce a given tumor-suppressing protein molecule known as “p16Ink4a” that works towards shortening the body’s lifespan and speeding the commencement of age-related diseases and illnesses.
In striking this molecule in the mouse genetic code, the scientists came up with a genetic line of mice that had cells, which could under right conditions, produce a very dominant protein known as caspace when the mice’ bodies start producing p16Ink4a. By doing that, the caspace would automatically act as a self-destruct switch that would kill the unwanted senescence cells. So to ensure success, the scientists manufactured a drug that had caspace that when injected into the mice, would automatically kill senescence cells.
Noting one downside of the breakthrough was that some senescence cells, especially those in the colon and liver somehow managed to survive by avoiding the caspace-related drug. Again, wounds that resulted from the removed dead senescence cells healed slowly, given that senescence cells are known to play a big role in healing wounds and scar formations.
Now, What Next for Humans?
Although this research was based on the mice, many scientists across various medical fields were quick to applaud Mayo Clinic scientists for their breakthrough on the removal of senescence cells from the body. Many noted that this was a new beginning and the same study could be possibly translated to humans so that future generations would grow up in a world free of aging. Sounds perfect? Of course, but there will be many challenges to overcome before this aspirations can come to fruition.