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We spoke with Dr Morgan Levine 2 years ago concerning the remarkable results that she and a team that included Dr David Sinclair had in restoring vision in mice. In that experiment, published in the journal Nature, older mice had tighter optic nerves crushed causing blindness. Then, using a combination of 3 of the 4 Yamanaka cellular programing factors, they were able to restore the mice’s vision by signally the underlying DNA, rebuilding what had been thought to be permanently damaged cells. This was a remarkable result, as it was restoring a damaged organ, essentially a part of the brain, to its original healthy state. When I spoke to Dr Levine about the next step in her research, she mentioned it may be a more complex organ, such as a mouse liver.

But they went further. In the January issue of Cell, Sinclair published results of their ability to age an entire mouse. That is, to signal the epigenome to cause the underlying mouse DNA to behave as if it were much older. They were also able to do the reverse: to take an older mouse and, by signaling the epigenome, bring its cells and organs to the state of a younger mouse. This is a truly remarkable achievement, and it seems to prove Sinclair’s theory that all of our cells have within them a pristine copy of their DNA, and that aging and the disease associated with aging are the result of miscues from the epigenome. If these miscues can be corrected then the cell can be restored, not to a blank stem cell but to its original condition.

A gene called BPIFB4, discovered in a population of centenarians, could help to reverse the aging of human hearts.

Carriers of healthy mutant genes, including people in so-called “blue zones” of the world, often live to 100 years or more and remain in good health. Cardiovascular complications are also rarer in these individuals. Scientists now believe that a gene may help to keep their hearts young by protecting them against diseases linked to aging.

Recent experiments conducted in Boston labs have shown reverse aging results among mice and could show similar results in people.

The combined experiments — which were conducted during a span of 13 years — published Thursday (January 12) in the scientific journal Cell reported that old, blind mice regained eyesight, developed smarter brains and built healthier muscle and kidney tissue, challenging the theory that DNA was the only cause of aging, as it proved that chemical and structural changes to chromatin played a factor without altering genetic code.

The research showed that a breakdown in epigenetic information caused the mice to age and the restoration of the epigenome reversed aging effects.

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This video explores aliens, mind uploading to other species (like in Avatar), genetic engineering, and future robots. Watch this next video about digital immortality: https://youtu.be/sZdWN9pbbew.
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💡 Future Business Tech explores the future of technology and the world.

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Source: Penn State

Understanding the neural interface within the brain is critical to understanding aging, learning, disease progression and more. Existing methods for studying neurons in animal brains to better understand human brains, however, all carry limitations, from being too invasive to not detecting enough information.

A newly developed, pop-up electrode device could gather more in-depth information about individual neurons and their interactions with each other while limiting the potential for brain tissue damage.

By ten years.


An anti-aging gene discovered in a population of centenarians has been shown to rewind the heart’s biological age by 10 years. The breakthrough, published in Cardiovascular Research and led by scientists at the University of Bristol and the MultiMedica Group in Italy, offers a potential target for patients with heart failure.

Associated with exceptional longevity, carriers of healthy mutant , like those living in blue zones of the planet, often live to 100 years or more and remain in . These individuals are also less prone to cardiovascular complications. Scientists believe the gene helps to keep their hearts young by protecting them against diseases linked to aging, such as .

In this new study, researchers demonstrate that one of these healthy mutant genes, previously proved particularly frequent in centenarians, can protect cells collected from patients with failure requiring cardiac transplantation.