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Category: genetics – Page 238

The researchers looked at multiple measures of cellular age. First, they used the epigenetic clock, where chemical tags throughout the genome indicate age. Secondly, they looked at the transcriptome, all the gene readouts produced by the cell. By these two measures, the reprogrammed cells matched the profile of cells that were 30 years younger, compared to reference data sets. In other words, cells from a woman of 53 now appeared like those of a woman aged 23.

The potential applications of this technique are dependent on cells not only appearing younger, but functioning like young cells too. Fibroblasts produce collagen – a molecule found in bones, skin tendons, and ligaments, helping provide structure to tissues and heal wounds. In this study, the rejuvenated fibroblasts produced more collagen proteins compared to control cells that did not undergo the reprogramming process. Fibroblasts also move into areas that need repairing. Researchers tested the partially rejuvenated cells by creating an artificial cut in a layer of cells in a dish, seen in the video below. The treated fibroblasts moved into the gap faster than older cells. This is a promising sign that one day this research could eventually be used to create cells that are better at healing wounds.

In the future, this research may also open up other therapeutic possibilities; the researchers observed that their method also influenced other genes linked to age-related diseases and symptoms. The APBA2 gene – associated with Alzheimer’s, and the MAF gene with a role in the development of cataracts – both showed changes towards youthful levels of transcription.

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Findings could lead to targeted approach for treating aging.

Research from the Babraham Institute has developed a method to ‘time jump’ human skin cells by 30 years, turning back the aging clock for cells without losing their specialized function. Work by researchers in the Institute’s Epigenetics research program has been able to partly restore the function of older cells, as well as rejuvenating the molecular measures of biological age. The research is published today (April 7, 2022) in the journal eLife and whilst at an early stage of exploration, it could revolutionize regenerative medicine.

What is regenerative medicine?

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At roughly 70 years human age, the mice looked elderly and unremarkable. Yet hidden underneath was a youthful cellular clock, turned back in time based on a Nobel-Prize-winning strategy. It’s also the latest bet for finding the fountain of youth, backed by heavy-hitter anti-aging startups in Silicon Valley.

At the center is partial cellular reprogramming. The technique, a sort of gene therapy, forces cells to make four proteins, collectively dubbed the Yamanaka factors. Like erasers, the factors wipe a cell’s genetic history clean, reverting adult cells—for example, skin cells—to a stem cell-like identity, giving them back the superpower to turn into almost any type of cell.

The process isn’t all-or-nothing. In a twist, scientists recently found that they can use the factors to rewind a cell’s genetic history tape rather than destroying it altogether. And if they stop at the right point, the cell dramatically loses its age, becoming more youthful but retaining its identity. The results spurred a wave of interest in moving the therapy to humans, with Calico Life Sciences—a sister company to Google—and Altos Labs, backed by Jeff Bezos, in the race.

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Summary: 15 newly discovered “hotspots” in the genome that either speed up or slow down brain aging could be new targets for the development of Alzheimer’s medications and therapies for other brain disorders.

Source: USC

Researchers from a USC-led consortium have discovered 15 “hotspots” in the genome that either speed up brain aging or slow it down—a finding that could provide new drug targets to resist Alzheimer’s disease and other degenerative brain disorders, as well as developmental delays.

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The only way life extension would remain financially out of reach is if we vote ourselves into a dystopia.

Dr David Sinclair explains why aging therapies will be eventually affordable to us in this clip.

David Sinclair is a professor in the Department of Genetics and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School, where he and his colleagues study sirtuins—protein-modifying enzymes that respond to changing NAD+ levels and to caloric restriction—as well as chromatin, energy metabolism, mitochondria, learning and memory, neurodegeneration, cancer, and cellular reprogramming.

Continue reading “Why AGING Therapies Will Be AFFORDABLE To Us | Dr David Sinclair Interview Clips” | >

Remember He Jiankui, the Chinese scientist who shocked the world when it emerged in late 2018 that he had used CRISPR to tinker with the genetic code of IVF embryos, leading to the birth of twins who are likely the world’s first genetically modified humans?

The news led to a broad outcry among scientists, ethicists and regulators, not the least because experts in the field later found the experiment to be tainted by “egregious scientific and ethical lapses.”

Long story shot, China ended up imprisoning He, who also lost his research position at the Southern University of Science and Technology in China — but now MIT Technology Review, which first broke the news of the experiment back in 2018, reports that he’s out of prison and even answered his cell phone for a brief call.

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Scientists at The University of Texas at Austin have redesigned a key component of a widely used CRISPR-based gene-editing tool, called Cas9, to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version, making it potentially much safer.

Other labs have redesigned Cas9 to reduce off-target interactions, but so far, all these versions improve accuracy by sacrificing speed. SuperFi-Cas9, as this new version has been dubbed, is 4,000 times less likely to cut off-target sites but just as fast as naturally occurring Cas9. Bravo says you can think of the different lab-generated versions of Cas9 as different models of self-driving cars. Most models are really safe, but they have a top speed of 10 miles per hour.

“They’re safer than the naturally occurring Cas9, but it comes at a big cost: They’re going extremely slowly,” said Bravo. “SuperFi-Cas9 is like a self-driving car that has been engineered to be extremely safe, but it can still go at full speed.”

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NOTE FROM TED: Research around aging discussed in this talk remains an ongoing field of study. Please do not look to this talk for health advice. TEDx events are independently organized by volunteers. The guidelines we give TEDx organizers are described in more detail here: http://storage.ted.com/tedx/manuals/tedx_content_guidelines.pdf.

Have you ever wondered how long you will live? And if so, how could you change that number to live drastically longer? The science might be in your favor: follow David Sinclair, Australian biologist and professor of genetics at Harvard University, as he shares his research on slowing and reversing the process of aging in mice, and how the same technology may someday be transferable to humans. David Sinclair, Australian biologist and professor of genetics at Harvard Universityhis insightful research into the science of age reversal and anti-aging medicine.

David Sinclair, Australian biologist and professor of genetics at Harvard Universityhis insightful research into the science of age reversal and anti-aging medicine. This talk was given at a TEDx event using the TED conference format but independently organized by a local community.

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a cardiac arrhythmia disorder associated with sudden death in young adults.

The findings expand possibilities for predictive risk scoring and provide new targets for therapeutic study, according to Alfred George, Jr., MD, chair and the Alfred Newton Richards Professor of Pharmacology and a co-author of the study.

“Prior to this work, there were only two genomic regions associated with Brugada syndrome risk that were identified by genome-wide studies. Data from the new study greatly expands this to 12 regions with a total of 21 genetic signals to better explain risk for Brugada syndrome,” George said. “The results also provide the basis for a polygenic risk score that can be used to assess risk in individuals.”

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A recent study published in Nature Genetics identified 10 new genetic regions associated with Brugada syndrome, a cardiac arrhythmia disorder associated with sudden death in young adults.

The findings expand possibilities for predictive risk scoring and provide new targets for therapeutic study, according to Alfred George, Jr., MD, chair and the Alfred Newton Richards Professor of Pharmacology and a co-author of the study.

“Prior to this work, there were only two genomic regions associated with Brugada syndrome risk that were identified by genome-wide studies. Data from the new study greatly expands this to 12 regions with a total of 21 genetic signals to better explain risk for Brugada syndrome,” George said. “The results also provide the basis for a polygenic risk score that can be used to assess risk in individuals.”

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