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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.

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.

ABOUT PETER DIAMANDIS

Peter is the founder and executive chairman of the XPRIZE Foundation, and has started over 20 companies in the areas of longevity, space, venture capital and education. He is also the New York Times bestselling author of several books, including his latest, Life Force, which he published early in 2020 with Tony Robbins.

Peter joined host Robert Glazer on the Elevate Podcast to discuss transformational changes needed in education, how the pandemic accelerated global trends, and the astonishing medical and health technologies he believes will be widely available, sooner than you think.

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.

The lethargy that many Alzheimer’s patients experience is caused not by a lack of sleep, but rather by the degeneration of a type of neuron that keeps us awake, according to a study that also confirms the tau protein is behind that neurodegeneration.

The study’s findings contradict the common notion that Alzheimer’s patients during the day to make up for a bad night of sleep and point toward potential therapies to help these patients feel more awake.

The data came from study participants who were patients at UC San Francisco’s Memory and Aging Center and volunteered to have their sleep monitored with electroencephalogram (EEG) and donate their brains after they died.

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The risk of morbidity and mortality increases exponentially with age. Chronic inflammation, accumulation of DNA damage, dysfunctional mitochondria, and increased senescent cell load are factors contributing to this. Mechanistic investigations have revealed specific pathways and processes which, proposedly, cause age-related phenotypes such as frailty, reduced physical resilience, and multi-morbidity. Among promising treatments alleviating the consequences of aging are caloric restriction and pharmacologically targeting longevity pathways such as the mechanistic target of rapamycin (mTOR), sirtuins, and anti-apoptotic pathways in senescent cells. Regulation of these pathways and processes has revealed significant health-and lifespan extending results in animal models. Nevertheless, it remains unclear if similar results translate to humans. A requirement of translation are the development of age-and morbidity associated biomarkers as longitudinal trials are difficult and not feasible, practical, nor ethical when human life span is the endpoint. Current biomarkers and the results of anti-aging intervention studies in humans will be covered within this paper. The future of clinical trials targeting aging may be phase 2 and 3 studies with larger populations if safety and tolerability of investigated medication continues not to be a hurdle for further investigations.

As age increases, so does the susceptibility to a series of chronic diseases which ultimately result in fatal endings. This is such a basic part of life that we rarely consider if there is anything we can do to postpone it. So far, the principal of “one-disease-one-treatment” has brought medical sciences far but this line of thought may soon be outdated when it comes to aging related conditions. It is like fighting a many-headed monster: If one condition is treated successfully, another emerges shortly after. This point is illustrated as eradicating the two leading causes of death (cancer and cardiovascular disease) extends mean life span by 3.3 and 4 years, respectively (Arias et al., 2013). Interestingly, the gain of treating multiple diseases combined exceeds the sum of these numbers.

Aging is the greatest risk factor for most diseases likely because as aging progresses, cells and tissue undergo a series of processes which result in gradually declining functionality, accumulation of damage, increased inflammation, and cell death. If these processes are reversable or treatable, all aging related chronical diseases may potentially be simultaneously treated—or postponed—and healthy aging could be achieved. This approach to treating aging itself could effectively treat chronic diseases among the world’s elderly, shifting from treating symptoms of aging to treating the cause of it. The fact that the number and proportion of elderly people (65 years) is growing in every country in the world underlines the relevance of this field of research (World Population Prospects — Population Division, 2021).

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.