Lifeboat Foundation

From Cryonics To Living In Android Bodies here are 10 Ways Humans Will Become Immortal by 2050.

#Technology #Science #Immortal

Today we’re going to talk to the godfather of longevity, Aubrey de Grey, in the most ironic of settings – a pub in London. Over a beer, Aubrey explains why he believes that many of the typical health practices, such as drinking a lot of water, are myths and what he has discovered about slowing down the aging process. He reckons that in as little as 17 years, aging will no longer be a concern, and he supports this radical standpoint with some fascinating research. He talks about the idea that health is an integral part of longevity and that the seven pillars of aging need to be addressed simultaneously.

Human and animal longevity is directly bound to their health span. While previous studies have provided evidence supporting this connection, therapeutic implementation of this knowledge has been limited. Traditionally, diseases are researched and treated individually, which ignores the interconnectedness of age-related conditions, necessitates multiple treatments with unrelated substances, and increases the accumulative risk of side effects. In this study, we address and overcome this deadlock by creating adeno-associated virus (AAV)-based antiaging gene therapies for simultaneous treatment of several age-related diseases. We demonstrate the modular and extensible nature of combination gene therapy by testing therapeutic AAV cocktails that confront multiple diseases in a single treatment. We observed that 1 treatment comprising 2 AAV gene therapies was efficacious against all 4 diseases.

Comorbidity is common as age increases, and currently prescribed treatments often ignore the interconnectedness of the involved age-related diseases. The presence of any one such disease usually increases the risk of having others, and new approaches will be more effective at increasing an individual’s health span by taking this systems-level view into account. In this study, we developed gene therapies based on 3 longevity associated genes (fibroblast growth factor 21 [FGF21], αKlotho, soluble form of mouse transforming growth factor-β receptor 2 [sTGFβR2]) delivered using adeno-associated viruses and explored their ability to mitigate 4 age-related diseases: obesity, type II diabetes, heart failure, and renal failure.

Human aging has been reversed in a new medical breakthrough. John Iadarola, Brooke Thomas, and Greg Fahy break it down on The Damage Report. Follow The Damage Report on Facebook: https://www.facebook.com/TheDamageReportTYT/

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Tissue injury‐induced senescence is conserved in zebrafish. Fin amputation in adult fish lead to the appearance of senescent cells at the site of damage, and their removal impairs tissue regeneration…

Scientists successfully extended the average lifespan of mice by breeding them using embryonic stem cells with extra-long telomeres. The findings are significant because the researchers managed to extend lifespan without genetic modification, and they also shed light on the aging process and techniques that might someday slow it.

The study — published October 17 in Nature Communications — focuses on telomeres, which are stretches of DNA found at the end of chromosomes.

Because telomeres protect the genetic material inside chromosomes, they’ve been likened to the plastic tips on the ends of shoelaces. But telomeres have also been compared to bomb fuses, or “molecular clocks,” because they become shorter each time a cell divides, eventually shrinking so much that the cell dies or stops dividing. This shortening of our telomeres is associated with aging, cancer, and death.

Liz Parish, CEO of BioViva and Bill Faloon, Co-Founder of Life Extension talk about new breakthroughs in age reversal.

This interview was conducted, by Richard Peritz during RAADfest 2019, to be included in a broadcast on ABC TV-25 in Palm Beach Florida, and other networks nationwide.

A new study from the Johns Hopkins University School of Medicine shows that selectively removing senescent cells—cells that no longer divide—from brains with a form of Alzheimer’s disease can reduce brain damage and inflammation and slow the pace of cognitive decline. These findings, say researchers, add to evidence that senescent cells contribute to the damage caused by Alzheimer’s disease.

“Our results show that eliminating these cells may be a viable route to treat Alzheimer’s disease in humans,” says Mark Mattson, a professor of neuroscience at the School of Medicine and a senior investigator in the Laboratory of Neurosciences at the National Institute on Aging.

A report on the work was published April 1 in Nature Neuroscience.

With ageing, intrinsic haematopoietic stem cell (HSC) activity decreases, resulting in impaired tissue homeostasis, reduced engraftment following transplantation and increased susceptibility to diseases. However, whether ageing also affects the HSC niche, and thereby impairs its capacity to support HSC function, is still widely debated. Here, by using in-vivo long-term label-retention assays we demonstrate that aged label-retaining HSCs, which are, in old mice, the most quiescent HSC subpopulation with the highest regenerative capacity and cellular polarity, reside predominantly in perisinusoidal niches. Furthermore, we demonstrate that sinusoidal niches are uniquely preserved in shape, morphology and number on ageing. Finally, we show that myeloablative chemotherapy can selectively disrupt aged sinusoidal niches in the long term, which is linked to the lack of recovery of endothelial Jag2 at sinusoids. Overall, our data characterize the functional alterations of the aged HSC niche and unveil that perisinusoidal niches are uniquely preserved and thereby protect HSCs from ageing.