Lifeboat Foundation

In 2006, scientists discovered a way to “reprogram” mature cells—adult skin cells, for example—into stem cells that could, in principle, give rise to any tissue or organ in the body. Many assumed it was only a matter of time until this groundbreaking technique found its way into the clinic and ushered in a regenerative medicine revolution.

Because the same patient would be both the donor and the recipient of cells derived from these so-called induced pluripotent stem cells (iPSCs), these cells would be seen as “self” by the immune system, the thinking went, and not subject to the problems of rejection that plague conventional transplants.

But iPSCs haven’t emerged as the cure-all that was originally envisioned, due to unforeseen setbacks, including the surprising preclinical finding that iPSC-derived cell transplants are often rejected, even after being reintroduced into the organism the cells were sourced from.

Each Cyclops had a single eye because, legend has it, the mythical giants traded the other one with the god Hades in return for the ability to see into the future. But Hades tricked them: the only vision the Cyclopes were shown was the day they would die. They carried this knowledge through their lives as a burden—the unending torture of being forewarned and yet having no ability to do anything about it.

Since ancient times, aging has been viewed as simply inevitable, unstoppable, nature’s way. “Natural causes” have long been blamed for deaths among the old, even if they died of a recognized pathological condition. The medical writer Galen argued back in the second century AD that aging is a natural process.

His view, the acceptance that one can die simply of old age, has dominated ever since. We think of aging as the accumulation of all the other conditions that get more common as we get older—cancer, dementia, physical frailty. All that tells us, though, is that we’re going to sicken and die; it doesn’t give us a way to change it. We don’t have much more control over our destiny than a Cyclops.

Today, we’re offering another discussion from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Today, we’re offering another talk from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Continue reading “Ronald Kohanski at Ending Age-Related Diseases 2019” »

Accelerating rejuvenation therapies to repair the damage of aging.…

Some people live much longer than average, partly thanks to their DNA. A study, published in the European Heart Journal, shows that it could be possible to replicate this genetic gift even for those lacking it. The way is now open to an innovative therapy model capable of preventing and fighting cardiovascular diseases through a real rejuvenation of blood vessels.

The study, conducted by the I.R.C.C.S. Neuromed, the I.R.C.C.S. Multimedica and the Department of Medicine, Surgery, and Dentistry, Salerno Medical School University of Salerno, with the support of the Cariplo Foundation and the Italian Ministry of Health, focuses on the gene that encodes the BPIFB4 protein. In the past, the same research group had identified a variant of this gene, the so-called LAV (“longevity associated variant”), which prevails in people over 100 years of age. Now, through a viral vector, researchers have inserted the LAV-BPIFB4 gene into the DNA of animal models particularly susceptible to atherosclerosis and, consequently, to cardiovascular diseases.

“The results—says Annibale Puca, coordinator of a research team at the University of Salerno and at I.R.C.C. MultiMedica—were extremely encouraging. We observed an improvement in the functionality of the endothelium (the inner surface of blood vessels), a reduction of atherosclerotic plaques in the arteries and a decrease in the inflammatory state.”

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For a core of longevity true believers, the time to intervene is now.

“How old are you?” James Clement wanted to know.

I turn 50 this year. There’s a new creaking in my bones; my skin doesn’t snap back the way it used to. It’s developed a dull thickness—you can’t tickle me at all. My gums are packing it in and retreating toward my jaw. These changes have been gradual or inexplicably sudden, like the day when I could no longer see the typed words that are my profession. Presbyopia, the ophthalmologist told me. Totally normal. You’re middle-aged.

Continue reading “The transhumanists who want to live forever” »

A new study outlines multiple ways in which epiblast stem cells can be reprogrammed back into a fully pluripotent state, paving the way for a better understanding of epigenetics.

The role of epigenetics

Epigenetics are why our cells, which all have the same DNA, differ in function. A bone cell has the same genetics as a nerve cell, but its epigenetic switches instruct it to perform the functions of a bone cell and not a nerve cell. Epigenetic alterations, however, are one of the primary hallmarks of aging. As we age, harmful epigenetic switches are activated and beneficial ones are deactivated, causing age-related dysfunction. This may even lead to inflammation, which causes further epigenetic damage, leading to a dangerous feedback loop.

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Ronald Kohanski, PhD. is the Deputy Director of the Division of Aging Biology at the National Institute on Aging, and he gave the keynote for day two of our recent conference in New York City.