Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

Previous research published earlier this year in Nature Medicine involving University of Minnesota Medical School faculty Paul D. Robbins and Laura J. Niedernhofer and Mayo Clinic investigators James L. Kirkland and Tamara Tchkonia, showed it was possible to reduce the burden of damaged cells, termed senescent cells, and extend lifespan and improve health, even when treatment was initiated late in life. They now have shown that treatment of aged mice with the natural product Fisetin, found in many fruits and vegetables, also has significant positive effects on health and lifespan.

As people age, they accumulate damaged . When the cells get to a certain level of damage they go through an aging process of their own, called cellular senescence. The cells also release inflammatory factors that tell the immune system to clear those damaged cells. A younger person’s immune system is healthy and is able to clear the damaged cells. But as people age, they aren’t cleared as effectively. Thus they begin to accumulate, cause low level inflammation and release enzymes that can degrade the tissue.

Robbins and fellow researchers found a natural product, called Fisetin, reduces the level of these damaged cells in the body. They found this by treating mice towards the end of life with this compound and see improvement in health and . The paper, “Fisetin is a senotherapeutic that extends health and lifespan,” was recently published in EBioMedicine.

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The universe is filled with uncountable amounts of mystery, discovery, opportunity, experiences, marvels and more. So, let’s not die if we don’t have to.

It’s much harder to make the case that radical longevity cannot be engineered into our biology than that it can. Humanity engineers cells in countless ways all the time now, and our knowledge, capability and tools keep growing exponentially.

Now, a mainstream amount of demand to create a bustling global industry of life extension R&D is the only thing standing between you and the ability to live indefinitely.” — Eric Schulke

Fifteen thousand years worth of Netflix are watched every day. Fifteen billion dollars are spent on the Super Bowl and fifteen billion dollars are spent on Valentine’s day. Those aren’t bad things but we need some perspective. Survival is humanity’s main and oldest occupation. We have what it takes to survive if we pay attention and get with the program.

“Yes, the future is transhumanism. Who would ask ‘Is the future being alive and prosperous?’ As if anyone should expect humanity to work for a future of hardship and death.” — Ray Keyes

People suffer in great existential voids these decades, not only do they need life, they need deep meaning and purpose. The movement for indefinite life extension is giving them both.

Today, we would like to share with you a talk by Dr. Michael West from AgeX Therapeutics, a company developing therapies to combat age-related diseases by encouraging the body to regenerate cells and tissues.

On July 12th, we hosted our first conference, Ending Age-Related Diseases: Investment Prospects & Advances in Research, at the Frederick P. Rose Auditorium, which is part of the Cooper Union campus in New York City. The packed event saw a range of people from research, investment, and the wider community coming together for a day of science and biotech business presentations and panels.

In his talk, “Hayflick Rewound: Somatic Restriction, Epigenetics, and the Reversibility of Human Aging”, Dr. Michael West, CEO of AgeX Therapeutics, discussed the breakthroughs in our understanding of biological regeneration and in induced tissue regeneration.

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LEAF’s Rejuvenation Roundup September 2018 is out!

Happy autumn—or spring, if you live in the southern hemisphere! Be as it may, in a post-aging world, the season of your health would always be summer; let’s see how much closer we got to that world during last September.

LEAF News

To get things started, the new episode of the Rejuvenation Roundup podcast is available today.

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Even with an increasing number of articles about aging and rejuvenation technologies in mass media, the general public’s lack of information remains a problem. Pro-longevity organizations try to spread useful information; however, it’s clear that this information is, quite often, only delivered to current members of the community instead of to a new audience. My work at LEAF is partially focused on finding ways to break this border and explore new social territories as often as possible. Last week, this journey brought me to a meeting with a title that speaks for itself: Death Cafe.

What is Death Cafe?

A Death Cafe is not a place. It is a meeting at which people are encouraged to discuss everything related to death over a cup of tea. The official mission of this community is defined as follows: “Our objective is to increase awareness of death with a view to helping people make the most of their (finite) lives.” It is not a form of group therapy, not a support group or a survivors’ group (though only the living can attend…); rather, it’s just a space where people can talk to each other about a topic that is usually excluded from public dialogue.

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Duca.

This announcement was made in the presence of the Ambassador Extraordinary and Plenipotentiary of the People’s Republic of China.

At the 69th anniversary of the founding of the People’s Republic of China reception.

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A recent open-access mouse study published by Xi’an Institute of Tissue Engineering and Regenerative Medicine scientists in the journal Bone Research describes how the ALPL gene affects bone aging and suggests that metformin might constitute a viable therapeutic option to prevent it [1].

Study abstract

Mutations in the liver/bone/kidney alkaline phosphatase (Alpl) gene cause hypophosphatasia (HPP) and early-onset bone dysplasia, suggesting that this gene is a key factor in human bone development. However, how and where Alpl acts in bone ageing is largely unknown. Here, we determined that ablation of Alpl induces prototypical premature bone ageing characteristics, including bone mass loss and marrow fat gain coupled with elevated expression of p16INK4A (p16) and p53 due to senescence and impaired differentiation in mesenchymal stem cells (MSCs). Mechanistically, Alpl deficiency in MSCs enhances ATP release and reduces ATP hydrolysis. Then, the excessive extracellular ATP is, in turn, internalized by MSCs and causes an elevation in the intracellular ATP level, which consequently inactivates the AMPKα pathway and contributes to the cell fate switch of MSCs.

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The Imagine Science Films Festival is happening on October 12-19th, 2018 in New York, at a variety of venues, and this year, it is featuring a theme close to home: survival.

Crisis. Entropy. Extinction. This year we look at the high stakes for all life on Earth and beyond. Between nuclear proliferation, species loss and dwindling resources, existence itself is not assured. But for every dystopia, a corresponding utopia may be within reach. It may be a struggle, but the record of all life is that of an eon-spanning fight to stay alive. We’ll feature tumultuous natural history and startling feats of adaptation. Apoptosis versus immortal cell lines. Half-lives and radical life extension. The deaths of stars and extraordinary paths to SURVIVAL.

With this year’s theme including life extension, we may well see some interesting and thought-provoking films on the topic. Lifespan.io is also an official event sponsor for the festival, as we strongly feel that the worlds of filmmaking and science can be a perfect match in helping to encourage a wider dialogue about aging and doing something about it.

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Today, we have an interview with Dr. Michael Bonkowski, an expert on NAD+ biology and aging from the David Sinclair Lab, Harvard Medical School.

Michael Bonkowski aims to advance our understanding of the links between metabolism, aging, and age-associated diseases. He has published 35 peer-reviewed journal articles and has conducted multiple successful longevity studies. In Dr. David Sinclair’s lab, his research efforts are focused on the role of nutrient sensors’ regulation of endocrine signaling and aging in the mouse. He is also working on direct and indirect ways to drive the activity of these nutrient sensors by using dietary manipulations, small molecules, and chemical treatments.

Michael is trained as a pharmacologist, physiologist, and animal scientist. Some of his areas of expertise include animal physiology, genetics, glucose, and insulin homeostasis, metabolism, assay development, protein biochemistry, and transmission electron microscopy imaging.

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