Lifeboat Foundation

As regenerative medicine expands, our ability to engineer organs is growing with it. Researchers can now grow a number of so called ‘organoids’ — mini-organs which can teach us more about developmental biology and enable vastly improved testing. In the latest addition to the bunch, a team from Ohio State University has successfully engineered the most complete model yet of a human brain, with a similar maturity to a 5 week old fetus.

Containing 99% of the genes present in the human fetal brain, and about the size of an eraser, the organoid was developed from transformed adult human skin. This method could allow more ethical and precise clinical trials, both speeding up and enabling more rigorous, personalized testing. As animal testing frequently fails to predict varied human responses, these organoid models offer an alternative approach which could revolutionize clinical trial methodology.

“It not only looks like the developing brain, its diverse cell types express nearly all genes like a brain. We’ve struggled for a long time trying to solve complex brain disease problems that cause tremendous pain and suffering. The power of this brain model bodes very well for human health because it gives us better and more relevant options to test and develop therapeutics other than rodents.”

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Checkout the latest Longevity Reporter Newsletter (22nd August, 2015), covering this week’s top news in health, aging, longevity.

This week: An Entire Nervous System Captured On Film; 10 Enduring Health Myths, Debunked By Science; Peto’s Paradox: Why Don’t Larger Animals Get Cancer More Often?; Antioxidants: Separating Myth From Reality; And more.

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If cancer is predominantly a random process, then why don’t organisms with thousands of times more cells suffer more from cancer? Large species like whales and elephants generally live longer, not shorter lives, so how are they protected against the threat of cancer?

While we have a great deal more to learn when it comes to cancer biology, the general belief is that it arises first from mutation. It’s becoming clear it’s actually an incredibly complicated process, requiring a range of variable factors such as mutation, epigenetic alteration and local environment change (like inflammation). While some students may have spent sleepless nights wondering how many mutated cells they contain after learning the fallibility of our replication mechanisms, the reality is that with such an error rate we should all be ridden with cancer in childhood — but we’re not. Our canine companions sadly often succumb around their 1st decade, but humans are actually comparatively good at dealing with cancer. We live a relatively long time in the mammal kingdom for our size and even in a modern environment, it’s predominantly an age-related disease.

While evolution may have honed replication accuracy, life itself requires ‘imperfection’ to evolve. We needed those occasional errors in germ cells to allow evolution. If keeping the odd error is either preferable or essentially not worth the energy tackling when you’re dealing with tens of trillions of cells, then clearly there is more to the story than mutation. In order to maintain a multi-cellular organism for a long enough period, considering that errors are essentially inevitable, other mechanisms must be in place to remove or quarantine problematic cells.

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Tony Wyss-Coray studies the impact of aging on the human body and brain. In this eye-opening talk, he shares new research from his Stanford lab and other teams which shows that a solution for some of the less great aspects of old age might actually lie within us all.

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Lifespan.io is running a SENS fundraiser to aid research into Mitochondrial repair. This is a new fundraiser platform to help get important regenerative medicine research funded and underway. Let us hope this is the start of how research could be funded and that it opens up faster progress.

Engineering backup copies of mitochondrial genes to place in the nucleus of the cell, aiming to prevent age-related damage and restore lost mitochondrial function.

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https://www.youtube.com/watch?v=y5zQpZ1BqXs&feature=youtu.be&app=desktop

An interesting little Bioviva clip about their upcoming gene therapy work.

CEO Liz Parrish discusses BioViva and gene therapy…. Diseases of aging beware.

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Ever since the free radical theory of aging was conceived in the 1950s, antioxidants have been a buzzword in health — saturating the cosmetic industry and contributing to a smoothie blending, supplement popping boom.

Ever since the free radical theory of aging was conceived in the 1950s, antioxidants have been a buzz word in health — saturating the cosmetic industry and contributing to a smoothie blending, supplement popping boom. While antioxidants can certainly play an essential role in health, there is growing evidence that additional supplementation has limited benefit and can actually be harmful in some cases.

Aging has yet to be ascribed to one, singular cause and the free radical theory has struggled to prove itself. While in some organisms reducing oxidative stress can prove beneficial and increasing mitochondria targeted catalase (an important antioxidant enzyme) production in mice showed a modest increase in lifespan, when important enzymes were knocked out in C. elegans (a model organism) there was curiously no reduction and reducing expression of various antioxidant mechanisms in mice also failed to reduce lifespan. While a certain amount of vitamins and antioxidant intake is necessary, as many are co-factors in essential reactions, it seems that aside from nutritional value there is little consensus regarding additional benefits.

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Checkout the latest Longevity Reporter Newsletter (15th August, 2015), covering this week’s top news in health, aging, longevity

This week: ‘Danielle’ — An Eye Opening Simulation Of The Aging Process; How Does Chronic Inflammation Lead To Cancer?; Low Inflammation and Telomere Maintenance Predict Healthy Longevity; 3-D Printing: Could Downloadable Medicine Be The Future?; And more.

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“A protein found in the blood of young animals called GDF-11 is inducing systemic rejuvenation effects on bone, muscle, heart, blood vessels, and brains of older animals.

“GDF” stands for growth differentiating factor. It functions to turn “on” senescent stem cells, which results in a restoration of youthful structure and function to senile tissues. This same protein (GDF-11) is found in young humans as well as animals.

Harvard, Stanford, and other universities are conducting remarkable studies showing age reversal in animal models. Researchers from these centers of medical innovation are optimistic that this approach might be applicable to humans.”

Continue reading “Report: Human Age Reversal Research” »