Lifeboat Foundation

Investments in Longevity Could Really Pay Off

With a ‘silver tsunami’ ahead, tackling aging makes all kinds of sense — and could reap rich rewards.

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AOL running an energetic 2-min video on transhumanism and longevity on their morning show:

Zoltan Istvan of the Transhumanist Party is running for President on one platform: longevity.

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Heales, The Healthy Life Extension Society, is dedicated to promoting and informing the public about life extension and longevity breakthroughs. In this spirit, Heales has announced a Short Film Competition with a grand prize of €3.000. Heales wants you to capture why living longer, healthier lives will be something to celebrate, not fear.

We caught up with Didier Cournelle, director of the society, to find out more about the competition:

Why do you think there are so few positive portrayals of longevity and life extension in the media? In general, the press prefers bad news to good news. Good news concerning longevity is difficult to describe because it is often made of small, incremental progress. Another aspect is that the idea of radical life extension looks fringe to many people. Last aspect: to speak about longevity is to speak about death and unconsciously, we tend to avoid what reminds us of our own death.

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Cool article on longevity science:

The search for the fountain of youth continues in Silicon Valley.

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California researchers opened the world’s largest publicly available stem cell bank Tuesday, which will aid in the search for cures for genetic diseases such as Alzheimer’s, epilepsy and autism.

Universities from around the state will contribute adult skin samples to the bank, while the Buck Institute for Research in Novato will store the material.

The Stem Cell Bank is funded through a $32 million grant awarded in 2013 by the California Institute for Regenerative Medicine, which itself was established in 2004 through voter approval of Proposition 71. That measure provided an initial $3 billion in state bonds to the institute.

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What would you say if I told you that aging happens not because of accumulation of stresses, but rather because of the intrinsic properties of the gene network of the organism? I’m guessing you’d be like: surprised .

So, here’s the deal. My biohacker friends led by Peter Fedichev and Sergey Filonov in collaboration with my old friend and the longevity record holder Robert Shmookler Reis published a very cool paper. They proposed a way to quantitatively describe the two types of aging – negligible senescence and normal aging. We all know that some animals just don’t care about time passing by. Their mortality doesn’t increase with age. Such negligibly senescent species include the notorious naked mole rat and a bunch of other critters like certain turtles and clams to name a few. So the paper explains what it is exactly that makes these animals age so slowly – it’s the stability of their gene networks.

What does network stability mean then? Well, it’s actually pretty straightforward – if the DNA repair mechanisms are very efficient and the connectivity of the network is low enough, then this network is stable. So, normally aging species, such as ourselves, have unstable networks. This is a major bummer by all means. But! There is a way to overcome this problem, according to the proposed math model.

Continue reading “Hacking Aging” »

My 4 min interview on transhumanism and longevity with BuzzFeed came out as a stand-alone video. About 800 comments under the YouTube video:

Because we all deserve a chance at immortality!

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Dr DePinho released a paper in 2012, this builds on previous papers and his theory of the “telomere-p53-PGC axis”. This is a big reason along with the work of Dr Michael Fossel I believe telomerase therapy is probably the best chance of radical life extension in the near future. This is one of a number of papers that implicate dysfunctional telomeres in a cascade that causes mitochondrial dysfunction and various other aging consequences.

ABSTRACT Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1α and PGC-1β, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1α expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1α and PGC-1β promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.

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An interesting paper that uses ALA to shore up telomerase activity, loss of telomeres inhibition of P53 expression and mitochondrial dysfunction in one go. They use ALA (alpha lipoic acid) to induce PGC-1α in this case though PGC1-alpha seems to be a potential target for intervention as I understand that ALA is difficult to deliver to cells. In this case this involves the vascular system and atherosclerosis.

http://www.cell.com/cell-reports/abstract/S2211-1247(15)00825-6

Short telomeres and Mitochondrial dysfunction are increasingly implicated as being closely linked as this 2012 Dephino paper demonstrates in the aging heart:

Continue reading “PGC-1α Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases” »