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Category: life extension – Page 648

Could an algorithm help to save people’s eyesight? Google thinks so

Google’s artificial intelligence research lab DeepMind is exploring whether its technology could be used to identify early signs of eye diseases that ophthalmologists might not spot.

DeepMind, which was acquired by Google in 2014, has struck an agreement with Moorfields Eye Hospital in London that gives it access to about a million anonymous retinal scans, which it will feed into its artificial intelligence software.

The algorithm will target two of the most common eye diseases: age-related macular degeneration and diabetic retinopathy, which affect more than 100 million people around the world.

Safer Gene Editing Without Cleaving DNA

It’s an add-on for CRISPR.

Researchers have created a new genome editing technique called Target-AID, which induces point mutations instead of cutting DNA

Gene editing technology has fantastic potential, but there are remaining issues and questions over safety and specificity. The major contender is currently CRISPR-Cas9, but this induces a double stranded break in DNA which is a slightly riskier approach — particularly if it cuts in other locations too that you don’t want it to. Research teams across the world are both optimising and customising the CRISPR system; creating more accurate versions or versions that regulate gene expression as opposed to editing it. One such team has now built an add-on to CRISPR, Target-AID.

Uncovering the genetic basis of ALT (Alternative Lengthening of Telomeres) — Harold Silva

Dr Haroldo Silva from SENS talks about ALT cancer in this short film.

As normal cells divide, the ends of their chromosomes (telomeres) progressively shorten until eventually the cells reach senescence or undergo apoptosis. Cancers, which disproportionally kill more individuals in the 65 years or above age group, often overcome this built-in replication limit by expressing the enzyme telomerase.

However, about 10–15% cancers do not use telomerase and at least a major subset of these exhibit hallmarks of Alternative Lengthening of Telomeres (ALT) activity, including long and heterogeneous telomere lengths, presence of ALT-associated PML nuclear bodies (APBs), and generation of high-levels of C-rich circular telomeric DNA repeats (C-circles). Although there are many telomerase-based anti-cancer therapies in clinical development at the moment, research on ALT has not produced any promising therapies so far. This lag is due in part to a lack of assays that are reliable and amenable to high-content/high-throughput (HTS) screens.

The OncoSENS team has made significant progress toward making some of these key ALT assays compatible with the HTS format, which should not only speed up the development of ALT-based anti-cancer therapies but also broaden the amount of research performed on ALT. Our team has already begun applying the assays above to test the involvement of several genes in the ALT pathway and the progress on that front will also be showcased. Undoubtedly, successfully shutting down both ALT- and telomerase-based pathways of telomere maintenance in cancers will move the field forward towards realizing the goal of a complete eradication of one of the main age-related fatal diseases burdening society.

Visit www.sens.org/videos to view the rest of our SENS6 videos.

Continue reading “Uncovering the genetic basis of ALT (Alternative Lengthening of Telomeres) — Harold Silva” | >

Menopause reversed as scientists successfully ‘rejuvenate women’s ovaries’

Time people rethought outdated ideas about biology and accepted that development and aging are not one way processess and they are amenable to intervention.

Scientists have announced they can now reverse the menopause in what is thought to be a major scientific breakthrough.

Trials claim to have ‘rejuvenated’ women’s ovaries using a blood treatment normally used to help wounds heal faster and have reversed menstrual cessation in multiple women, including 40-year-old woman who underwent the menopause five years ago.

The research, undertaken by scientists in Athens, has been presented at the European Society of Human Reproduction and Embryology’s annual meeting in Finland, The New Scientist reports.

Aubrey de Grey — Pushing back Death

Even insurance companies are taking longevity seriously now!

Source: http://www.riskmindslive.com/will-rea…

Is ageing a disease? Can it be cured? Can death be pushed back? Will you live to 1000 years? Aubrey de Grey, Chief Science Officer, SENS Research Foundation divulges the truth behind longevity and the ensuing risks and discover how you should transform your life insurance models. He spoke to Markus Salchegger, Managing Director at Accenture Risk & Finance at RiskMinds Insurance 2016, Amsterdam.

Website: http://sens.org

YouTube: https://www.youtube.com/user/SENSFVideo

Continue reading “Aubrey de Grey — Pushing back Death” | >

Anti-aging effects (in mice) of a dietary supplement called alpha lipoic acid

Shortened telomeres, the protective caps at the ends of chromosomes (credit: NIGMS)

Scientists at Emory University School of Medicine have found that the dietary supplement alpha lipoic acid (ALA) can stimulate telomerase, the enzyme that lengthens telomeres, with positive effects in a mouse model of atherosclerosis.

In human cells, shortened telomeres, the protective caps at the ends of chromosomes, are a sign of aging and also contribute to aging.

​The Jesus Singularity

I’m super excited to share my first fiction since writing “The Transhumanist Wager” four years ago. Vice Motherboard has published this short story of mine on the challenge of AI becoming religious—and what that might mean for humanity. It’s a short read and the story takes place just a few years into the future. And yes, the happenings in this story could occur.

For the second installment of our series exploring the future of human augmentation, we bring you a story by the Transhumanist Party’s presidential candidate (and occasional Motherboard columnist), Zoltan Istvan. Though he’s spent most of the last year traveling the nation in a coffin-shaped bus, spreading the gospel of immortality and H+, he’s no stranger to fiction. His novel, The Transhumanist Wager, is about the impact of evolving beyond this mortal coil. This story is even bolder. Enjoy the always provocative, always entertaining, Zoltan Istvan. –the editor.

Paul Shuman’s phone rang. He struggled to open his eyes. ‘Who the hell is calling me in the middle of the night?’ he thought. He rolled out of bed and walked naked to his desk to see. His phone showed it was his secretary.

“What is it?” he sharply asked on speaker phone.

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.

The model very generally describes what happens with a gene network over time – the majority of the genes are actually working perfectly, but a small number doesn’t. There are repair mechanisms that take care of that. Also, there are mechanisms that take care of defected proteins like heat shock proteins, etc. Put together all of this in an equasion and solve it, and bam! here’s an equasion that gives you the Gompertz law for all species that have normal aging, and a time independent constant for the negligibly senescent ones.

What’s the difference between those two aging regimes? The model suggests it’s the right combination of DNA repair efficiency and the combined efficiency of proteolysis and heat shock response systems, mediating degradation and refolding of misfolded proteins. So, it’s not the accumulation of damages that is responsible for aging, but rather the properties of the gene network itself. The good news is that even we are playing with a terrible hand at first, there is a chance we can still win by changing the features of our network and making it stable. For example, by optimizing misfolded protein response or DNA repair.