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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.

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Will Ichor Therapeutics be the first to clinic with a SENS based approach?


As I mentioned last week, earlier this year Fight Aging! invested a modest amount in the Ichor Therapeutics initiative to develop a treatment for macular degeneration, joining a number of other amateur and professional investors in helping to get this venture started. The approach taken here is based on the results of research carried out at the Methuselah Foundation and SENS Research Foundation over much of the past decade, funded by philanthropists and the support of our community of longevity science enthusiasts. This is how we succeed in building the future: medical science in the laboratory leads to medical development in startup companies, each new stage bringing treatments capable of repairing specific forms of age-related molecular damage that much closer to the clinic.

Ichor Therapeutics is one of a growing number of success stories to emerge from the SENS rejuvenation research community. Young scientists, advocates, and donors involved in earlier projects — years ago now — have gone on to build their own ventures, while retaining an interest in stepping up to do something meaningful to help bring an end to aging. Back in 2010, Kelsey Moody worked on the LysoSENS project to find ways to break down damaging metabolic waste in old tissues; fast-forward six years, and he is the now the CEO of a successful small biotechnology company with a great team, taking that very same technology and putting it to good use. I recently had the chance to ask Kelsey a few questions about the future of SENS rejuvenation research, as well as how the Ichor scientists intend to construct a new class of therapy for macular degeneration, one based on removing one of the root causes of the condition.

Quote:

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And, a few words from Ray.


According to Ray Kurzweil, we’re approaching a time when humans will begin to radically extend their lifespans. This sounds good on the surface, but will we have enough resources to support everyone? And won’t living indefinitely get boring eventually? Not so much, Kurzweil says.

Kurzweil suggests that by the time we’ve significantly extended our average lifespan, we’ll no longer be in a scarcity-driven world competing for finite resources. Take energy, for example. Kurzweil notes solar is on an exponential curve and has been doubling every two years.

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More info. on some research that I came across a few weeks ago on a new bioimaging technique to help map and understand the nervous system which is one of the hardest areas of the brain to map and monitor — this is truly groundbreaking on so many fronts such as precision meds. research, computer mapping of the brain and neuro pathways, etc. If will be very impressive to see how much this accelerates the efforts in finding a cure for diseases such as Dystonia.


MUNICH, Germany, Aug. 22 (UPI) — Scientists at Ludwig Maximilian University have developed a technique for turning the body of a deceased rodent entirely transparent, revealing the central nervous system in unprecedented clarity.

Researchers are hopeful the new and improved view will help scientists understand how traumatic brain injuries, strokes and aging yield chronic disorders like dementia and epilepsy.

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“Researchers Successfully Implant Living, Functional 3D Printed Human Tissue Into Animals”

My question is “why?”


The news has been full of stories about new advancements in 3D printed tissue. Companies such as Organovo and research institutions such as the University of California San Diego are leading the charge in the development of 3D printed, functional human tissue, particularly liver tissue. So far, printed tissue is being used mostly for pharmaceutical drug testing, but everyone in the 3D printing biosphere professes the ultimate goal of eventually producing whole, fully functional human organs that can be transplanted into patients. Most experts agree that it will happen; it’s just a matter of when.

It’s also a matter of who. The race to be the first to 3D print a transplantable human organ is an intense one, and Wake Forest Baptist Medical Center may have just pulled into the lead. Regenerative medicine researchers at the North Carolina hospital have announced that they have printed ear, bone and muscle structures and successfully implanted them into animals. The structures, after being implanted, matured into functional tissue and sprouted new systems of blood vessels, and their strength and size mean that they could feasibly be implanted into humans in the future.

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My exclusive interview with Libertarian presidential candidate Gary Johnson on some hard science & tech issues, including transhumanism, longevity, AI, and gene editing. This is also my first story for Futurism. For the record, I am trying, along with millions of others, to get Gary Johnson into the Presidentia l debates! No matter who you plan to vote for, it would be good for America to have him in the debates so a third voice is heard:


Libertarian Presidentia l candidate Gary Johnson wants humans to live a lot longer and isn’t worried about AI becoming the Terminator. Here, Futurist Zoltan Istvan gains an exclusive interview with Johnson, who is polling double digits nationally and hopes to be in the Presidentia l debates with Trump and Clinton in October.

Disclaimer: The views and opinions expressed are solely those of the author. They do not necessarily represent the views of Futurism or its affiliates.

I recently sat down with Libertarian Presidentia l candidate Gary Johnson at his home in New Mexico and watched an episode of Orphan Black, the hit sci-fi show. Between his CNN Town Hall meetings and endless speeches on the campaign trail, you’re probably asking: How did Gary get the time to watch a television show? It’s a good question, but the former Governor made the time, because he’s interested in the future and willing to explore how it might unfold.

Johnson is excited about using radical science and technology to make America stronger and help the human race.

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(credit: NIH National Institute on Aging)

Anti-inflammatory drug mefenamic acid completely reversed memory loss and brain inflammation in mice genetically engineered to develop symptoms of Alzheimer’s disease and amyloid beta-induced memory loss, a team led by David Brough, PhD, from the University of Manchester has discovered.

The non-steroidal anti-inflammatory drug (NSAID) drug targets an important inflammatory pathway called the NLRP3 inflammasome, which damages brain cells, according to Brough. This is the first time a drug has been shown to target this inflammatory pathway, highlighting its importance in the disease model, Brough said.

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