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Category: life extension – Page 504

Now that some time has passed since the release of Avengers: Infinity War, we should probably talk about Thanos, the nigh-omnipotent “Mad Titan” at the heart of Marvel’s latest blockbuster, and how he perfectly embodies one of the most pervasive societal misconceptions circling the topic of life extension. This might, therefore, be the first post here on LEAF that necessitates a spoiler warning, so here it is!

SPOILER ALERT — IF YOU CARE ABOUT HAVING INFINITY WAR, WHICH IS AN EXCELLENT MOVIE THAT YOU SHOULD SEE, SPOILED, PLEASE ABANDON SHIP AND HEREUPON RETURN AFTER WATCHING

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An interesting interview with one of the Dog Aging Project’s lead scientists, Dr. Matt Kaeberlein.

As we discussed in a recent article about Prof. George Church’s new startup, endeavors to undo aging aren’t directed exclusively toward human aging; extending the healthy lifespan of our pet dogs and cats is also currently being researched. The Dog Aging Project (DAP) has been around quite a bit longer than Prof. Church’s startup, and today, we have the pleasure to bring you an interview with one of the lead scientists behind it, Dr. Matt Kaeberlein.

In much the same way that other projects are aiming to extend healthy human lifespan, the DAP team intends to do the same, targeting the aging processes directly. Given the rate of progress in geroscience over the past years, Dr. Kaeberlein and his team are optimistic that, in the near future, the interventions that have been shown to slow down aging in mice and rats could do the same in our furry companions.

Besides Dr. Kaeberlein—who is a Professor of Pathology and an Adjunct Professor of both Genome Sciences and Oral Health Sciences at the University of Washington in Seattle—the DAP team is comprised of Dr. Daniel Promislow, Professor of the Departments of Pathology and Biology at the University of Washington; Dr. Kate Crevy, Associate Professor of Small Animal Internal Medicine at Texas A&M University’s College of Veterinary Medicine; Dr. Tammi Kaeberlein, a research scientist at the Department of Pathology at the University of Washington; Dr. Silvan Urfer, a veterinarian and Senior Fellow of Washington University’s Department of Pathology; and Kelly Jin, a doctoral student currently pursuing a Ph.D. in Molecular Medicine and Mechanisms of Disease at the University of Washington.

Continue reading “Dr. Matt Kaeberlein – The Dog Aging Project” | >

Long story in The Independent: https://www.independent.co.uk/…/biohacking-transhumanism-aa… #transhumanism #biohacking

On the morning of 29 April, staff at the Soulex spa in Washington DC discovered the lifeless body of one of its clients lying face down in a sensory deprivation tank. The body was that of 28-year-old Aaron Traywick, who less than three months earlier had injected himself live on stage at an event in Austin, Texas, with an untested gene therapy that he claimed could cure herpes.

Stories soon spread about the discovery of Traywick’s body, with some inferring a potential link between the DIY herpes treatment and his untimely death. But those who knew the young entrepreneur and were familiar with the work he did suspected something much more sinister.

Continue reading “Live forever or die trying: Meet the biohackers who fear their work could get them killed” | >

This in depth story has recently been translated to English: https://ciencias.uautonoma.cl/…/we-want-to-declare-ageing-a…?

Zoltan Istvan is currently a Libertarian candidate for Governor in California, also former 2016’s US presidential candidate for the Transhumanist Party and he is known around the world as someone that advocates for Transhumanism, a public figure in science and technology.

Dr. Marcela Gatica-Andrades and Nadia Politis from Science Communication Center interviewing Zoltan Istvan.

Continue reading “We want to declare ageing a disease” | >

Professor George Church of Harvard Medical School has co-founded a new startup company, Rejuvenate Bio, which has plans to reverse aging in dogs as a way to market anti-aging therapies for our furry friends before bringing them to us.

Dogs first, humans next

The company has already carried some initial tests on beagles and plans to reverse aging by using gene therapy to add new instructions to their DNA. If it works, the goal is ultimately to try the same approach in people, and George Church may be one the first human volunteers.

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Vascular risk and accumulation of beta-amyloids seem to accelerate the rate of cognitive decline in elderly adults.

Vascular risk appears to be a strong predictor of dementia, especially in older individuals with high levels of brain beta-amyloids, and the interaction between these two risk factors might lead to a higher rate of cognitive decline, according to a recent study at the Massachusetts General Hospital.

Alzheimer’s disease (AD) is an age-related neurological disorder whose most feared outcome is dementia, along with other symptoms, such as behavioral issues, loss of motivation, and even the inability to take care of oneself. Patients suffering from AD exhibit an accumulation of plaques in their brains; these plaques, resulting from the build-up of amyloid-beta protein, have long been thought to be the cause of the disease, though other hypotheses have been put forward as well.

However, the presence of excess beta amyloids is a constant in all AD patients, and a recent study by researchers at the Massachusetts General Hospital has discovered that increased cardiovascular risk, combined with higher brain amyloid levels, is a predictor of faster cognitive decline in clinically normal elderly. [1].

Continue reading “Vascular risk appears to accelerate cognitive decline in old age” | >

After NAD+ is consumed, it is broken down into nicotinamides and ADP-ribose; the researchers concluded that this means that NAD+ must be resynthesized following this in order for normal cellular functions to continue. This converges with previous studies, which suggest that NAD+ decline leads to changes in metabolism and an increased risk factor for some diseases; this typically happens as the result of aging, as NAD+ levels begin to fall.

With this in mind, the research team thought that cellular metabolism and gene regulation were potentially connected to NAD+ synthesis. They discovered evidence suggesting that compartmentalized NAD+ synthesis and the subsequent consumption are integrated with glucose metabolism and adipogenic transcription as part of the adipocyte differentiation process.

NAD+ synthesis acts as a mediator of PARP-1-regulated transcription during the differentiation of adipocytes, linking cellular metabolism and the adipogenic transcription process. During adipogenesis, nuclear NAD+ levels fall, causing the induction of NMNAT-2, the cytoplasmic NAD+ synthase. This increased level of NMNAT-2 then reduces the availability of NMN and leads to a reduction of nuclear NAD+ synthesis via NMNAT-1. The drop in NAD+ levels then results in decreased PARP-1 activity, which then reduces levels of inhibitory ADP-ribosylation of the adipogenic transcription factor C/EBPβ. Reduced ADP-ribosylation of C/EBPβ means that it is able to bind its target genes, thus promoting the differentiation of preadipocytes into adipocytes. In other words, a decline of NAD+ encourages an increase of preadipocytes turning into adipocyte fat cells.

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Today, as part of our series of articles that cover the Hallmarks of Aging, we are going to take a look at the role of proteins in cellular function and how they play a key role in aging.

Proteins are essential for cellular function

Proteins are large, complex molecules that regulate almost everything in your body, either directly or indirectly. They do the majority of the work in cells and are critical for the function, regulation, and structure of tissues and organs.

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Researchers at Brown University have discovered a way to stimulate cellular autophagy, which is a natural recycling system built into every cell in the body. This has the potential to combat many age-related neurodegenerative diseases.

What is autophagy?

Autophagy means “eating of self” (from Ancient Greek “auto” = self, “phagein” = to devour). Autophagy is how cells break down broken or dysfunctional organelles and proteins in the cell [1,2]. This essentially means that autophagy can consume organelles, such as mitochondria, peroxisomes, and the endoplasmic reticulum, as part of this process. There is also evidence to support that high levels of autophagy are linked to longevity.

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