Lifeboat Foundation

A new finding from the UVA School of Medicine suggests that fatty liver disease and other effects of aging may be the result of our cells’ nuclei getting wrinkly.

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

Continue reading “Thanos, Overpopulation, and How to Save the Universe” »

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.

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.

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.

Continue reading “We want to declare ageing a disease” »

Aging (Albany NY). 2017 Feb 14;9:419–446. doi: 10.18632/aging.101168.

Quach A, Levine ME, Tanaka T, Lu AT, Chen BH, Ferrucci L, Ritz B³ Bandinelli S, Neuhouser ML, Beasley JM, Snetselaar L, Wallace RB, Tsao PS^9,10, Absher D¹¹, Assimes TL, Stewart JD¹², Li Y^13,14, Hou L^15,16, Baccarelli AA¹⁷, Whitsel EA^12,18, Horvath S^1,19.

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.

Continue reading “New Harvard Startup Wants to Reverse Aging in Dogs and then Humans” »

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.

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.