Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

For centuries humans have sought the ‘elixir of life’ – a mythical potion that supposedly would grant the drinker eternal life.

Now Exeter scientists believe they may have found the secret to a longer, healthier life.

New compounds developed and tested at the University of Exeter have brought the dream a step closer and paved the way for “anti-degeneration” drugs that could not only extend life, but also extend health and may help treat age-related diseases like cancer, dementia and diabetes.

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The compounds — AP39, AP123 and RT01 — have been designed to selectively deliver minute quantities of the gas hydrogen sulphide to the mitochondria in cells and help the old or damaged cells to generate the ‘energy’ needed for survival and to reduce senescence.

In the samples used, the number of senescent cells — older cells that have deteriorated and stopped dividing — was reduced by up to 50 per cent.

The team also identified two splicing factors — a component of cells — that play a key role in when and how endothelial cells become senescent.

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A team of researchers from several institutions in Iceland and the U.S. has conducted a unique blood serum investigation and discovered multiple protein networks that are involved in the aging process. In their paper published in the journal Science, the group describes their study and what they found.

Prior research has shown that when older mice have their blood systems connected to younger mice, the older mice experience improvements in age-related organ deterioration. This finding has led scientists to suspect that aging might be caused by something in the blood. In this new effort, the researchers sought to test this idea by studying proteins in the circulatory system.

The study consisted of analyzing blood samples from 5,457 people living in Iceland, all of whom were over the age of 65 and who were participants in an ongoing study called Age, Gene/Environment Susceptibility. The volunteers had also been chosen specifically to represent a cross section of the people living in Iceland. The major part of the analysis involved creating a panel of DNA aptamers (short sequences that bind to proteins) that could be used to recognize proteins, both known and unknown. Blood serum from the volunteers was then compared against the panels and the results were analyzed by a computer looking for patterns.

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There is a 3-day conference in Brussels on November 8–10 for those of you in Europe interested in aging research.

The Eurosymposium on Healthy Ageing (EHA) is an international event that provides a unique opportunity for researchers, government officials, biotech executives, entrepreneurs, and non-governmental institutions from around the world to meet, network, and forge new scientific collaborations.

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Evolutionary theory predicts that reproduction entails costs that detract from somatic maintenance, accelerating biological aging. Despite support from studies in human and non-human animals, mechanisms linking ‘costs of reproduction’ (CoR) to aging are poorly understood. Human pregnancy is characterized by major alterations in metabolic regulation, oxidative stress, and immune cell proliferation. We hypothesized that these adaptations could accelerate blood-derived cellular aging. To test this hypothesis, we examined gravidity in relation to telomere length (TL, n = 821) and DNA-methylation age (DNAmAge, n = 397) in a cohort of young (20–22 year-old) Filipino women. Age-corrected TL and accelerated DNAmAge both predict age-related morbidity and mortality, and provide markers of mitotic and non-mitotic cellular aging, respectively. Consistent with theoretical predictions, TL decreased (p = 0.031) and DNAmAge increased (p = 0.007) with gravidity, a relationship that was not contingent upon resource availability. Neither biomarker was associated with subsequent fertility (both p 0.3), broadly consistent with a causal effect of gravidity on cellular aging. Our findings provide evidence that reproduction in women carries costs in the form of accelerated aging through two independent cellular pathways.

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This is part of our ongoing series of articles that discuss the Hallmarks of Aging. Published in 2013, the paper divides aging into distinct categories (“hallmarks”) of damage to explain how the aging process works and how it causes age-related diseases. Today, we will be looking at the hallmark of cellular senescence.

What are senescent cells?

As you age, increasing numbers of your cells enter into a state known as senescence. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals that encourage nearby healthy cells to enter the same senescent state. Their presence causes many problems: they reduce tissue repair, increase chronic inflammation, and can even eventually raise the risk of cancer and other age-related diseases.

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Fantastic Video Set of Aubrey De Grey discussing Indefinite Longevity.

This video is a compilation of the biogerontologist Aubrey de Grey. He has been pushing the scientific frontier of indefinite longevity for the last few decades and predicts that science and technology will be advanced enough 20 years from now so that we can all achieve longevity escape velocity.

Video One:

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Life extension would give us more time to enjoy; why not?

At times, meeting people feels like going to the theater. Conversations tend to revolve around the same topics and can sound so cliché that they seem scripted. Of course, it depends on the people—close friends tend to be far more genuine than that—but if you pay attention during a conversation, a certain topic will pop up several times: aging.

Depending on the age of the people involved, the way they discuss aging will be different. Teenagers probably won’t even touch the subject; it generally starts creeping up in conversations once working life has begun or is about to begin. At this stage, chronological and biological aging are mostly conflated; responsibilities, more demanding schedules, and abandoning student life are all seen as hallmarks of growing older, when, in fact, they are only signs of growing up and are not absolute.

Still, it is largely true that we become more busy as we get older, independent of biological aging. This is, in fact, a common complaint that subtly slips into most “grown-up conversations”; this is especially true in the case of parents, whose free time is understandably even more curtailed. Wouldn’t we all like to have more time?

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