Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 506

Today, we wanted to draw your attention to a review of aging and the role that the gut microbiome plays in it.

There is an increasing amount of evidence for the contribution of microbial burden in the chronic, age-related background of inflammation known as “inflammaging”. There are a number of proposed sources of inflammaging, including senescent cells, immunosenescence, cell debris, and microbial burden.

We have delved into the topic of the gut microbiome in the past and its possible role as the origin point of inflammaging in a previous article, but we wanted to highlight this publication for people interested in reading further about this rapidly evolving area of aging research [1].

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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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