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Category: life extension – Page 475

Many mutations accumulate in the esophagus as we age.

Scientists at the MRC Cancer Unit of the Wellcome Sanger Institute and other departments of the University of Cambridge discovered that healthy esophageal tissue accumulates very high numbers of mutations with age, to the point that, by the time middle age is reached, it is likely to contain more cells with a particular mutation than cells without it [1].

Abstract

The extent to which cells in normal tissues accumulate mutations throughout life is poorly understood. Some mutant cells expand into clones that can be detected by genome sequencing. We mapped mutant clones in normal esophageal epithelium from nine donors (age range, 20 to 75 years). Somatic mutations accumulated with age and were caused mainly by intrinsic mutational processes. We found strong positive selection of clones carrying mutations in 14 cancer genes, with tens to hundreds of clones per square centimeter. In middle-aged and elderly donors, clones with cancer-associated mutations covered much of the epithelium, with NOTCH1 and TP53 mutations affecting 12 to 80% and 2 to 37% of cells, respectively. Unexpectedly, the prevalence of NOTCH1 mutations in normal esophagus was several times higher than in esophageal cancers. These findings have implications for our understanding of cancer and aging.

Continue reading “Mutations Accumulate in Healthy Esophageal Tissue With Age” | >

Judith Campisi as a speaker for the 2019 Undoing Aging Conference.

At Lawrence Berkeley National Laboratory and at the Buck Institute for Research on Aging, Dr. Judith Campisi established a broad program to understand the relationship between aging and age-related disease.

Judith Campisi says: “Aging research has entered an era of unprecedented hope for interventions that can prevent, delay and, in some cases, reverse much of the functional decline that is a hallmark of aging. There is still a lot of research to be done! I am delighted to be among the speakers at Undoing Aging 2019, where I will discuss the opportunities and challenges of our recent research.”

“Judy has been a towering figure in the field of senescent cells for decades; among other things she pioneered the idea that senescent cells could be actively toxic to their environment and the discovery that cell senescence has a beneficial physiological role in wound healing. She was also one of the first senior gerontologists to appreciate the merits of the SENS approach when I first proposed it in 2000, and her support for it and us ever since has been of incalculable benefit in helping it achieve the mainstream status it enjoys today.” says Aubrey de Grey.

Continue reading “We are happy to announce Dr” | >

To paraphrase Churchill’s words following the Second Battle of El Alamein: Google’s announcement about their new venture to extend human life, Calico, is not the end, nor even the beginning of the end, but it is, perhaps, the end of the beginning.

(MORE: Google vs. Death)

Since the dawn of civilization, humanity has been enslaved by the knowledge that no lifestyle choice, no medicine, no quirk of fate can enable anyone to live for more than a few decades without suffering progressive, inexorable decline in physical and mental function, leading inevitably to death. So soul-destroying has this knowledge been, for almost everyone, that we have constructed our entire society and world view around ways to put it out of our minds, mostly by convincing ourselves that the tragedy of aging is actually a good thing. And why not? After all, why be preoccupied about something one cannot affect?

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Today we are delighted to announce there is to be a third fund match for the NAD+ Mouse Project!

Today, we are delighted to announce that there is to be a third funding match for the NAD+ Mouse Project!

Dr. David Sinclair will be personally matching the next $5000 in donations for the last 10 days of the campaign to help reach the final $60,000 goal. Now, that is what we call a devoted scientist!

If the project can reach this final fundraising goal, the project will greatly increase in scope and become a full-on lifespan study, including the collection of months of long-term data for NMN. This is the ultimate goal of the project and will allow the research team at Harvard Medical School to obtain enough NMN to be able to investigate a wide range of health measures as well as get a detailed picture of how long-term treatment with NMN affects the aging processes.

Continue reading “David Sinclair Supports NAD+ Mouse Project with a 5k Fund Match” | >

A team of researchers led by Principal Investigator Dr. Jan Gruber from Yale-NUS College has discovered a combination of pharmaceutical drugs that not only increases healthy lifespan in the microscopic worm Caenorhabditis elegans (C. elegans), but also delays the rate of ageing in them, a finding that could someday mean longer, healthier lives for humans.

The study, published in the peer-reviewed international journal Developmental Cell on 8 October 2018, lays crucial groundwork for further research into designing combinations that produce the same effect in mammals.

“Many countries in the world, including Singapore, are facing problems related to ageing populations,” said Dr. Gruber, whose lab and research team made the discovery. “If we can find a way to extend healthy lifespan and delay ageing in people, we can counteract the detrimental effects of an ageing population, providing countries not only medical and , but also a better quality of life for their people.”

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Cancer is the poster child of age-related diseases, and a recent study sheds light on why the risk of cancer rises dramatically as we age.

Abstract

For many cancer types, incidence rises rapidly with age as an apparent power law, supporting the idea that cancer is caused by a gradual accumulation of genetic mutations. Similarly, the incidence of many infectious diseases strongly increases with age. Here, combining data from immunology and epidemiology, we show that many of these dramatic age-related increases in incidence can be modeled based on immune system decline, rather than mutation accumulation. In humans, the thymus atrophies from infancy, resulting in an exponential decline in T cell production with a half-life of ∼16 years, which we use as the basis for a minimal mathematical model of disease incidence. Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data.

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In support of the NAD+ Mouse Project over at Lifespan.io, Dr. David Sinclair will be doing an AMA on Reddit Futurology Tuesday, October 23, 2018 from 11:00 – 12:00 AM EDT. Dr. Sinclair will be answering questions from the community about his work with NAD+ biology, Sirtuins, and why the NAD+ Mouse Project is important for aging research. To ask your question please visit the AMA thread on Reddit Futurology here.

For those not familiar with NAD+ biology we did the NAD+ World series recently which explores this area of the biology of aging. We also took a look at why NAD+ appears to decline as we age and what is one of the most likely reasons for this.

Dr. Sinclair and his team at Harvard Medical School are currently hosting the NAD+ Mouse Project with us at Lifespan.io which is aiming to conduct long-term studies into the ability of NAD+ precursor molecule, NMN, to delay or even reverse some aspects of aging.

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