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On the 23rd of this month, Dr. David Sinclair did an Ask Me Anything over at the Futurology subreddit in support of the NAD+ Mouse Project on Lifespan.io. There were a range of interesting questions from the community about his work in aging research, particularly the role of NAD+ in aging.

Dr. David A. Sinclair is a Professor in the Department of Genetics at Harvard Medical School and a co-joint Professor in the Department of Physiology and Pharmacology at the University of New South Wales. He is the co-Director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging and a Senior Scholar of the Ellison Medical Foundation. He obtained his Ph.D. in Molecular Genetics at the University of New South Wales, Sydney in 1995. He worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente; there, he co-discovered a cause of aging for yeast as well as the role of Sir2 in epigenetic changes driven by genome instability.

More recently, he has been in the spotlight for his work with NAD+ precursors and their role in aging and has been helping to develop therapies that replace NAD+, which is lost with aging, in order to delay the diseases of old age. Below are a selection of questions and answers from the AMA, and we urge you to head over to Reddit Futurology to check out the other questions that people asked.

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Flu sufferers now have a new option for relieving symptoms. Xofluza (baloxavir marboxil), a single-dose, oral prescription drug, was approved by the US Food and Drug Administration on Wednesday. The antiviral is the first new flu treatment approved by the FDA in nearly 20 years, FDA Commissioner Dr. Scott Gottlieb said in a statement.

“With thousands of people getting the flu every year, and many people becoming seriously ill, having safe and effective treatment alternatives is critical,” said Gottlieb.

The pill is intended for patients who are 12 or older and who have had symptoms for no more than 48 hours. When patients with the flu, a respiratory illness, are treated within 48 hours of becoming sick, antiviral drugs can reduce symptoms and duration of illness, according to the FDA.

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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.

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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.

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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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