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The consortium, called LifeTime, aims to use three emerging technologies—machine learning, the study of single cells, and lab-grown organlike tissues called organoids—to map how human cells change over time and develop diseases. It is one of six candidates in the latest round of ambitious proposals for European flagships, billion-euro research projects intended to run for 10 years. There is just one snag: The European Commission has decided that it won’t launch any of them.


Six candidate research proposals lost in limbo.

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On senescent cells, mechanism of interaction and (potential?!) side effects of NAD+ supplements. “… Those people self-experimenting with NAD+ precursor supplementation should consider keeping a close eye on markers of inflammation…”


Enhancing levels of NAD+ in mitochondria via delivery of various precursor compounds as supplements is growing in popularity as an approach to boost faltering mitochondrial function and thus modestly slow the progression of aging. A human trial demonstrated improved vascular function as a result of nicotinamide riboside supplementation, for example. Researchers here show that increased NAD+ will likely make worse the inflammatory signaling of senescent cells, however. Senescent cells accumulate with age, and are an important cause of the chronic inflammation of aging that drives the progression of many age-related diseases.

The results here suggest that efficient senolytic treatments to selectively destroy senescent cells should proceed any of the current approaches to raising levels of NAD+ in older individuals — and it is an open question as to whether any of the existing available options are efficient enough to make NAD+ enhancement safe in the longer term. Those people self-experimenting with NAD+ precursor supplementation should consider keeping a close eye on markers of inflammation.

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May have posted this, but this is very cool. “We can now generate insulin-producing cells that look and act a lot like the pancreatic beta cells you and I have in our bodies,” explains one of the team, microphysiologist Matthias Hebrok from the University of California San Francisco (UCSF).


Although treatment of type 1 diabetes has come a long way since it was first described in Ancient Egypt, insulin injections and finger pricks are a daily part of life for many diabetics.

But researchers have just made a breakthrough that might one day make these technologies obsolete, by transforming human stem cells into functional insulin-producing cells (also known as beta cells) – at least in mice.

“We can now generate insulin-producing cells that look and act a lot like the pancreatic beta cells you and I have in our bodies,” explains one of the team, microphysiologist Matthias Hebrok from the University of California San Francisco (UCSF).

I am writing this shortly after returning from the third edition of RAADfest, a conference created two years ago by a team led by Jim Strole. I go to a lot, I mean a lot, of conferences, not least because outreach is such a big part of my role in our crusade. But I think this is the first time I have chosen to devote an editorial to one. You may wonder what’s so special.

Well, RAADfest is … not your typical conference. Its organizers—Strole and his team, most notably his partner Bernadeane—have, for a couple of decades, led a group in Arizona named “People Unlimited”, which has acquired a reputation—and, I have to report, a well-deserved one—for, let’s say, placing excessive emphasis on the principle that ‘‘where there’s a will there’s a way’’ in relation to the defeat of aging (Yeah, I can still do classic British understatement when I try). Accordingly, when they first let it be known that they planned to do something bigger, the initial reaction was decidedly mixed. I don’t know how many credentialed biogerontologists declined speaking invitations, but only a few of us accepted—and of those, as I recall, only the perennially fearless Michael Rose was a university professor. I myself, though happy to lend my support to this new initiative as a speaker, was rather more diffident in response to Strole’s entreaties to promote the event through my outreach channels.

But the doubters were wrong—very wrong. The event was a storming success, in terms of both attendance—Strole had secured significant sponsorship from the Life Extension Foundation under the expectation of a budgetary shortfall but was actually able to give it back, yes you read that correctly—and also content, which, while being necessarily a little light on science given the paucity of scientist speakers, was coherent, rousing, and informative.

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Stressful life events most likely contribute to autoimmune diseases, but scientists don’t have a deep understanding of the underlying chain of events. A study on mice published this week in mSystems suggests that the gut microbiota may play a significant role in that connection. Researchers found that the onset of stress caused changes in the intestinal bacteria that, in turn, stimulated the activity of immune cells in a way that increased the likelihood that the body would a…


Chronic social stress in mice induces the expression of virulent genes in the gut microbiota. The altered microbiota increases the presence of effector T helper cells in the lymph nodes and induces myelin autoreactive cells. Exposure to chronic stress, therefore, may increase the risk of developing autoimmune diseases for some individuals with a susceptibility.

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