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Scientists successfully extended the average lifespan of mice by breeding them using embryonic stem cells with extra-long telomeres. The findings are significant because the researchers managed to extend lifespan without genetic modification, and they also shed light on the aging process and techniques that might someday slow it.

The study — published October 17 in Nature Communicationsfocuses on telomeres, which are stretches of DNA found at the end of chromosomes.

Because telomeres protect the genetic material inside chromosomes, they’ve been likened to the plastic tips on the ends of shoelaces. But telomeres have also been compared to bomb fuses, or “molecular clocks,” because they become shorter each time a cell divides, eventually shrinking so much that the cell dies or stops dividing. This shortening of our telomeres is associated with aging, cancer, and death.

A new study from the Johns Hopkins University School of Medicine shows that selectively removing senescent cells—cells that no longer divide—from brains with a form of Alzheimer’s disease can reduce brain damage and inflammation and slow the pace of cognitive decline. These findings, say researchers, add to evidence that senescent cells contribute to the damage caused by Alzheimer’s disease.

“Our results show that eliminating these cells may be a viable route to treat Alzheimer’s disease in humans,” says Mark Mattson, a professor of neuroscience at the School of Medicine and a senior investigator in the Laboratory of Neurosciences at the National Institute on Aging.

A report on the work was published April 1 in Nature Neuroscience.

With ageing, intrinsic haematopoietic stem cell (HSC) activity decreases, resulting in impaired tissue homeostasis, reduced engraftment following transplantation and increased susceptibility to diseases. However, whether ageing also affects the HSC niche, and thereby impairs its capacity to support HSC function, is still widely debated. Here, by using in-vivo long-term label-retention assays we demonstrate that aged label-retaining HSCs, which are, in old mice, the most quiescent HSC subpopulation with the highest regenerative capacity and cellular polarity, reside predominantly in perisinusoidal niches. Furthermore, we demonstrate that sinusoidal niches are uniquely preserved in shape, morphology and number on ageing. Finally, we show that myeloablative chemotherapy can selectively disrupt aged sinusoidal niches in the long term, which is linked to the lack of recovery of endothelial Jag2 at sinusoids. Overall, our data characterize the functional alterations of the aged HSC niche and unveil that perisinusoidal niches are uniquely preserved and thereby protect HSCs from ageing.

51-year-old astronaut Scott Kelly lived in the International Space Station for almost a year while his identical twin brother Mark continued with life on earth. As an astronaut, Scott is a member of group that’s been studied in greater depth than any other living humans. As part of a special study, so was his earthbound twin.

The many negatives of space travel were expected to take their toll on Scott’s health — and they did.

The scene last weekend at the Westgate, a Las Vegas mega resort, was like many others in Sin City. Alongside the one-armed bandits and craps tables, around 1,000 people milled around a mega convention centre. Many would have been close to pensionable age, and came from all corners of the Earth. But all the attendees at the event, RAADfest, were pursuing something out of the ordinary: immortality.


‘Immortalists’ say they have discovered how to slow and perhaps even reverse the ageing process — but is that really a good thing?