Killing old cells to stay young.

I want to pass on one of Science Magazine's choices for the top ten scientific breakthroughs of the year.

Pricey plastic surgery won't stop you from getting old. Nor will dietary supplements, testosterone injections, or those wrinkle creams that imply they'll make you look 21 again. But this year, researchers demonstrated one way to postpone some ravages of time—at least in mice. When they selectively weeded out rundown cells, the animals lived longer and remained healthier as they aged.

The infirm cells the scientists targeted had undergone a partial shutdown known as senescence, in which they lose the ability to divide. Researchers think senescence may prevent worn-out, cancer-prone cells from initiating tumors, but it may also promote aging. As we grow older, more and more cells stop reproducing, potentially robbing our tissues of the ability to replace dead or injured cells. Senescent cells also discharge molecules that can cause problems such as abnormal cell growth and inflammation.

The first study showing that eliminating senescent cells can produce health and longevity benefits, at least in middle-aged mice, came out in February. Deterioration of the animals' hearts and kidneys slowed, and they didn't sprout tumors until later in their lives. Some age-related declines, such as in memory and muscle coordination, didn't abate. Nonetheless, the rodents outlived their contemporaries by more than 20%.

In October, the same research team took aim at senescent cells from the immune system that amass in artery-clogging plaques and may drive their formation. Removing these cells from mice that are prone to atherosclerosis reduced the amount of fatty buildup in the animals' arteries by 60%, even though the rodents gorged on fat-laden food.

The multibillion-dollar question: Will taking out senescent cells help humans stay young longer? Both studies used genetically modified mice that clear away their senescent cells in response to a particular compound—a technique that isn't feasible in humans. But researchers have created several so-called senolytic drugs that slay senescent cells without genetic tinkering. Next year, scientists will launch the first clinical trial of one of those drugs in people who have arthritis.

References:

D. J. Baker et al., “Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders,” Nature 479, 232 (2 November 2016)

D. J. Baker et al., “Naturally occurring p16Ink4a-positive cells shorten healthy lifespan,,” Nature 530, 184 (11 February 2016)

B. G. Childs et al., “Senescent intimal foam cells are deleterious at all stages of atherosclerosis,” News from Science 354, 472 (28 October 2016)