{"id":465,"date":"2016-02-08T21:39:32","date_gmt":"2016-02-08T21:39:32","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=465"},"modified":"2016-02-08T21:39:32","modified_gmt":"2016-02-08T21:39:32","slug":"one-of-the-most-important-aging-discoveries-ever","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/02\/08\/one-of-the-most-important-aging-discoveries-ever\/","title":{"rendered":"‘one of the most important aging discoveries ever’"},"content":{"rendered":"

The science <\/i>news circuits have been buzzing<\/i><\/a> about <\/i>Jan van Deursen\u2019s recent paper<\/i><\/a>, in which mice stayed younger, longer when their senescent cells were removed. \u00a0They\u2019re right to call this technology a game changer for anti-aging medicine. \u00a0They\u2019re wrong to say this is new\u2014in fact, the recent paper advances only incrementally over <\/i>van Deursen\u2019s stunning results from 2011<\/i><\/a>. \u00a0But what they don\u2019t explain very well is that so far this technology only works for specially-prepared mice. \u00a0The mice are genetically engineered (before birth) to make their senescent cells vulnerable to a trigger that can be administered later, when they are old. \u00a0We don\u2019t yet have a way to selectively kill senescent cells in a natural mouse, or a natural human.<\/i><\/p>\n

(Background is in my blog post of last spring<\/a>.)<\/p>\n

As we get older, a tiny minority (~1 in 10,000) of cells becomes senescent, usually through telomere shortening that goes so far as to compromise the integrity of the chromosomes. \u00a0The number of cells is small, but they do outsized damage, by secreting signals into the surrounding region and even into the body as a whole that turn on inflammaging, <\/i><\/b>which is one of the primary modes by which the body destroys itself. \u00a0<\/i>Chronic, systemic inflammation is linked to all the diseases of old age, especially arthritis, cancer, arterial diseases and Alzheimer\u2019s.<\/p>\n

The original paper from 2011 reported on a novel idea to test the hypothesis that getting rid of this tiny number of cells could have a positive impact on the whole body. \u00a0The experiment required genetically engineered mice. \u00a0That means their genes were modified in the egg stage, when the incipient mouse is still a single cell, and there\u2019s only one set of genes to modify. \u00a0Mice could be prepared in such a way that a particular gene called p16 was associated with an added gene that made the cells extremely vulnerable to a drug that wouldn\u2019t otherwise have damaged them. \u00a0This was done because senescent cells express p16, while normal cells don\u2019t. \u00a0So administration of the drug would kill just the senescent cells, while leaving normal cells alone.<\/p>\n

The results of the experiment were dramatic. \u00a0Animals that had their senescent cells removed lived 20-25% longer, and were healthier and more active at an age when other mice were in steep decline. \u00a0In the recent paper, life extension was bumped up marginally to 24-27%.<\/p>\n

From my perspective as theorist<\/a>, I take this as confirmation of the idea that aging is part of the developmental program, not an unavoidable side-effect or \u201caccumulated damage\u201d as standard thinking allows.<\/p>\n