{"id":350,"date":"2015-03-13T18:16:01","date_gmt":"2015-03-13T18:16:01","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=350"},"modified":"2015-03-13T22:16:22","modified_gmt":"2015-03-13T22:16:22","slug":"kill-senescent-cells-before-they-kill-you","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/03\/13\/kill-senescent-cells-before-they-kill-you\/","title":{"rendered":"Kill Senescent Cells Before They Kill You"},"content":{"rendered":"

Several readers have asked me to comment on the<\/i> press release<\/a> and <\/i>preprint<\/a> that came out of the Mayo Clinic this week. \u00a0Researchers searched for ways to eliminate cells in the body that have become senescent and destructive. \u00a0Their tests in cell cultures and in genetically-modified mice turned up two substances, one natural and cheap, the other patented and dear. \u00a0I think theirs is a promising approach, and will soon offer substantial life extension in humans with minimal side-effects, but my guess is that the particular cocktail they have found will be left in the dust.<\/i><\/p>\n

Here\u2019s the Theory<\/b><\/p>\n

Our stem cells divide through a lifetime, renewing our muscles, blood vessels, and especially skin and blood cells that turn over rapidly. \u00a0But in the process, chromosomes in those stem cells lose their telomeres. \u00a0When its chromosomes have telomeres that are too short, a cell becomes \u201csenescent.\u201d \u00a0Senescent cells are not just sluggish and moribund, they actually poison the nearby tissue (creating more senescent cells) and poison the body with chemical signals (cytokines) that fan the flames of inflam-aging. \u00a0This is called SASP, for \u201csenescent-associated secretory phenotype\u201d. \u00a0A tiny number of senescent cells can do a great deal of damage.<\/p>\n

Would we be better off without senescent cells? \u00a0It was the insight of the Mayo Clinic\u2019s Jan van Deursen to ask this question with an experiment four years ago. \u00a0He genetically modified mice in such a way that senescent cells had a bomb and a trigger attached. \u00a0By feeding the mice a molecule that matched the trigger, he could cause the senescent cells to self-destruct, leaving normal cells intact. \u00a0He did a controlled experiment, comparing the same genetically-modified mice, with and without pulling the trigger. \u00a0The result was eye-popping life extension in the mice that had their senescent cells removed. \u00a020 to 25% increase in life span from a single treatment, fairly late in life [ref<\/a>].<\/p>\n

Just a decade ago, such discoveries would remain languishing in the lab for a maddeningly-long time. \u00a0But it is a sign of the times that venture capital and even Big Pharma are investing in longevity science. \u00a0Van Deursen\u2019s discovery was quickly seized by half a dozen different labs around the world (including a for-profit spinoff by van Deursen himself). \u00a0What they are looking for is a drug that will attack the 0.01% of senescent cells while leaving 99.99% of non-senescent cells unharmed.<\/p>\n

\u00a0<\/strong><\/strong><\/span><\/p>\n

The Research Strategy<\/b><\/p>\n

The research group at Mayo\/Scripps<\/a> started with gene expression profiles for senescent cells, comparing them to profiles for non-senescent cells. \u00a0This was used to identify targets for the drug. \u00a0Van Deursen had used p16 to identify senescent cells. \u00a0P16 is a gene that keeps senescent cells alive when they really should be eliminating themselves. \u00a0The Mayo\/Scripps team identified several other drug targets, but did not use p16. \u00a0They used RNA interference to silence these genes, one at a time, to help identify effective strategies for differentially targeting the senescers. \u00a0Then they screened 46 compounds to see which would best attack the targets they had identified.<\/p>\n

The result was two drugs: quercetin<\/a> seemed to work best for endothelial cells (in arteries), and dasatinib<\/a> was best for fat stem cells. \u00a0Quercetin is cheap and found in many herbs and berries; dasanatib is a patented chemotherapy agent, sold for a scandalously high price<\/a> by Bristol Myers Squib. \u00a0The team tested the combination Q+D for short-term health effects in mice, and found encouraging results.<\/p>\n

Q + D<\/b><\/p>\n

Quercetin is a common flavonoid, polycyclic, found in black currents, cilanthro, red onion, watercress, cranberries, and smaller amounts in many fruits and herbs. \u00a0It is an anti-oxidant, but you know I\u2019m not much impressed by that<\/a>. Though it is natural, it is a mutagen, which means it breaks DNA. Substances like this would never be approved by the FDA, if they had to be approved by the FDA, but they don\u2019t because they escape regulation as GRAS — \u201cgenerally recognized as safe\u201d. \u00a0This is not to damn the stuff–many toxins have a beneficial effect in small doses. \u00a0This is hormesis<\/a>, a paradoxical but common and well-documented fact of longevity science.<\/p>\n

But in the case of quercetin, it has been tried in longevity tests with mammals, and the results are not promising. \u00a0In 1982, the first published study<\/a> showed no life extension, and perhaps a slight shortening of life span in male mice. Stephen Spindler, our reality check for life extension claims, found that quercetin had zero effect on mouse life span in a 2013 study<\/a>.<\/p>\n

\"\"<\/p>\n

Dasatinib is a chemotherapy agent, sold by Bristol-Myers Squibb as Sprycel at thousands of dollars per dose for treatment of leukemia. \u00a0\u00a0Dasaitinib has been tested for toxicity<\/a> but never for life extension.<\/p>\n

\"\"<\/p>\n

\u00a0<\/strong><\/strong><\/span><\/p>\n

To put this in perspective…<\/b><\/p>\n

The gold standard for a life extension drug is that it works to extend life span in rodents. \u00a0That\u2019s because it\u2019s too easy to extend life span in simpler lab models like worms and flies, but tests in humans overtax our patience. \u00a0Even for mice, the test requires three years and hundreds of thousands of dollars, so researchers are motivated to screen different compounds with tests that can be done in a petri dish, or with short-term studies of physiological changes in live mice. \u00a0This is exactly what the Mayo\/Scripps team did, and it should have yielded good candidates for life extension drugs. \u00a0But the result was a \u201cgood candidate\u201d that had already been tried, and didn\u2019t do so well.<\/p>\n

\"\"<\/p>\n

The reason that short-term benefits to the metabolism are not<\/i><\/b> a good indicator of what might increase longevity is that body chemistry is complicated. \u00a0Life span is tightly regulated, with a mind of its own. \u00a0Some substances have short-term benefits, and the body over-compensates with a shorter life span. \u00a0Anti-oxidants are a good example. \u00a0Other substances do short-term damage, and again the body over-compensates and the result is a longer life span. \u00a0Look at the way paraquat affects life span in worms<\/a>!<\/p>\n

\u00a0<\/strong><\/strong><\/span><\/p>\n

The Bottom Line<\/b><\/p>\n

I\u2019m betting that the search for strategies that differentially kill senescent cells will soon lead to better drugs than quercetin or dasatinib.<\/p>\n

\u00a0<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

Several readers have asked me to comment on the press release and preprint that came out of the Mayo Clinic this week. \u00a0Researchers searched for ways to eliminate cells in the body that have become senescent and destructive. \u00a0Their tests in cell cultures and in genetically-modified mice turned up two substances, one natural and cheap, … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"jetpack_post_was_ever_published":false,"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-350","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nKill Senescent Cells Before They Kill You - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/03\/13\/kill-senescent-cells-before-they-kill-you\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Kill Senescent Cells Before They Kill You\" \/>\n<meta property=\"og:description\" content=\"Several readers have asked me to comment on the press release and preprint that came out of the Mayo Clinic this week. \u00a0Researchers searched for ways to eliminate cells in the body that have become senescent and destructive. \u00a0Their tests in cell cultures and in genetically-modified mice turned up two substances, one natural and cheap, ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\/\/mathforum.org\/~josh","sameAs":["http:\/\/AgingAdvice.org"],"url":"https:\/\/scienceblog.com\/joshmitteldorf\/author\/joshmitteldorf\/"}]}},"jetpack_featured_media_url":"","jetpack_shortlink":"https:\/\/wp.me\/pgtN8h-5E","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/350","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/users\/65"}],"replies":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/comments?post=350"}],"version-history":[{"count":0,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/350\/revisions"}],"wp:attachment":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/media?parent=350"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/categories?post=350"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/tags?post=350"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}