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“Current treatments for diseases related to ageing “just exchange one disease for another”, says physician Nir Barzilai of the Albert Einstein College of Medicine in New York. That is because people treated for one age-related disease often go on to die from another relatively soon thereafter. “What we want to show is that if we delay ageing, that’s the best way to delay disease.”

Barzilai and other researchers plan to test that notion in a clinical trial called Targeting Aging with Metformin, or TAME. They will give the drug metformin to thousands of people who already have one or two of three conditions — cancer, heart disease or cognitive impairment — or are at risk of them. People with type 2 diabetes cannot be enrolled because metformin is already used to treat that disease.
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http://www.nature.com/news/anti-ageing-pill-pushed-as-bona-fide-drug-1.17769

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987618/

Aging Pathways: insulin-foxo, mTOR, AMPK, Sirtuin

Ageing does not have to bring…frailty http://www.telegraph.co.uk/news/science/science-news/11326136/Ageing-does-not-have-to-bring-poor-health-and-frailty-say-Kings-College-scientists.html Good #cyclists are as fit at 79 as 55 but how many are there at 79 HT @timjph

Sequenced genomes reveal mutations that disable single genes and can point to new drugs.

Ewen Callaway

28 October 2014 Corrected:
29 October 2014

http://www.nature.com/news/geneticists-tap-human-knockouts-1.16239

You should also read the Corrections to this article
http://www.nature.com/news/geneticists-tap-human-knockouts-1.16239#/correction1

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The poster child for human-knockout efforts is a new class of drugs that block a gene known as PCSK9 (see Nature 496, 152–155; 2013). The gene was discovered in French families with extremely high cholesterol levels in the early 2000s. But researchers soon found that people with rare mutations that inactivate one copy ofPCSK9 have low cholesterol and rarely develop heart disease. The first PCSK9-blocking drugs should hit pharmacies next year, with manufacturers jostling for a share of a market that could reach US$25 billion in five years.

“I think there are hundreds more stories like PCSK9 out there, maybe even thousands,” in which a drug can mimic an advantageous
loss-of-function mutation, says Eric Topol, director of the Scripps Translational Science Institute in La Jolla, California. Mark Gerstein, a bio­informatician at Yale University in New Haven, Connecticut, predicts that human knockouts will be especially useful for identifying drugs that treat diseases of ageing. “You could imagine there’s a gene that is beneficial to you as a 25-year-old, but the thing is not doing a good job for you when you’re 75.”

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