https://www.economist.com/technology-quarterly/2023/09/25/some-claim-human-lifespans-can-be-lengthened-indefinitely
QT:{{”
There is a story about a blues musician who, when questioned on his 100th birthday about his decades of smoking and drinking, responded that if he’d known he was going to live so long, he’d have taken better care of himself. Bryan Johnson is that apocryphal bluesman’s polar opposite. He has been taking care of himself for years to a degree as remarkable, in its way, as the deepest devotion to bourbon and bad choices. …
The daily regime which he and his many doctors have devised makes life in Biosphere 2 look sybaritic. A kilogram of vegetables, all before 11am, rigorous workouts lasting 45-60 minutes, and 100 pills, including metformin and rapamycin. His vital functions are subjected to the sort of continuous scrutiny more usually associated with laboratory animals. He says he is ageing at 69% of the normal rate. Mr Johnson, who has been described as the most measured man in the world, can afford the team of medics, trainers and dieticians who minister to him because selling Braintree, an electronic-payments company which he founded, left him with a net worth of more than $100m. For mere mortals, however, a range of less intensive options are available.
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Posts Tagged ‘aging’
Some claim human lifespans can be lengthened indefinitely
December 11, 2023Eating fewer calories can ward off ageing
December 11, 2023https://www.economist.com/technology-quarterly/2023/09/25/eating-fewer-calories-can-ward-off-ageing
QT:{{”
Take the mtorc1 pathway. The complex of proteins which gives it its name first came to attention because an immune suppressant called rapamycin has a strong effect on it: hence “mechanistic target of rapamycin complex 1”. That gives no real clue, however, to the fact that the signalling pathway in which mtorc1 sits is a complex set of controls and feedbacks designed to regulate metabolism in response both to the availability of nutrients …
The ambit of this regulatory power is broad; it influences the rate at which cells break down damaged internal structures (“autophagy”), the balance of their protein content (“proteostasis”) and the reproduction of their mitochondria, components responsible for turning the calories it receives into a form of energy its proteins can use. Autophagy, proteostasis and mitochondrial reproduction are three more of the 12 hallmarks of aging.
What is more, rapamycin, the effects of which give mtorc1 its name, turns out to lengthen the lives of lab animals even though it curbs their immune responses. …There is thus a search for “rapalogs” which provide the benefits of a tuned-up mtorc1 pathway without so many costs.
Another pathway which calorie-restriction studies have marked out as promising is named after a protein called ampk (don’t ask). This regulates the production of ATP, a small energy-carrying molecule produced in mitochondria. When atp levels fall, the ampk pathway increases a cell’s sensitivity to insulin.
Metformin, a drug used to treat type-2 diabetes, does so by activating the ampk pathway. Like rapamycin, it extends the lifespans of healthy mice.
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NRGN Gene – GeneCards | NEUG Protein | NEUG Antibody
May 9, 2022https://www.genecards.org/cgi-bin/carddisp.pl?gene=NRGN
Aging related gene in capstone4
Anti-ageing pill pushed as bona fide drug
July 4, 2017QT:{{‘
“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
Can we hit the snooze button on aging? | March 6, 2017 Issue – Vol. 95 Issue 10 | Chemical & Engineering News
April 23, 2017Can we hit the snooze button on #aging?
http://CEN.acs.org/articles/95/i10/hit-snooze-button-aging.html Various ways to tackle this timeless issue; for me more pertinent by the day
Aging increases cell-to-cell transcriptional variability upon immune stimulation | Science
April 21, 2017#Aging increases cell-to-cell transcriptional variability upon immune stimulation, but just for 225 up-reg. genes http://science.ScienceMag.org/content/355/6332/1433
The Aging Stress Response
February 12, 2016http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987618/
Aging Pathways: insulin-foxo, mTOR, AMPK, Sirtuin
Ageing does not have to bring poor health and frailty, say King’s College scientists – Telegraph
January 26, 2015Ageing 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
Geneticists tap human knockouts
November 1, 2014Sequenced 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
QT:{{”
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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