Yuli is confident in proto/first generation AGI before the end of 2024.
It's my #1 most wanted future need.... errr... I mean, technological breakthrough I look forward to.wjfox wrote: ↑Thu May 20, 2021 7:51 am
Aside from climate change, I can't think of any other subject that's more important to me. Without a cure for aging, we're all dead within a century and won't get to experience a single damn thing after that. It should be in everyone's top 3 for their most-wanted future breakthroughs.
If you're going to live to 2132, you'll most certainly going to live to 2500 and even beyond sans a freak accident.Yuli Ban wrote: ↑Wed May 26, 2021 10:21 pm Analysis of blood markers predicts human lifespan limit.
I'm not the healthiest man alive, but I would like to live for a good long while to see all that the Future™ has in store. Presuming I do somehow magically make it to 138 through arcane magic and extreme luck, that would mean I'd live to 2132.
https://metro.co.uk/2021/06/10/is-150-y ... i=14745298Thursday 10 Jun 2021
While most of us can expect to live to around 80, some people defy expectations and live to be over 100. In places such as Okinawa, Japan and Sardinia, Italy, there are many centenarians. The oldest person in history — a French woman named Jeanne Calment — lived to 122. When she was born in 1875, the average life expectancy was roughly 43.
But just how long could a human actually live? It’s a question people have been asking for centuries. While average life expectancy (the number of years a person can expect to live) is relatively easy to calculate, maximum lifespan estimates (the greatest age a human could possibly reach) are much harder to make. Previous studies have placed this limit close to 140 years of age. But a more recent study proposes that the limit to human lifespan is closer to 150.
Calculating lifespan
The oldest and still most widely used method for calculating life expectancy, and thus lifespan, relies on the Gompertz equation. This is the observation, first made in the 19th century, that human death rates from disease increase exponentially with time. Essentially, this means your chance of death — from cancer, heart disease and many infections, for example — roughly doubles every eight to nine years.
There are many ways the formula can be tweaked to account for how different factors (such as sex or disease) affect the lifespan within a population. Gompertz calculations are even used to calculate health insurance premiums — which is why these companies are so interested in whether you smoke, whether you are married and anything else that might allow them to more accurately judge the age at which you will die.
Another approach to figuring out how long we can live is to look at how our organs decline with age, and run that rate of decline against the age at which they stop working. For example, eye function and how much oxygen we use while exercising show a general pattern of decline with ageing, with most calculations indicating organs will only function until the average person is around 120 years old.
Sinclair and his team restored vision in old mice and in mice with damaged retinal nerves by resetting some of the thousands of chemical marks that accumulate on DNA as cells age. They are now working to rejuvenate the brains of old mice. This work is so promising that Sinclair believes he can get to human trials within two years. Sinclair is using three genes to reset the age of cells.
Several different causes of aging have been discovered, but the question remains whether there are common underlying mechanisms that determine aging and lifespan. Researchers from the Max Planck Institute for Biology of Ageing and the CECAD Cluster of Excellence in Ageing research at the University Cologne have now come across folate metabolism in their search for such basic mechanisms. Its regulation underlies many known aging signaling pathways and leads to longevity. This may provide a new possibility to broadly improve human health during aging.
In recent decades, several cellular signaling pathways have been discovered that regulate the lifespan of an organism and are thus of enormous importance for aging research. When researchers altered these signaling pathways, this extended the lifespan of diverse organisms. However, the question arises whether these different signaling pathways converge on common metabolic pathways that are causal for longevity.
Research conducted by Qiang et al has discovered a link between a protein in red blood cells and age-related decline in cognitive performance. Published in the open access journal PLOS Biology on 17th June 2021, the study shows that depleting mouse blood of the protein ADORA2B leads to faster declines in memory, delays in auditory processing, and increased inflammation in the brain.
As life expectancies around the world increase, so are the number of people who will experience age-related cognitive decline. Because the amount of oxygen in the blood also declines with age, the team hypothesized that aging in the brain might be naturally held at bay by adenosine receptor A2B (ADORA2B), a protein on the membrane of red blood cells which is known to help release oxygen from the blood cells so it can be used by the body. To test this idea, they created mice that lacked ADORA2B in their blood and compared behavioral and physiological measures with control mice.
