Molecule Kills Elderly Cells, Reduces Signs of Aging In Mice (sciencemag.org)
An anonymous reader shares an excerpt from a Science Magazine report: Even if you aren't elderly, your body is home to agents of senility -- frail and damaged cells that age us and promote disease. Now, researchers have developed a molecule that selectively destroys these so-called senescent cells. The compound makes old mice act and appear more youthful, providing hope that it may do the same for us. As we get older, senescent cells build up in our tissues, where researchers think they contribute to illnesses such as heart disease, arthritis, and diabetes. In the past, scientists have genetically modified mice to dispatch their senescent cells, allowing the rodents to live longer and reducing plaque buildup in their arteries. Such genetic alterations aren't practical for people, but researchers have reported at least seven compounds, known as senolytics, that kill senescent cells. A clinical trial is testing two of the drugs in patients with kidney disease, and other trials are in the works. However, current senolytic compounds, many of which are cancer drugs, come with downsides. They can kill healthy cells or trigger side effects such as a drop in the number of platelets, the cellular chunks that help our blood clot. Cell biologist Peter de Keizer of Erasmus University Medical Center in Rotterdam, the Netherlands, and colleagues were investigating how senescent cells stay alive when they uncovered a different strategy for attacking them. Senescent cells carry the type of DNA damage that should spur a protective protein, called p53, to put them down. Instead, the researchers found that a different protein, FOXO4, latches onto p53 and prevents it from doing its duty. To counteract this effect, De Keizer and colleagues designed a molecule, known as a peptide, that carries a shortened version of the segment of FOXO4 that attaches to p53. In a petri dish, this peptide prevented FOXO4 and p53 from hooking up, prompting senescent cells to commit suicide. But it spared healthy cells. The researchers then injected the molecule into mutant mice that age rapidly. These rodents live about half as long as normal mice, and when they are only a few months old, their fur starts to fall out, their kidneys begin to falter, and they become sluggish. However, the peptide boosted the density of their fur, reversed the kidney damage, and increased the amount of time they could scurry in a running wheel, the scientists report online today in Cell. When the researchers tested the molecule in normal, elderly mice, they saw a similar picture: In addition to helping their kidneys and fur, the molecule also increased their willingness to explore their surroundings.
More hair and better kidney function?
In other words, it's like washing down Rogaine with beer?
We used to have a Bill of Rights. Now, with the rights gone, all we have left is the bill.
We're finding all these awesome ways to extend and enrich their lives. God I wish I was a rat...
I tend to rant.
I'm glad we seem to be on track to tackling frailty with age... however, we're nowhere when it comes to tackling our resource problems...
A cynical though: Will we stay healthy and strong longer just so we can send the 50 year olds to war over water instead of just the 20 to 30 year olds?
Well, are you off the meth ?
New things are always on the horizon
Countries with longer lifespans have lower population growth, or even decline. This is plausible because people in those countries don't have to have extra children to be certain that some will survive. If life extension also increases the maximum reproductive age, people could put off having children which would reduce population growth even more. A lot of people in developed countries only choose to have children because their biological clock is ticking.
Correlation or causation?
After all, education and prosperity are in that mix too.
"I don't know, therefore Aliens" Wafflebox1
If this allows you to live a health life until 100 they will put retirement age up to 90.
2015 - A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan
http://www.cell.com/cell-metab...
2016 - Fasting: Awakening the Rejuvenation from Within | Valter Longo | TEDxEchoPark
https://www.youtube.com/watch?...
2017 - Fasting-Mimicking Diet Promotes Ngn3-Driven -Cell Regeneration to Reverse Diabetes
http://www.cell.com/cell/fullt...
You can replicate the study at home with 4 days of a ketogenic fasting mimic diet every 10 days for six cycles with a %5 carb ( 20 net carbs of nuts/greens/dairy) / %75 fat (nuts/olives/fish/eggs/butter) / %20 protein (nuts/fish/eggs/greens/bacon) macro and 50% then 20% , 20% , 20% calorie restriction (the 3 day 10% restriction of the study on mice was extreme and not for the faint of heart). Throw in multi vitamin and probiotic day 3 and 4 and lots and lots of water with pinch of salt now and then/mineral water/coffee/tea during the fast and... amazing. You lose fat, feel better, and if the studies are right; get some nice anti-cancer, anti-aging, anti-disease, body regeneration benefits.
For me, the following was one of the more interesting pieces:
Senescent cells carry the type of DNA damage that should spur a protective protein, called p53, to put them down. Instead, the researchers found that a different protein, FOXO4, latches onto p53 and prevents it from doing its duty. To counteract this effect, De Keizer and colleagues designed a molecule, known as a peptide, that carries a shortened version of the segment of FOXO4 that attaches to p53.
Does this mean we have an internal cleanup mechanism, but somehow it's gotten subverted over the years? Our ancestors may have had the benefit of p53, until something changed and we started developing FOXO4 when we hadn't before? Or somewhere along the line the amount of FOXO4 in our bodies increased? That seems fascinating to me.
My first reaction was also to think, "That doesn't seem like a very useful mutation/bit of evolution" but of course most of the age-related stuff won't be important until you're beyond the age of reproduction, so it's probably relatively easier for that kind of problem to sneak in than something that affects the young. I also wonder if it's *just* a mutation, or if the FOXO4 is doing something else more useful for us when we're young, that the tradeoff is worth it?
The Quirkz Handbook of Self-Improvement for People Who Are Already Pretty Okay
Kill off all my elderly brain cells:
a) Pretty much nothing left in my head.
b) Nobody will notice any change.
Don't step on the baby.
Death really is unnecessary from an evolutionary standpoint. We have grown beyond the need to pass on genetic traits that allow us to adapt to changing environments since mankind uses technology to do this. Medicines are preventing the need to evolve immunities naturally so the fact that we die is simply the product of inefficiencies on cellular replication. The three things needed for immortality are negative apoptosis, efficient waste removal, and efficient genetic error checking. There is no need for the skin cells you have at 50 to be any different than at 20.