Oneskin — the first skin cream that destroys senescent cells:
Longevity, Health, Long Lifespans, and Halthspans, Psychology, Spirituality — I and Carolina Reis Oliveira talk about all these things in relation to the skin. Find out how you can have very healthy skin with OneSkin!
NOT curing aging is immoral.
El libro de José Luis Cordeiro y David Wood, “La Muerte de la Muerte”, cuya publicación en español cubrimos en su día, se ha presentado ahora en francés. Los autores han hecho esta presentación en inglés para promocionarlo.
Continue reading “Presentación de ‘La Mort de la Mort’ (inglés)” »
The maximal reduction for biological age when using the biological age calculator, Phenotypic Age, is ~20 years. In other words, if I’m 80 years old and my biomarkers are all reflective of youth, the lowest possible biological age will be ~60 years old. One reason for that is the inclusion of chronological age in the prediction of biological age, which adds strength to the correlation while simultaneously limiting the maximal biological age reduction.
To account for the possibility that youthful biomarkers at an older chronological age can yield a biological age that is more than 20 years younger, it’s important to quantify biological age using a tool that doesn’t include chronological age in its calculation. Aging.ai fits that criterion, and in the video I present biological age data with use of aging.ai for 24 blood tests since 2009.
A new study shows that humans express a powerful hormone during exercise and that treating mice with the hormone improves physical performance, capacity and fitness. Researchers say the findings present new possibilities for addressing age-related physical decline.
The research, published on Wednesday in Nature Communications, reveals a detailed look at how the mitochondrial genome encodes instructions for regulating physical capacity, performance and metabolism during aging and may be able to increase healthy lifespan.
Scientists in Beijing may be one step closer to having the answer to living longer and reversing the effects of ageing. A group of biologists at the Chinese Academy of Sciences say they have developed a world-first new gene therapy and have been running tests on mice. It involved screening around 10000 genes in search of particularly strong drivers of cellular ageing. They identified 100 genes in that pool, but the one that really stood out was the kat7. They then inactivated that kat7 gene in the livers of mice, Professor Qu Jing explained some of their findings: “These mice show after six to eight months, they show overall improved appearance and grip strength and most importantly they have extended lifespan for about 25%.” Kat7 is one of tens of thousands of genes found in the cells of mammals. The scientists also tested the function of the gene in human stem cells, human liver cells and more. So far there have been no side effects of cellular toxicity. Despite this, the method still has a long way to go from being ready for human trials and will require a lot of funding and much more research. “In the end we do hope that we can find a way to delay ageing even by a very minor percentage we want to delay the human ageing in the future.” For now, there’s no final answer to cheating death, but the scientists plan on testing the function of kat7 in other cell types of humans and other organs of mice.
Whereas cellular senescence is known to promote aging, many of the mechanisms controlling this process remain poorly understood. Using human mesenchymal precursor cells (hMPCs) carrying pathogenic mutations of the premature aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome, the authors conducted a genome-wide CRISPR-Cas9–based screen to identify genes that could affect cellular senescence. They identified KAT7, a histone acetyltransferase gene, as a driver of senescence. Inactivation of Kat7 in mice aging normally and in prematurely aging progeroid mice extended their life span. Although KAT7 requires further study in other cell types, these experiments highlight the utility of genome-wide CRISPR-Cas9 screens and shed further light on mechanisms controlling senescence.
Understanding the genetic and epigenetic bases of cellular senescence is instrumental in developing interventions to slow aging. We performed genome-wide CRISPR-Cas9–based screens using two types of human mesenchymal precursor cells (hMPCs) exhibiting accelerated senescence. The hMPCs were derived from human embryonic stem cells carrying the pathogenic mutations that cause the accelerated aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome. Genes whose deficiency alleviated cellular senescence were identified, including KAT7, a histone acetyltransferase, which ranked as a top hit in both progeroid hMPC models. Inactivation of KAT7 decreased histone H3 lysine 14 acetylation, repressed p15INK4b transcription, and alleviated hMPC senescence.
A brain aging link ~~~.
Suppose Smokey the Bear were to go on a tear and start setting forest fires instead of putting them out. That roughly describes the behavior of certain cells of our immune system that become increasingly irascible as we grow older. Instead of stamping out embers, they stoke the flames of chronic inflammation.
Biologists have long theorized that reducing this inflammation could slow the aging process and delay the onset of age-associated conditions, such as heart disease, Alzheimer’s disease, cancer and frailty, and perhaps even forestall the gradual loss of mental acuity that happens to nearly everyone.
Continue reading “Study reveals immune driver of brain aging” »
From cryonics to time travel, here are some of the (highly speculative) methods that might someday be used to bring people back to life.
The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. But this doesn’t only affect the individual, it also creates a significant burden on public healthcare. And yet, research efforts into the biological processes and biomarkers that define muscle aging have not yet defined the underlying causes.
Now, a team of scientists from lab of Johan Auwerx at EPFL’s School of Life Sciences looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. They have discovered protein aggregates that deposit in skeletal muscles during natural aging, and that blocking this can prevent the detrimental features of muscle aging. The study is published in Cell Reports.
“During age-associated muscle diseases, such as inclusion body myositis (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles,” explains Auwerx. “The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease.”
NRF2 is just one of thousands of critical proteins in the cell, but it is one that we now know a lot about. Once any molecule achieves a certain level of celebrity status, it tends to acquire a groupie following in the supplement market. Today, we have all manner of NRF enhancers, releasers, activators and synergizers ready to arrive on your doorstep at the click of a button. But what could any of these things possibly do for us, and how much is too much of a good thing?
At the risk of overstating the obvious, if a little extra NRF2 is good for every cell in your body, and every cell in your body is good, then NRF2 must be good for your body. The weak link in that argument, however, is that all cells are not good. Nobody wants harmful bacterial cells to flourish, and nobody wants cancer cells to flourish. A paper recently published in Nature now suggests that inhibiting NRF2 can block the migration and invasion of non-small-cell lung cancer cells through the body. If anyone is going to derive benefit from NRF2, they may need to be smart about it.
The main reason NRF2, or Nuclear factor-erythroid 2-related factor 2, is so highly sought, is because it is a key transcriptional regulator of several antioxidant and anti-inflammatory enzymes. Unfortunately, as the authors above have revealed, it also moonlights as an activator of the Rho-ROCK pathway, which promotes actin filamentation and movement of cells. The researchers were able to block this activity of NRF2 by giving an inhibitor known as brusatol.
