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Category: life extension – Page 300

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.

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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.

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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 and delay the onset of age-associated conditions, such as , Alzheimer’s disease, cancer and frailty, and perhaps even forestall the gradual loss of mental acuity that happens to nearly everyone.

Yet the question of what, exactly, causes particular of the immune system to kick into inflammatory overdrive has lacked a definitive answer.

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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 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 (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 , just like in the in the brains of patients with Alzheimer’s disease.”

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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 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 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.

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No that’s not clickbait.
Being able to stop and reverse aging is probably something every single person has yearned for at some point in their life. Now researchers are finally seeing successful implementations of methods for reversing aging in Animal cells. This creates the potential for countless benefits for humans. These range from simply preventing age related illness all the way to allowing women the opportunity to have kids at any point in their life when they are ready. We are living in very exciting scientific times.

References:

Reprogramming to recover youthful epigenetic information and restore vision — https://doi.org/10.1038/s41586-020-2975-4

NAD+ Repletion Rescues Female Fertility during Reproductive Aging — https://doi.org/10.1016/j.celrep.2020.01.

Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16 — https://doi.org/10.1007/s10522-009-9225-3

Age-related NAD+ decline — https://doi.org/10.1016/j.exger.2020.

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Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans. Looking at the brain cells of aging flies, they found that better glucose uptake compensates for age-related deterioration in motor functions, and led to longer life. The effect was more pronounced when coupled with dietary restrictions. This suggests healthier eating plus improved glucose uptake in the brain might lead to enhanced lifespans.

The brain is a particularly power-hungry part of our bodies, consuming 20% of the oxygen we take in and 25% of the glucose. That’s why it’s so important that it can stay powered, using the glucose to produce (ATP), the “energy courier” of the body. This , known as glycolysis, happens in both the intracellular fluid and a part of cells known as the mitochondria. But as we get older, our become less adept at making ATP, something that broadly correlates with less glucose availability. That might suggest that more food for more glucose might actually be a good thing. On the other hand, it is known that a healthier diet actually leads to longer life. Unraveling the mystery surrounding these two contradictory pieces of knowledge might lead to a better understanding of healthier, longer lifespans.

A team led by Associate Professor Kanae Ando studied this problem using Drosophila . Firstly, they confirmed that brain cells in older flies tended to have lower levels of ATP, and lower uptake of glucose. They specifically tied this down to lower amounts of the enzymes needed for glycolysis. To counteract this effect, they genetically modified flies to produce more of a glucose-transporting protein called hGut3. Amazingly, this increase in glucose uptake was all that was required to significantly improve the amount of ATP in cells. More specifically, they found that more hGut3 led to less decrease in the production of the enzymes, counteracting the decline with age. Though this did not lead to an improvement in age-related damage to mitochondria, they also suffered less deterioration in locomotor functions.

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