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Category: life extension – Page 318

The number of mutations that can contribute to aging may be significantly higher than previously believed, according to new research on fruit flies. The study by scientists at Linköping University, Sweden, supports a new theory about the type of mutation that can lie behind aging. The results have been published in BMC Biology.

We live, we age and we die. Many functions of our bodies deteriorate slowly but surely as we age, and eventually an organism dies. This thought may not be very encouraging, but most of us have probably accepted that this is the fate of all living creatures—death is part of life. However, those who study find it far from clear why this is the case.

“The evolution of aging is, in a manner of speaking, a paradox. Evolution causes continuous adaptation in organisms, but even so it has not resulted in them ceasing to age,” says Urban Friberg, senior lecturer in the Department of Physics, Chemistry and Biology at Linköping University and leader of the study.

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Not too much here, but longevity research fans might like.

Time may be our worst enemy, and aging its most powerful weapon. Our hair turns gray, our strength wanes, and a slew of age-related diseases represent what is happening at the cellular and molecular levels. Aging affects all the cells in our body’s different tissues, and understanding its impact would be of great value in fighting this eternal enemy of all ephemeral life forms.

The key is to first observe and measure. In a paper published in Cell Reports, scientists led by Johan Auwerx at EPFL started by asking a simple question: how do the tissues of aging mice differ from those of mice that are mere adults?

To answer the question, the researchers used the multiple techniques to measure the expression of everyone one of the thousands of mouse’s genes, and to identify any underlying epigenetic differences. The researchers not only measured different layers of information, but they did it across three different tissues: liver, heart, and muscle.

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Stopping the cannibalistic behavior of a well-studied enzyme could be the key to new drugs to fight age-related diseases, according to a new study published online in Nature Cell Biology. For the first time, researchers in the Perelman School of Medicine at the University of Pennsylvania show how the self-eating cellular process known as autophagy is causing the SIRT1 enzyme, long known to play a role in longevity, to degrade over time in cells and tissue in mice. Identifying an enzymatic target is an important step that may lead to new or modified existing therapeutics.

“Blocking this pathway could be another potential approach to restore the level of SIRT1 in patients to help treat or prevent age-related organ and immune system decline,” said first author Lu Wang, Ph.D., a postdoctoral researcher in the lab of Shelly Berger, Ph.D., a professor of Cell and Developmental Biology in the Perelman School of Medicine and a professor of Biology in the School of Arts and Sciences at Penn. Berger also serves as senior author on the paper.

“The findings may be of most interest to the immune aging field, as autophagy’s role in SIRT1 in immune is a concept that hasn’t been shown before,” Wang added. “Exploiting this mechanism presents us with a new possibility of restoring immune function.”

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A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.

In a study, published in the journal eLife on Sept. 29, the researchers identified a factor that acts like a molecular switch in the of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goose bumps, an ability that is lost in adult human scars.

“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”

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David Sinclair wants to slow down and ultimately reverse aging. Sinclair sees aging as a disease and he is convinced aging is caused by epigenetic changes, abnormalities that occur when the body’s cells process extra or missing pieces of DNA. This results in the loss of the information that keeps our cells healthy. This information also tells the cells which genes to read. David Sinclair’s book: “Lifespan, why we age and why we don’t have to”, he describes the results of his research, theories and scientific philosophy as well as the potential consequences of the significant progress in genetic technologies.

At present, researchers are only just beginning to understand the biological basis of aging even in relatively simple and short-lived organisms such as yeast. Sinclair however, makes a convincing argument for why the life-extension technologies will eventually offer possibilities of life prolongation using genetic engineering.

He and his team recently developed two artificial intelligence algorithms that predict biological age in mice and when they will die. This will pave the way for similar machine learning models in people.
The loss of epigenetic information is likely the root cause of aging. By analogy, If DNA is the digital information on a compact disc, then aging is due to scratches. What we are searching for, is the polish.

Every time a cell divides, the DNA strands at the ends of your chromosomes replicate in order to copy all the genetic information to each new cell, and this process is not perfect. Over time, however, the ends of your chromosomes can become scrambled.

However, the progress in genetic engineering has proved that these changes can be reversed even at the cellular level, and it is possible to restore the information in our cells, thus improving the functioning of our organs and slowing the aging process.

#Aging #DavidSinclair #Lifespan

Continue reading “Harvard Professor Wants to Slow Down & Reverse Aging: David Sinclair’s Approach For a Longer Life” | >

11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.

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In order to slow aging, it’s important to know how circulating biomarkers change during aging, and how these biomarkers are associated with risk of death for all causes. In this video, I discuss blood test data for the oldest old, including centenarians (100 — 104y), semi-centenarians (105 — 109y), and super-centenarians (110y+).

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Lil bits of info on DNA methylation, clocks.

Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7–8 million years ago when our ancestors branched away from the lineage of chimps.

Slower ticker

There are tens of thousands of genes in the human genome, but that doesn’t mean all of them are active. For instance, through the methylation of DNA across certain sites of the genetic sequence, genes are locked in the “off” position. These modifications, known as epigenetic changes (‘epi’ means ‘above’ in Greek), do not alter the DNA sequence itself but, rather, simply regulate the activity of genes.

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WEDNESDAY, Sept. 23, 2020 (HealthDay News) — A common type 2 diabetes drug called metformin may have an unexpected, but positive, side effect: New research suggests that people taking the drug appear to have significantly slower declines in thinking and memory as they age.

“Our six-year study of older Australians with type 2 diabetes has uncovered a link between metformin use and slower cognitive [mental] decline and lower dementia rates,” said study author Dr. Katherine Samaras. She’s the leader of the healthy aging research theme at the Garvan Institute of Medical Research in New South Wales, Australia.

“The findings provide new hope for a means of reducing the risk of dementia in individuals with type 2 diabetes, and potentially those without diabetes,” Samaras said.

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