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Scooped by Dr. Stefan Gruenwald!

Young poo: Gut microbes of young killifish can extend the lifespans of older fish

Young poo: Gut microbes of young killifish can extend the lifespans of older fish | Amazing Science |

The gut microbes of young killifish can extend the lifespans of older fish – hinting at the microbiome’s role in aging.


It may not be the most appetizing way to extend life, but researchers have shown for the first time that older fish live longer after they consumed microbes from the poo of younger fish. The findings were posted to the preprint server on 27 March1 by Dario Valenzano, a geneticist at the Max Planck Institute for Biology of Ageing in Köln, Germany, and his colleagues.


So-called ‘young blood’ experiments that join the circulatory systems of two rats — one young and the other old — have found that factors coursing through the veins of young rodents can improve the health and longevity of older animals. But the new first-of-its-kind study examined the effects of 'transplanting' gut microbiomes on longevity.


“The paper is quite stunning. It’s very well done,” says Heinrich Jasper, a developmental biologist and geneticist at the Buck Institute for Research on Aging in Novato, California, who anticipates that scientists will test whether such microbiome transplants can extend lifespan in other animals.


Life is fleeting for killifish, one of the shortest-lived vertebrates on Earth: the fish hits sexual maturity at three weeks old and dies within a few months. The turquoise killifish (Nothobranchius furzeri) that Valenzano and his colleagues studied in the lab inhabits ephemeral ponds that form during rainy seasons in Mozambique and Zimbabwe.


Previous studies have hinted at a link between the microbiome and aging in a range of animals. As they age, humans2 and mice3 tend to lose some of the diversity in their microbiomes, developing a more uniform community of gut microbes, with once-rare and pathogenic species rising to dominance in older individuals4. The same pattern holds true in killifish, whose gut microbiomes at a young age are nearly as diverse as those of mice and humans, says Valenzano. “You can really tell whether a fish is young or old based on its gut microbiota.”


To test whether the changes in the microbiome had a role in ageing, Valenzano’s team ‘transplanted’ the gut microbes from 6-week-old killifish into middle-aged 9.5-week-old fish. They first treated the middle-aged fish with antibiotics to clear out their gut flora, then placed them in a sterile aquarium containing the gut contents of young fish for 12 hours. Killifish don’t usually eat faeces, Valenzano notes, but they would probe and bite at the gut contents to see whether it was food, ingesting microbes in the process. The transplanted microbes successfully recolonized the guts of the fish that received them, the team found. At 16 weeks of age, the gut microbiomes of middle-aged fish that received 'young microbes' still resembled those of 6-week-old fish.  


The young microbiome ‘transplant’ also had dramatic effects on the longevity of fish that got them: their median lifespans were 41% longer than fish exposed to microbes from middle-aged animals, and 37% longer than fish that received no treatment (antibiotics alone also lengthened lifespan, but to a lesser extent).

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Study identifies key factor in DNA damage associated with aging 

Study identifies key factor in DNA damage associated with aging  | Amazing Science |

In a recent study, Rochester scientists made two important contributions to DNA damage research. First, though scientists could previously point to an association between DNA damage and aging, the Rochester group has demonstrated a causal relationship between reduced DNA damage and extended lifespan. Second, the researchers have identified a cellular factor—an enzyme called topoisomerase 2, or Top2, implicated in DNA damage—that can be targeted to reduce that damage. The findings are published in the journal Aging.


“This part of the puzzle has been missing from the DNA damage theory of aging,” says David Goldfarb, professor of biology. There are many examples of DNA damage being associated with aging, but never has a reduction in DNA damage been shown to extend lifespan. The study also shows how this information may have therapeutic potential.


Goldfarb’s lab exposed yeast—which ages much like humans—to a lifespan-shortening, drug-like molecule that acts on Top2 and helped the lab uncover Top2’s role. Top2 introduces double strand breaks into DNA as part of its catalytic cycle. The breaks must then be resealed. “Every once in a while Top2 gets trapped on the DNA before it can seal the breaks,” Goldfarb says. “When that happens, at least in young cells, there are a number of back-up systems that recognize the breaks and repair them.”


However, a number of researchers have shown that DNA damage repair systems decline as cells age, causing the unrepaired DNA breaks created by Top2 to persist. The unrepaired double strand breaks cause aging, diseases like cancer, and, ultimately, death.

Via Integrated DNA Technologies
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The limits to human lifespan must be respected

The limits to human lifespan must be respected | Amazing Science |
Lengthening our lives will come at a cost.


A study published online in Nature uses demographic data to reveal a lifespan that human beings cannot exceed, simply by virtue of being human. It’s like running, as an accompanying News and Views article points out. Elite athletes might shave a few milliseconds off the world record for the 100-meter sprint, but they’ll never run the same distance in, say, five seconds, or two. Human beings are simply not made that way. The same is true for longevity. The consequences of myriad factors related to our genetics, metabolism, reproduction and development, all shaped over millions of years of evolution, means that few humans will make it past their 120th birthdays. The name of Jeanne Calment, who died in 1997 at the age of 122, is likely to remain as long in the memory in the Methuselah stakes as that of Usain Bolt on the Olympic track.


Maximum lifespan is a bald measure of years accumulated. It is not the same as life expectancy, which is an actuarial measure of how long one is expected to live from birth, or indeed from any given age. Life expectancy at birth has increased in most countries over the past century, not because people have longer lifespans, but mainly because infectious disease does not kill as many infants as it once did. Factors such as poverty and warfare conspire to decrease life expectancy. Although life expectancy at birth has risen steadily for both men and women in France since 1900, for example, there are dramatic and poignant drops that coincide with the two world wars.


In Britain in the early twentieth century, many children still died from infectious diseases, and men would die shortly after retiring from physically demanding jobs. The National Health Service was the political response. It has become, in some ways, the victim of its own success. People live longer than they did even a few decades ago, and die (eventually) of different (and more expensive) complaints. As any beginning medical student is soon taught, gerontology is far from a dying discipline. So if we owe our increases in life expectancy to better public health, nutrition, sanitation and vaccination, is it not fair to ask whether more-effective treatments for diseases such as cancer, Parkinson’s disease and Alzheimer’s might also yield dividends in maximum lifespan? Will 120th birthday parties become routine, outmatched by a small yet increasing number of sesquicentenarians? The demographic data say no. People are living longer, and the population as a whole is greying, but the rate of increase in the number of centenarians is slowing, and might even have peaked.

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Start-up Humai wants to transfer consciousness to an artificial body to live forever

Start-up Humai wants to transfer consciousness to an artificial body to live forever | Amazing Science |
Forever young?


With the rise of brain-controlled robotic limbs, advanced biomedical implants, and life-saving medical treatments, it seems as though in the modern day, we're closer than ever to conquering death. Some hope to extend the human lifetime indefinitely. Singularity proponents hope that eventually we'll be able to upload our consciousness to computers.


Now the company Humai aims to bring people back from the dead. From their website:


  • We're using artificial intelligence and nanotechnology to store data of conversational styles, behavioral patterns, thought processes and information about how your body functions from the inside-out. This data will be coded into multiple sensor technologies, which will be built into an artificial body with the brain of a deceased human.


If it sounds like something out of science fiction, that's because it is. The challenges are significant: taking a dead brain and bringing it back to life; wiring up the brain so that it can control a silicon-based machine; and trying to replicate that vital thing that is you--your personality, your past experiences, your mind. We wouldn't bet on this thing working, at least not anytime soon. But hopefully it won't hurt to try.


The CEO and founder of Humai explains: "Our mission is fairly simple to understand but obviously difficult to execute. We'll first collect extensive data on our members for years prior to their death via various apps we're developing. After death we'll freeze the brain using cryonics technology. When the technology is fully developed we'll implant the brain into an artificial body. The artificial body functions will be controlled with your thoughts by measuring brain waves. As the brain ages we'll use nanotechnology to repair and improve cells. Cloning technology is going to help with this too. Every step we take toward understanding how to get your thoughts to control an artificial body will be huge progress. I'm confident that in the process we'll develop a technology that will even save lives. However, the ultimate test will be when we perform the first surgical procedure to implant a human brain to an artificial body."


Humai CEO's answer is: "in Bionics, nanotechnology and artificial intelligence. I think the body has limitations and I don't believe the body was evolved with the best possible functions. I think an artificial body will contribute more to the human experience. It will extend the human experience. So much so, that those who accept death will probably change their mind."

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Greenland Sharks are the Longest-Lived Vertebrates on Earth, up to 400 Years Old

Greenland Sharks are the Longest-Lived Vertebrates on Earth, up to 400 Years Old | Amazing Science |
Greenland sharks (Somniosus microcephalus) live at least as long as 400 years, according to a team of marine biologists led by Dr. Julius Nielsen from the University of Copenhagen, Denmark.


Traditional methods for determining the age of a species involve analyzing calcified tissue, a feature that’s sparse in Greenland sharks. Therefore, to determine the average age of this species, Dr. Nielsen and his colleagues from Denmark, Greenland, Norway, UK and the United States applied radiocarbon dating techniques to the eye lenses of 28 female Greenland sharks (2.7 to 16.5 feet, or 81 cm to 5.02 m, in total length) caught as by-catch.


The team’s analysis suggests an average lifespan of at least 272 years. The two largest sharks in the study, at 16.2 and 16.5 feet (4.93 and 5.02 m) in length, were estimated to be roughly 335 and 392 years old, respectively.


“Our results demonstrate that the Greenland shark is among the longest-lived vertebrate species surpassing even the bowhead whale (Balaena mysticetus, estimated longevity of 211 years),” Dr. Nielsen and co-authors said.


“The life expectancy of the Greenland shark is exceeded only by that of theocean quahog (Arctica islandica, 507 years).”


“What’s more, since previous reports suggest that females of this species reach sexual maturity at lengths greater than 4 m (13 feet), the corresponding age would be at least 156 years old,” the scientists added.


Based on these results, published in Science, the Greenland shark is now the oldest-known vertebrate roaming our planet.


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Blood of world’s oldest woman hints at current limits of life

Blood of world’s oldest woman hints at current limits of life | Amazing Science |
She lived to 115, but a study of Hendrikje van Andel-Schipper's blood hints at factors limiting lifespan


Death is the one certainty in life – a pioneering analysis of blood from one of the world’s oldest and healthiest women has given clues to why it happens. Born in 1890, Hendrikje van Andel-Schipper was at one point the oldest woman in the world. She was also remarkable for her health, with crystal-clear cognition until she was close to death, and a blood circulatory system free of disease. When she died in 2005, she bequeathed her body to science, with the full support of her living relatives that any outcomes of scientific analysis – as well as her name – be made public. Researchers have now examined her blood and other tissues to see how they were affected by age.


What they found suggests, as we could perhaps expect, that our lifespan might ultimately be limited by the capacity for stem cells to keep replenishing tissues day in day out. Once the stem cells reach a state of exhaustion that imposes a limit on their own lifespan, they themselves gradually die out and steadily diminish the body’s capacity to keep regenerating vital tissues and cells, such as blood.


In van Andel-Schipper’s case, it seemed that in the twilight of her life, about two-thirds of the white blood cells remaining in her body at death originated from just two stem cells, implying that most or all of the blood stem cells she started life with had already burned out and died. “Is there a limit to the number of stem cell divisions, and does that imply that there’s a limit to human life?” asks Henne Holstege of the VU University Medical Center in Amsterdam, the Netherlands, who headed the research team. “Or can you get round that by replenishment with cells saved from earlier in your life?” she says.


The other evidence for the stem cell fatigue came from observations that van Andel-Schipper’s white blood cells had drastically worn-down telomeres – the protective tips on chromosomes that burn down like wicks each time a cell divides. On average, the telomeres on the white blood cells were 17 times shorter than those on brain cells, which hardly replicate at all throughout life.


The team could establish the number of white blood cell-generating stem cells by studying the pattern of mutations found within the blood cells. The pattern was so similar in all cells that the researchers could conclude that they all came from one of two closely related “mother” stem cells.


“It’s estimated that we’re born with around 20,000 blood stem cells, and at any one time, around 1000 are simultaneously active to replenish blood,” says Holstege. During life, the number of active stem cells shrinks, she says, and their telomeres shorten to the point at which they die – a point called stem-cell exhaustion.


Holstege says the other remarkable finding was that the mutations within the blood cells were harmless – all resulted from mistaken replication of DNA during van Andel-Schipper’s life as the “mother” blood stem cells multiplied to provide clones from which blood was repeatedly replenished. She says this is the first time patterns of lifetime “somatic” mutations have been studied in such an old and such a healthy person. The absence of mutations posing dangers of disease and cancer suggest that van Andel-Schipper had a superior system for repairing or aborting cells with dangerous mutations.


The study is novel because it is the first to investigate the accumulation of somatic mutations within the tissues of an old individual, says Chris Tyler-Smith of the Wellcome Trust Sanger Institute in Hinxton, UK. “This contrasts to the germ-line mutations [present at birth] measured in previous studies,” he says.

Via Khannea Suntzu
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How Craig Venter is fighting ageing with genome sequencing

How Craig Venter is fighting ageing with genome sequencing | Amazing Science |

Nine years ago, Craig Venter sequenced the first complete individual human genome - his own. Now, he's finally starting to decode what it means for his future. 

Via Integrated DNA Technologies
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Removing senescent cells makes mice live longer and prosper

Removing senescent cells makes mice live longer and prosper | Amazing Science |

Killing worn-out cells helps middle-aged mice live longer, healthier lives, a new study suggests. Removing those worn-out or “senescent” cells increased the median life span of mice from 24 to 27 percent over that of rodents in which senescent cells built up normally with age, Mayo Clinic researchers report online February 3 in Nature. Clearing senescent cells also improved heart and kidney function, the researchers found.

If the results hold up in people, they could lead to an entirely new way to treat aging, says gerontology and cancer researcher Norman Sharpless at the University of North Carolina School of Medicine in Chapel Hill. Most prospective antiaging treatments would require people to take a drug for decades. Periodically zapping senescent cells might temporarily turn back the clock and improve health for people who are already aging, he says. “If this paper is right, I believe it will be one of the most important aging papers ever,” Sharpless says.

Senescent cells are ones that have ceased to divide and do their usual jobs. Instead, they hunker down and pump out inflammatory chemicals that may damage surrounding tissues and promote further aging. “They’re zombie cells,” says Steven Austad, a biogerontologist at the University of Alabama at Birmingham. ”They’ve outlived their usefulness. They’re bad.”

Cancer biologist Jan van Deursen of the Mayo Clinic in Rochester, Minn., and colleagues devised the strategy for eliminating senescent cells by making the cells commit suicide. A protein called p16 builds up in senescent cells, the researchers had previously discovered. The team hooked up a gene for a protein that causes cells to kill themselves to DNA that helps turn on p16 production, so that whenever p16 was made the suicide protein was also made.

The suicide protein needs a partner chemical to actually kill cells, though. Once mice were a year old — 40 to 60 years old in human terms — the researchers started injecting them with the partner chemical. Mice got injections about every three days for six months. Mice that got the cell-suicide cocktail were compared with genetically engineered mice that were injected with a placebo mix.

Senescent cells were easier to kill in some organs than others, the researchers found. Colon and liver senescent cells weren’t killed, for instance. But age-related declines in the function of organs in which the treatment worked — eyes, fat, heart and kidney —were slowed.

Genetic engineering and regular shots would not be feasible for use in people, but several companies are developing drugs that might clear the zombie cells from humans, Austad says. Some side effects to the treatment in mice also would be important to consider if those drugs are ever used in people. Senescent cells have previously been shown to be needed for wound healing, and mice that got the killing cocktail couldn’t repair wounds as well as those that didn’t get the treatment. Once treatment stopped, the mice were able to heal normally again. That result suggests that people undergoing senescent-cell therapy might need to stop temporarily to heal wounds from surgery or accidents.

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Species found with 20 copies of p53, and it almost never develops cancer

Species found with 20 copies of p53, and it almost never develops cancer | Amazing Science |
Elephants’ genomes possess 20 copies of a tumor suppressing gene called P53, new research shows.

A longstanding mystery in biology is why the rate of cancer incidence in a species does not scale up with body size and longevity. Take elephants for instance, which live to approximately the same age as humans and have 100 times more cells, yet hardly ever develop cancer, a disease which is estimated to affect 40 percent of Americans at some point in their lives.

ou'd expect elephants would have higher rates of cancer, because elephants have significantly more cells than humans and more cells means more opportunities for cancerous mutations to occur. The fact that this isn’t the case gives rise to the conundrum known as Peto’s Paradox, the resolution of which may provide valuable insight into preventing cancer in humans.

Recently a team of geneticists led by Joshua Schiffman at the University of Utah made major headway in this direction when they studied the cells of Asian and African elephants from the San Diego Frozen Zoo and found that elephants’ genomes possessed 20 copies of a tumor suppressing gene called P53.

For the sake of comparison, the team looked at the genomes of more than 60 other species (including humans) and found that most only possess a single copy of this gene, suggesting that this redundancy in the elephant genome may finally explain the low rate of cancer in the species. The results of the study were published today in an editorial for the Journal of the American Medical Association.

“If you’re interested in cancer the first gene to look at is P53, it is the master tumor suppressor,” said Vincent Lynch, a human geneticist at the University of Chicago who published supporting research in a preprint study on Biorxiv. “We thought maybe elephants have another copy, but certainly not 19 more copies than other animals. This discovery is a big deal.”

According to Lynch, the canonical copy of the P53 gene along with the 19 retrogene copies make elephants more sensitive to DNA damage during cell replication. This hypersensitivity to genetic anomalies means that cells are quicker to ‘commit suicide’ when they are found to be damaged, halting the proliferation of potentially cancerous cells before it begins.

While multiple copies of the P53 gene might seem like a wholly positive evolutionary development, the overexpression of this gene likely comes with some tradeoffs, such as reproductive senescence or rapid aging.

“There is definitely a tradeoff, or else many other species would have evolved duplicate P53 genes by now,” said Lynch. “We don’t know what the tradeoff was, but elephants either found a way to deal with it or broke whatever constraint prevented organisms from evolving many P53 copies.”

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Despite research breakthroughs, an anti-aging pill is still a long way off

Despite research breakthroughs, an anti-aging pill is still a long way off | Amazing Science |

Last month a team of doctors and scientists made the case to regulators at the Food and Drug Administration (FDA) to consider approving anti-aging drugs as a new pharmaceutical class. Such a designation would treat aging as disease rather than a natural process, potentially opening the door to government funding for anti-aging drug trials.

To some, such a drug may seem impossible. Yet, the physiologic basis for it exists. In fact, some candidate drugs, such as metformin, used to treat diabetes, are already being safely used for treating other conditions. Many scientists believe that designing an anti-aging medication is a matter of “when,” not “if.”

Yet the very idea of a quick-fix pill for stopping, and perhaps even reversing, nature’s intricate biologic clock thus far has proven to be a hubristic notion. There is much we need to learn about how the aging process works. And while some drugs have shown promise as anti-aging treatments in the lab, we don’t know how well, or even if, they will work in humans.

Aging remains a mystery. While the visible changes of gray hair and wrinkles are unmistakable, what goes on inside your body is less clear. According to leading theories, aging is an accumulation of damage inside your cells, the building blocks of your tissues.

Cells continually receive cues from your body and the environment that can accelerate age-driving processes such as oxidative damage and inflammation. These processes are interdependent – woven in a complex maze that is perplexing and daunting for researchers.

Rather than trying to extend life by individually targeting prevention and treatment of common age-related diseases such as heart disease, stroke and cancer, scientists are looking for a “master control switch” that can regulate the divergent and overlapping pathways that contribute to aging itself.

Since aging is the biggest risk factor for developing such diseases, an anti-aging medication that can flip this switch would theoretically not only slow or stop aging but would also defer many diseases associated with aging. And that is what some of the drugs scientists are investigating may be able to do.

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How aging cripples the immune system

How aging cripples the immune system | Amazing Science |

Aging cripples the production of new immune cells, decreasing the immune system’s response to vaccines and putting the elderly at risk of infection, but antioxidants in the diet may slow this damaging process.

That’s a new finding by scientists from the Florida campus of The Scripps Research Institute (TSRI), published in an open-access paper in the journal Cell Reports. The problem is focused on an organ called the thymus, which produces T lymphocytes (a type of white blood cell) — critical immune cells that must be continuously replenished so they can respond to new infections. “The thymus begins to atrophy rapidly in very early adulthood, simultaneously losing its function,” said TSRI Professor Howard Petrie“This new study shows for the first time a mechanism for the long-suspected connection between normal immune function and antioxidants.”

Scientists have been hampered in their efforts to develop specific immune therapies for the elderly by a lack of knowledge of the underlying mechanisms of this process. To explore these mechanisms, Petrie and his team developed a computational approach for analyzing the activity of genes in two major cell types in the thymus — stromal cells and lymphoid cells — in mouse tissues, which are similar to human tissues in terms of function and age-related atrophy. The team found that stromal cells were specifically deficient in an antioxidant enzyme called catalase. That resulted in elevated levels of the reactive oxygen byproducts of metabolism, which cause accelerated metabolic damage.*

Taken together, the findings provide support for the “free-radical theory” of aging, which proposes that reactive oxygen species (such as hydrogen peroxide), produced during normal metabolism (and from other sources) cause cellular damage that contributes to aging and age-related diseases. Free radicals are especially reactive atoms or groups of atoms that have one or more unpaired electrons.  Besides those produced in the body as a by-product of normal metabolism, they can also be introduced from an outside source, such as tobacco smoke or other toxins.

Other studies have suggested that sex hormones, particularly androgens such as testosterone, play a major role in the aging process. But according to the researchers, those studies have failed to answer the key question: why does the thymus atrophy so much more rapidly than other body tissues?

“There’s no question that the thymus is remarkably responsive to androgens,” Petrie noted, “but our study shows that the fundamental mechanism of aging in the thymus, namely accumulated metabolic damage, is the same as in other body tissues. However, the process is accelerated in the thymus by a deficiency in the essential protective effects of catalase, which is found at higher levels in almost all other body tissues.”

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Altering RNA helicases in roundworms doubles their lifespan, something that could be tried in humans

Altering RNA helicases in roundworms doubles their lifespan, something that could be tried in humans | Amazing Science |
The things we do to extend our lives -- quitting smoking, cutting back on carbs, taking up jogging -- all have some impact on our longevity, if only just a little. But no matter how hard we work towards chasing the dream of forever staying fit and youthful, our efforts all end the same way and we must come to terms with the fact that we are mortal beings living on a finite timeline. There is nothing we can do to stop the aging process, and most things people do only serve to delay the inevitable: we can't stop death.

If someone was going to attempt to stop it, what would be the first step? Researchers at the Center for Plant Aging Research with support from the Institute for Basic Science (IBS) in Korea have made a breakthrough in decoding the aging process and how to dramatically slow it down.

The team used a mutated form of the roundworm in which they restricted a gene called daf-2 which is responsible for the rate of aging, reproductive development, resistance to oxidative stress, thermotolerance, resistance to hypoxia, and resistance to bacterial pathogens. In this case the daf-2 gene was altered so its IIS (insulin/insulin-like growth factor 1 (IGF1) signaling) would be restricted. These daf-2 mutants display increased resistance against diverse stresses, including heat stress, pathogenic bacteria, and oxidative stress and most importantly, the daf-2 mutants displayed double the lifespan compared to wild Caenorhabditis elegans roundworms.

The team believes that HEL-1 may act as a transcription regulator, which control how cells convert DNA to RNA since other RNA helicases do the same thing now. According to the team, "In contrast to the expectation that RNA helicases have general housekeeping roles in RNA metabolism, our findings reveal that the RNA helicase HEL-1 has specific roles in a specific longevity pathway."

Even if immortality isn't an immediate result of this work, there are other possible applications. Something called DDX39 (the mammalian version of the roundworm's HEL-1) is found in increased levels in the frontal cortex of patients with Alzheimer's disease. The ability to regulate DDX39 and other RNA helicases may give us an insight into finding the ability to control Alzheimer's disease, among other brain disorders.

Using the technique of altering RNA helicases to extend life in humans looks promising as human and roundworm both have HEL-1 and IIS which can be manipulated in similar ways. It isn't clear if the same mechanism is responsible for cellular aging regulation in humans, but evidence suggests that it might be. This research hasn't given humanity a cure to any diseases or made any claims of human life extension but it is an important first step in more fully understanding the lifecycle and function of cells.

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Rescuing memory: Blocking beta2-microglobulin could stop memory loss at old age

Rescuing memory: Blocking beta2-microglobulin could stop memory loss at old age | Amazing Science |

There might be a way to stave off the memory loss people experience as they get older. As people age, a protein that disrupts brain cell repair gradually builds up in the blood and cerebrospinal fluid. The offending protein, called beta2-microglobulin (B2M), has now been shown to affect how mice perform in memory tests. Work is already under way to identify drugs that mop up or destroy B2M which will allow the researchers to test if the same applies to humans. If so, the same drug could offer a solution.

"Right now, the idea is to develop antibodies or small molecules that can either block the effects of the protein or help to remove it from old blood," says Saul Villeda of the University of California at San Francisco. Villeda's discovery is the first detailed investigation of a so-called "anti-elixir" factor, in other words one that builds up with age and causes brain degeneration. Most research aimed at reversing ageing so far has focused on "elixir" factors – agents that bring back lost youth. For example, when the the blood of young mice is injected into old mice, it halts brain and muscle degeneration, helps fractured bones heal and prevents heart damage.

B2M's main job is to help the immune system tell the difference between foreign cells and those from the body, but it also plays a role in development of the nervous system. When Villeda's team injected B2M into the brains or blood of young mice, they performed almost as badly as elderly mice on two kinds of memory test. When the molecule had been naturally eliminated from their bodies – around 30 days later - the animals' performances returned to normal, suggesting the effect of B2M is reversible.

Some mice had been genetically engineered so that they couldn't make B2M. These animals performed equally well regardless of age. "It may not be this factor alone that causes the memory loss," says Benjamin Alman of the Hospital for Sick Children in Toronto, Canada, who is trying to find molecules in young blood that heal bones faster. "But it does raise the possibility that failing memory can be rescued by drugs that interfere with these circulating factors," he says. "The concept is very exciting, and would have been unthinkable a few years ago."

eduardo marcelo levingston's curator insight, July 9, 2015 9:02 AM

El papel de la B2microglobulina en la perdida de memoria y la esperanza de su bloqueo como medida terapéutica en un futuro no tan lejano 

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FOXO4-peptides kill elderly cells, reduce signs of aging in rodents

FOXO4-peptides kill elderly cells, reduce signs of aging in rodents | Amazing Science |

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.


“It’s definitely a landmark advance in the field,” says cell and molecular biologist Francis Rodier of the University of Montreal in Canada who wasn’t connected to the study. “This is the first time that somebody has shown that you can get rid of senescent cells without having any obvious side effects.”


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.


The proof-of-concept study, published March 23, 2017 in Cell, found that an anti-senescent cell therapy could reverse age-related loss of fur, poor kidney function, and frailty. It is currently being tested whether the approach also extends lifespan, and human safety studies are being planned.


The peptide took over four years of trial and error to develop and builds on nearly a decade of research investigating vulnerabilities in senescent cells as a therapeutic option to combat some aspects of aging (Trends in Molecular Medicine, 10.1016/j.molmed.2016.11.006). It works by blocking the ability of a protein implicated in senescence, FOXO4, to tell another protein, p53, not to cause the cell to self-destruct. By interfering with the FOXO4-p53 crosstalk, the peptide causes senescent cells to go through apoptosis, or cell suicide.


"Only in senescent cells does this peptide cause cell death," says senior author Peter de Keizer, a researcher of aging at Erasmus University Medical Center in the Netherlands. "We treated mice for over 10 months, giving them infusions of the peptide three times a week, and we didn't see any obvious side effects.


FOXO4 is barely expressed in non-senescent cells, so that makes the peptide interesting as the FOXO4-p53 interaction is especially relevant to senescent cells, but not normal cells."


Senescent cell therapy is one of several strategies being tested in mice aimed at reversing aging or lengthening healthspan. In 2015, the Valter Longo laboratory at the University of Southern California reported that mice on a calorie-restricted diet that mimics fasting benefited from a longer life, a reduction in inflammatory disease, and improved memory (Cell Metabolism, 10.1016/j.cmet.2015.05.012).


In December 2016, Juan Carlos Izpisua Belmonte at the Salk Institute of Biological Science and colleagues made headlines with their discovery that cellular reprogramming of epigenetic marks could extend lifespan and improve health in fast-aging mice (Cell, 10.1016/j.cell.2016.11.052). "This wave of research on how we can fight aging is complementary, and not in competition," says de Keizer. "The common thread I see for the future of anti-aging research is that there are three fronts in which we can improve: The prevention of cellular damage and senescence, safe therapeutic removal of senescent cells, to stimulate stem cells--no matter the strategy--to improve tissue regeneration once senescence is removed."

I Am A Science Lady's curator insight, April 4, 9:16 PM
Who wants to live forever?  What about in a changing world?
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Cellular reprogramming turns back the aging clock in mice

Cellular reprogramming turns back the aging clock in mice | Amazing Science |

Salk Institute scientists have extended the average lifespan of live mice by 30 percent, according to a study published December 15, 2016 in Cell. They did that by rolling back the “aging clock” to younger years, using cellular reprogramming.

The finding suggests that aging is reversible by winding back an animal’s biological clock to a more youthful state and that lifespan can be extended. While the research does not yet apply directly to humans, it promises to lead to improved understanding of human aging and the possibility of rejuvenating human tissues.


To achieve this, the scientists worked with “progeria” mouse models — mice that had been genetically modified to carry a mutation that leads to premature aging, allowing the aging effects to be isolated and studied. Rather than attempting to correct the genetic mutations that cause premature aging (a difficult challenge), the Salk team instead focused on restoring the epigenome.

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Physics, Not Biology, Makes Aging Inevitable

Physics, Not Biology, Makes Aging Inevitable | Amazing Science |

The inside of every cell in our body is like a crowded city, filled with tracks, transports, libraries, factories, power plants, and garbage disposal units. The city’s workers are protein machines, which metabolize food, take out the garbage, or repair DNA.


Cargo is moved from one place to another by molecular machines that have been observed walking on two legs along protein tightropes. As these machines go about their business, they are surrounded by thousands of water molecules, which randomly crash into them a trillion times a second. This is what physicists euphemistically call “thermal motion.” Violent thermal chaos would be more apt.


How any well-meaning molecular machine could do good work under such intolerable circumstances is puzzling. Part of the answer is that the protein machines of our cells, like tiny ratchets, turn the random energy they receive from water bombardment into the very directed motion that makes cells work. They turn chaos into order.


In this sense, life pits biology against physics in mortal combat. So why do living things die? Is aging the ultimate triumph of physics over biology? Or is aging part of biology itself?


Medawar himself argued for the “wearing out” theory—the physics viewpoint on aging. First, he said, it is difficult to see how natural selection could have selected for senescence, because we don’t reproduce in our elderly years and natural selection is driven by differences in reproduction rates. Second, it is unnecessary to actively kill off older individuals to keep an aging population small. Random chance can accomplish this on its own.


Medawar argued that a biological master clock for aging is unnecessary. To illustrate why, he pointed to a decidedly non-living example: Test tubes in a lab. Assume test tubes break from time to time by accident. To keep the total number of test tubes constant, a fresh supply is purchased every week. After a few months pass, how many young test tubes are there, and how many are old? If we assume that the probability of accidental breakage is independent of age (a sensible assumption), and plot the number of test tubes versus the age of each test tube, we get a concave, exponential decay curve that looks like a child’s slide. This “life curve” has a steep drop at the top, and it’s flat on the bottom.

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Short transient rapamycin treatment increases lifespan in mice by over 50%

Short transient rapamycin treatment increases lifespan in mice by over 50% | Amazing Science |

Old age is the single greatest risk factor for many diseases including heart disease, arthritis, cancer and dementia. By delaying the biological aging process, it may be possible to reduce the impact of age-related diseases, which could have great benefits for society and the quality of life of individuals. A drug called rapamycin, which is currently used to prevent organ rejection in transplant recipients, is a leading candidate for targeting aging. Rapamycin increases lifespan in several types of animals and delays the onset of many age-related conditions in mice.


Nearly all of the aging-related studies in mice have used the same dose of rapamycin given throughout the lives of the animals. Lifelong treatment with rapamycin wouldn’t be practical in humans and is likely to result in undesirable side effects. For example, the high doses of rapamycin used in transplant patients cause side effects including poor wound healing, elevated blood cholesterol levels, and mouth ulcers. Before rapamycin can be used to promote healthy aging in humans, researchers must better understand at what point in life the drug is most effective, and what dose to use to provide the biggest benefit while limiting the side effects.


Now, Bitto et al. show that treating mice with rapamycin for a short period during middle age increases the life expectancy of the mice by up to 60%. In the experiments, mice were given two different doses of rapamycin for only three months starting at 20 months old (equivalent to about 60-65 years old in humans). After receiving the lower dose, both male and female mice lived about 50% longer than untreated mice, and showed improvements in their muscle strength and motor coordination. When given the higher dose, male mice showed an even greater increase in life expectancy, but the female mice did not. These female mice had an increased risk of developing rare and aggressive forms of blood cancer, but were protected from other types of cancer.


Both drug treatments also caused substantial changes in the gut bacteria of the male and female mice, which could be related to effects of rapamycin on metabolism, immunity and health. More studies are needed to uncover precisely how such short-term treatments can yield long-term changes in the body, and how such changes are related to lifespan and healthy aging.

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Organisms age in myriad ways, but some just don't seem to age at all

Organisms age in myriad ways, but some just don't seem to age at all | Amazing Science |

Death rates in humans increase dramatically in later life, leading to an upsweeping mortality curve (far right, 2009 data from Japanese women). But the mortality curves of plants and animals vary greatly, according to a recent data analysis. Hydra don’t appear to age at all, and the death rates of desert tortoises can actually decline later in life. 

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The Real Secret of Youth Is Complexity

The Real Secret of Youth Is Complexity | Amazing Science |
Youthful health and vigor depend, in many ways, on complexity. Bones get strength from elaborate scaffolds of connective tissue. Mental acuity arises from interconnected webs of neurons. Even seemingly simple bodily functions like heartbeat rely on interacting networks of metabolic controls, signaling pathways, genetic switches, and circadian rhythms. As our bodies age, these anatomic structures and physiologic processes lose complexity, making them less resilient and ultimately leading to frailty and disease.
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America's richest men live 15 years longer than poor men

America's richest men live 15 years longer than poor men | Amazing Science |

Men in the Top 1% can expect to live until age 87.3, nearly 15 years longer than those in the Bottom 1%, according to research by Stanford economics professor Raj Chetty and seven co-authors.


America's wealthiest men live longer than their counterparts in any other country, while the poorest have life expectancies comparable to men in Sudan and Pakistan. The richest women, meanwhile, have life expectancies just shy of 89 years, a full decade longer than the poorest women.

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Scientists identify protein (GPR3) that may be key to Alzheimer's treatment

Scientists identify protein (GPR3) that may be key to Alzheimer's treatment | Amazing Science |

A protein that appears to be key in the development of Alzheimer's disease has been identified by scientists who say the discovery could provide a new drug target for dementia. Known as GPR3, the protein is believed to play an important role in reducing the buildup of amyloid plaques in the brain, a hallmark of Alzheimer's disease, said the findings in Wednesday's edition of Science Translational Medicine.

Research on mice with four different varieties of dementia showed that genetically deleting GPR3 resulted in cognitive improvement and reduced signs of disease in the brain. But since mouse models of Alzheimer's disease are not directly equivalent to the human condition, more research is needed to determine if the same process could work in people.

Researchers are encouraged by the fact that about half of all drugs currently on the market target this type of receptor, known as a G protein-coupled receptor. Also, autopsies on the brains of people with Alzheimer's have shown that a subset of patients show high levels of GPR3, and that these levels were associated with advancement of the disease.

The new study "is an example of how testing a drug target in multiple disease-relevant models can build a strong case to convince the pharmaceutical industry to launch a drug development program for Alzheimer's disease," the authors wrote. There is no cure for Alzheimer's disease, the most common type of dementia, and no drug treatment that has been shown to stop its progressions. More than 46 million people worldwide suffer from dementia, and cases are expected to balloon to 131.5 million by 2050 due to the aging population.

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How tech billionaires are using money and data to solve for death

How tech billionaires are using money and data to solve for death | Amazing Science |
How tech billionaires are using money and data to solve for death.
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Search for Immortality: Google Says Humans Could Live to be 500 Years Old

Search for Immortality: Google Says Humans Could Live to be 500 Years Old | Amazing Science |

Google has invested in taxi firms, smart thermostats and even artificial intelligence but it is also setting its sights on immortality - or at least increasing our lives five-fold. In an interview with Bloomberg, Google Ventures' president Bill Maris said he thinks it's possible to live to 500 years old. And this will be helped by medical breakthroughs as well as a rise in biomechanics. Bill Maris has $425 million to invest this year, and the freedom to invest it however he wants. He's looking for companies that will slow aging, reverse disease, and extend life.

He has already sank money into genetics firms and cancer diagnostic startups and said: 'We have the tools in the life sciences to achieve anything that you have the audacity to envision. I just hope to live long enough not to die.' Mr Maris has advised Aurolab in the development of a hydrophobic acrylic lens for cataract blindness, and helped develop Google’s Calico project.

Calico is a research and development company set up in 2013 by Google and Apple to tackle 'aging and associated diseases.'

Google co-founder Larry Page said the project would focus on 'health, wellbeing and longevity' and last September Calico partnered with AbbVie to open a research centre into neurodegeneration and cancer. Although these firms are focused on extending life naturally, there is also a group that believes machines will be the key to extending lives beyond 120 - an age that has been quoted as the 'real absolute limit to human lifespan'.

Maris has a team of 70, most of whom are in the room this day or patched in by phone or video. The group includes the fund’s 17 investing partners, who are in charge of finding startups. Among the investing partners are Joe Kraus, co-founder of Excite; Rich Miner, co-founder of Android; and David Krane, employee No. 84 at Google.

The mood in the room is casual. Some staffers sit cross-legged on the floor; others curl up on soft felt couches. There are a lot of jokes. One partner starts his presentation with a slide entitled “Secret Project”—which most people in the room already know about—and concludes it with a doctored-up photo of Maris’s head superimposed on the body of someone playing tambourine. It’s a jab at the boss, who married the singer-songwriterTristan Prettyman last August and recently went on tour with her. Everyone laughs. Maris smiles, but immediately he’s back to business. “Time is the one thing I can’t get back and can’t give back to you,” he says, turning to an agenda on the screen behind him.

“I know you’re all aware of the conference happening this week,” Maris says. An hour away in San Francisco, JPMorgan Chase is hosting its annual health-care confab, nicknamed the Super Bowl of Health Care.

Thousands of pharmaceutical executives and investors have gathered for what has become a huge part of the industry’s dealmaking. Most of Google Ventures’ life sciences startups are attending. One,Foundation Medicine, which uses genetic data to create diagnostic oncology tools, is generating huge buzz this year. In January, Roche Holding announced plans to take a majority stake in the company, in a transaction valued at $1 billion. The stock more than doubled the next day. Google Ventures has a 4 percent stake in the company.

For Maris, Foundation Medicine represents the beginning of a revolution. “The analogy I use is this,” he says, holding up his iPhone 6. “Even five years ago, this would have been unimaginable. Twenty years ago, you wouldn’t have been able to talk to anyone on this.”

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Scientists discover important genetic pathway for aging

Scientists discover important genetic pathway for aging | Amazing Science |

It’s no secret that corporate America has declared a war on death. Fueled by the collective fears of 76 million baby boomers, heavyweights like Google and Synthetic Genomics have waded in to the life extension business, bringing with them millions of dollars in funding. The result has been an uptick in the number of discoveries made in gerontology – the study of aging. But despite swamping the issue with money and media attention –an actual cure to aging remains elusive. That may soon change.

Last week, a discovery published by scientists at Northwestern University detailed a new genetic switch that may prove to be a watershed in the fight against aging. It also sheds light on one of the most significant controversies in longevity research – whether aging is the result of numerous bodily systems independently breaking down, or is controlled by a single genetic pathway.

Needless to say, much rests on the result of this question. If aging is a result of multiple independent processes, than the problem is something of a Medusa’s head, where each source of decrepitude must be tackled individually. If on the other hand, aging has a single genetic source, one could hypothetically throw the switch and cure aging in one swoop.

Unfortunately, in biological systems the more complex answers tend to be the right ones. This is why perhaps many scientists were reluctant to believe there could be a single genetic pathway controlling the aging process. However, in what might turn out to be a stroke of luck, there does indeed seem to be a single switch responsible for the aging process — at least in the C. elegans worms on which the research at Northwestern was conducted.  Fortunately for us, humans possess the same genetic pathway as the worms, so there is reason to believe the research will apply to homo-sapiens and many other animals as well.

So what exactly is the genetic switch that Dr. Morimoto and his colleagues at Northwester discovered? The story begins eight hours into the life of the C. elegans worm, when their stress protective mechanisms suddenly go into decline. After the first telltale indicators of cellular stress begin occurring, the worm’s body rapidly deteriorates and in a number of weeks the creature is dead.

The researchers traced the decline to the gamete cells within the worm, and from there to a particular genetic pathway that is initialized when the worm reaches sexual maturity. Their research indicates that at the very time the worm reaches sexual maturity and starts creating gamete cells, it begins sending a signal to other cell tissues to turn off protective mechanisms, thereby setting into motion the aging process. Now that the exact pathway has been discovered, scientists will begin working on ways to foil that process and block the signal that causes the decline in cellular resilience.

Many ancient eastern traditions such as the yogic system in India and Taoists of ancient China also connected longevity with gamete cells. In Vedic mythology, the God possessing the knowledge of the Sanjivani mantra capable of bestowing immortality is named Sukracharya, which literally translates as “semen teacher.” While it remains unclear whether Morimoto and his colleagues have discovered the fabled Sanjivani, one thing is sure: they will not be the last to go looking for it. And with the deep pockets of Google and Big Pharma backing this quest, it’s increasingly likely that results will be forthcoming.

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Quantification of aging in young adults - Aging rates vary widely, study shows

Quantification of aging in young adults - Aging rates vary widely, study shows | Amazing Science |

A study of people born within a year of each other has uncovered a huge gulf in the speed at which their bodies age. The report, in Proceedings of the National Academy of Sciences, tracked traits such as weight, kidney function and gum health. Some of the 38-year-olds were ageing so badly that their "biological age" was on the cusp of retirement. The team said the next step was to discover what was affecting the pace of aging.

The international research group followed 954 people from the same town in New Zealand who were all born in 1972-73. The scientists looked at 18 different ageing-related traits when the group turned 26, 32 and 38 years old. The analysis showed that at the age of 38, the people's biological ages ranged from the late-20s to those who were nearly 60.

"They look rough, they look lacking in vitality," said Prof Terrie Moffitt from Duke University in the US. The study said some people had almost stopped aging during the period of the study, while others were gaining nearly three years of biological age for every twelve months that passed. People with older biological ages tended to do worse in tests of brain function and had a weaker grip. Most people's biological age was within a few years of their chronological age. It is unclear how the pace of biological ageing changes through life with these measures.

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