Category Archives: Human Longevity

PUBLIC RELEASE DATE:

8-May-2014

Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine

PHILADELPHIA - Ancient philosophers looked to alchemy for clues to life everlasting. Today, researchers look to their yeast. These single-celled microbes have long served as model systems for the puzzle that is the aging process, and in this week's issue of Cell Metabolism, they fill in yet another piece.

The study, led by researchers at the University of Pennsylvania, identifies a new molecular circuit that controls longevity in yeast and more complex organisms and suggests a therapeutic intervention that could mimic the lifespan-enhancing effect of caloric restriction, no dietary restrictions necessary. After all, says senior author Shelley Berger, PhD, "who wants to live on 500 calories a day?"

Berger, a Penn Integrates Knowledge Professor in the departments of Genetics and Cell and Developmental Biology at the Perelman School of Medicine and the department of Biology in the School of Arts and Sciences, studies epigenetics, the science of the control of genetic information. Epigenetics comprises multiple regulatory layers, including chromatin packaging -- the orderly wrapping of DNA around histone proteins in the cell nucleus. By altering this DNA packaging, cells can control when and how genes are expressed.

"Aging is, in part, the accumulation of cellular stress," she explains. "If you can better respond to these stresses, this ameliorates the damage it can cause."

Berger and her team looked for chromatin-associated genes that could influence longevity by searching for genes that already were implicated in epigenetic regulation that might extend lifespan when deleted in the yeast, Saccharomyces cerevisiae. One such gene improved lifespan by about 25 percent this would correspond to an increased lifespan in humans from 75 years to about 95 years a substantial benefit to longevity, notes Berger. The research, conducted by postdoctoral fellow Weiwei Dang, PhD, aimed to unravel how this increase in longevity was achieved and if it was related to cellular stress.

First, the team asked whether the gene ISW2 is part of previously identified longevity pathways, especially those associated with caloric restriction, a well-known strategy for extending lifespan. But pathways involving a form of chromatin modification (histone acetylation) came up empty, as did an alternate pathway involving growth control, suggesting ISW2 functions through a never-before-seen mechanism.

The team then looked for answers in the function of the ISW2 protein, and found that its absence alters the expression of genes involved in protecting cells from such stresses as DNA damage. Deletion of ISW2 increases the expression and activity of genes in DNA-damage repair pathways an effect also seen during calorie restriction.

Originally posted here:
Penn yeast study identifies novel longevity pathway

Ancient philosophers looked to alchemy for clues to life everlasting. Today, researchers look to their yeast. These single-celled microbes have long served as model systems for the puzzle that is the aging process, and in this week's issue of Cell Metabolism, they fill in yet another piece.

The study, led by researchers at the University of Pennsylvania, identifies a new molecular circuit that controls longevity in yeast and more complex organisms and suggests a therapeutic intervention that could mimic the lifespan-enhancing effect of caloric restriction, no dietary restrictions necessary. After all, says senior author Shelley Berger, PhD, "who wants to live on 500 calories a day?"

Berger, a Penn Integrates Knowledge Professor in the departments of Genetics and Cell and Developmental Biology at the Perelman School of Medicine and the department of Biology in the School of Arts and Sciences, studies epigenetics, the science of the control of genetic information. Epigenetics comprises multiple regulatory layers, including chromatin packaging -- the orderly wrapping of DNA around histone proteins in the cell nucleus. By altering this DNA packaging, cells can control when and how genes are expressed.

"Aging is, in part, the accumulation of cellular stress," she explains. "If you can better respond to these stresses, this ameliorates the damage it can cause."

Berger and her team looked for chromatin-associated genes that could influence longevity by searching for genes that already were implicated in epigenetic regulation that might extend lifespan when deleted in the yeast, Saccharomyces cerevisiae. One such gene improved lifespan by about 25 percent -- this would correspond to an increased lifespan in humans from 75 years to about 95 years -- a substantial benefit to longevity, notes Berger. The research, conducted by postdoctoral fellow Weiwei Dang, PhD, aimed to unravel how this increase in longevity was achieved and if it was related to cellular stress.

First, the team asked whether the gene ISW2 is part of previously identified longevity pathways, especially those associated with caloric restriction, a well-known strategy for extending lifespan. But pathways involving a form of chromatin modification (histone acetylation) came up empty, as did an alternate pathway involving growth control, suggesting ISW2 functions through a never-before-seen mechanism.

The team then looked for answers in the function of the ISW2 protein, and found that its absence alters the expression of genes involved in protecting cells from such stresses as DNA damage. Deletion of ISW2 increases the expression and activity of genes in DNA-damage repair pathways -- an effect also seen during calorie restriction.

The gene ISW2, it turns out, is involved in chromatin remodeling -- it controls the spacing and distribution of the histone "spools" around which DNA wraps. Normally, ISW2 dampens stress-response pathways, possibly because overactivation of these pathways is deleterious early in life, Berger speculates. Deletion or inactivation of the ISW2 gene activates those pathways, priming the cells to more effectively handle stress-associated genetic scars as cells age.

This effect is not limited to yeast. When Berger's team reduced the levels of a related gene in the nematode worm, Caenorhabditis elegans, they observed a 15 percent improvement in longevity, which is similar in magnitude to the lifespan extension observed in other worm longevity pathways. Similarly, knocking down expression of a human homolog in cultured human cells boosted the expression of stress-response genes that, again, like yeast, occur in DNA-damage repair pathways.

These findings suggest a pathway analogous to the one identified in yeast performs a similar function in humans, keeping stress-response genes in check -- and if inhibited, could boost these pathways. But that has yet to be established. And, it is far from clear if tweaking these pathways can actually extend healthy human lifespan -- but, of course, a goal worthy of further investigation, say the authors.

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Yeast study identifies novel longevity pathway

The plague preferentially killed the very old and those already in poor health. Natural selection or better diets may have allowed those who remained to thrive

A depiction of the black death from a 15th-century Bible

The Black Death, a plague that first devastated Europe in the 1300s, had a silver lining. After the ravages of the disease, surviving Europeans lived longer, a new study finds.

An analysis of bones in London cemeteries from before and after the plague reveals that people had a lower risk of dying at any age after the first plague outbreak compared with before. In the centuries before the Black Death, about 10 percent of people lived past age 70, said study researcher Sharon DeWitte, a biological anthropologist at the University of South Carolina. In the centuries after, more than 20 percent of people lived past that age.

"It is definitely a signal of something very important happening with survivorship," DeWitte told Live Science. [Images: 14th-Century Black Death Graves]

The plague years

The Black Death, caused by the Yersinia pestis bacterium, first exploded in Europe between 1347 and 1351. The estimated number of deaths ranges from 75 million to 200 million, or between 30 percent and 50 percent of Europe's population. Sufferers developed hugely swollen lymph nodes, fevers and rashes, and vomited blood. The symptom that gave the disease its name was black spots on the skin where the flesh had died.

Scientists long believed that the Black Death killed indiscriminately. But DeWitte's previous research found the plague was like many sicknesses: It preferentially killed the very old and those already in poor health.

That discovery raised the question of whether the plague acted as a "force of selection, by targeting frail people," DeWitte said. If people's susceptibility to the plague was somehow genetic perhaps they had weaker immune systems, or other health problems with a genetic basis then those who survived might pass along stronger genes to their children, resulting in a hardier post-plague population.

In fact, research published in February in the journal Proceedings of the National Academy of Sciences suggested that the plague did write itself into human genomes: The descendants of plague-affected populations share certain changes in some immune genes.

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Black Death Survivors and Their Descendants Went On to Live Longer

Its long been thought that vampires live forever by drinking the blood of young victims and new research may just be proving this theory.

Today, three very interesting studies published in the journals Science and Nature Medicine analyzed older mice and how they were affected when injected with blood, and blood proteins, of younger mice.

RELATED: Young blood reverses aging in mice

Conducted by researchers at Harvard University, University of California San Francisco and Stanford University, these studies found that post-injections, the aging mice had higher levels of strength and endurance, as well as improved memory. The younger blood also caused the older mice to develop more blood vessels and more blood flow to the brain.

Its not clear exactly why these changes occurred, though researchers suspect a particular protein called GDF11 may play a role, as it is much more abundant in the blood of younger mice.

So what can we learn from this experiment? As we age, certain components in our blood decrease over time, and because of advancements in life-saving technologies, the global population is growing much older overall. Therefore research must continue searching for bodily substances that get depleted over time, so that we might replace them in the future.

A perfect example includes research surrounding adult stem cells. There are many scientists that argue that young adults should consider harvesting their stem cells for potential use in the future when theyre older. There is a whole new field of medicine called regenerative medicine, in which stem cells are already being used for organ regeneration and human transplantation.

Recently, researchers at the Wake Forest Institute of Regenerative Medicine, known for conducting the first-ever lab-grown bladder transplants, made another incredible breakthrough in this field. They successfully implanted fully functioning vaginas into four women using cells taken from the patients own tissues.

Since we are on the topic of longevity, I would also like to point out some of the interesting findings from an ongoing study called 90+, conducted by Dr. Claudia Kawas of the University of California, Irvine. Utilizing medical questionnaires from 14,000 residents of a retirement community in Laguna Woods, California, Kawas and her team focused on the members who were still alive past age 90, examining them physically and cognitively for six months.

Their ongoing analysis has revealed a number of lifestyle habits and factors associated with longer life including moderate consumption of alcohol, moderate physical activity, putting on a little weight, maintaining healthy blood pressure, and finally, socialization. Thank goodness most of these seniors didnt care much about their computers. Instead, they were more preoccupied with dancing and having dinner with each other than being hooked on Facebook or Twitter.

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Key to longevity discovered?

Transfusions of young blood could hold the key to reversing the signs of ageing, scientists believe.

Transfusions of young blood could reverse the ageing process and even cure Alzheimer's disease, American scientists believe.

In a breakthrough that could herald a new dawn in anti-ageing treatments, researchers found that young blood "recharges" the brain, forms new blood vessels and improves memory and learning.

Meanwhile, in parallel research, scientists at Harvard University discovered that a "youth protein" which circulates in the blood, is responsible for keeping the brain and muscles young and strong.

The protein, known as "GDF11", is present in the bloodstream in large quantities when we are young but peters out as we age.

Although both the discoveries were made in mice, researchers are hoping to begin human trials in the next two to three years, in studies that could bring rapid improvements for human longevity and health.

"This should give us all hope for a healthier future," said Professor Doug Melton, from Harvard's department of stem cell and regenerative biology.

"We all wonder why we were stronger and mentally more agile when young, and these two unusually exciting papers actually point to a possible answer.

"There seems to be little question that GDF11 has an amazing capacity to restore ageing muscle and brain function."

Last year, the team discovered that the protein could repair damaged hearts. But the new study showed that raising the levels of the GDF11 protein in older mice improved the function of every organ in the body.

Continued here:
'Vampire therapy' reverses ageing

San Francisco, CA (PRWEB) May 02, 2014

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Visit link:
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The protein, known as GDF11, is present in the bloodstream in large quantities when we are young but peters out as we age.

Although both the discoveries were made in mice, researchers are hoping to begin human trials in the next two to three years, in studies which could bring rapid improvements for human longevity and health.

This should give us all hope for a healthier future, said Prof Doug Melton, of Harvard's Department of Stem Cell and Regenerative Biology.

We all wonder why we were stronger and mentally more agile when young, and these two unusually exciting papers actually point to a possible answer.

There seems to be little question that, GDF11 has an amazing capacity to restore aging muscle and brain function.

Last year the team discovered that the protein could repair damaged hearts. But the new study showed that that raising the levels of the GDF11 protein in older mice improved the function of every organ in the body.

Harvard stem cell biologist Prof Lee Rubin added: We do think that, at least in principal, there will be a way to reverse some of the decline of aging with a single protein.

"It isn't out of question that GDF11, or a drug developed from it, might be worthwhile in Alzheimer's Disease.

It is likely that the protein is at least partly responsible for the parallel finding by Stanford University that young blood can reverse the signs of ageing.

In the study, the blood of three-month-old mice was repeatedly injected into 18-month-old mice near the end of their natural life span.

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'Vampire therapy' could reverse ageing, scientists find

Beloved by young and old, Nellie the oldest dolphin in human care, has died at age 61, according to her caretakers at Marineland Dolphin Adventure.

We are saddened to announce that Nellie, the oldest Atlantic bottlenose dolphin in human care, has passed away. She lived to the incredible age of 61. Though we are saddened by her loss, her memory will live on in the lives she touched. She fostered a love of the ocean and promoted marine conservation to thousands throughout her lifetime. We will miss her dearly, the marine park announced on its Facebook page about 7 p.m. Thursday.

An Atlantic bottlenose dolphin, Nellie was born on Feb, 27, 1953 at Marineland. She was adopted as Jacksonville Universitys mascot in 1970. Last year, JU awarded Nellie an honorary doctorate degree in health sciences and longevity during her 60th birthday celebration.

Nellie brought such joy to so many, and was an inspiration to generations with her spirit and longevity, said JU President Tim Cost. We are honored to have had her as our mascot, and share our condolences with her caregivers at Marineland and with all those who shared such a special bond with her.

The certificate was Nellies third. The first was when she was proclaimed an honorary JU Dolphin when named its mascot. She then received an honorary masters degree in marine science in 2008.

She was also the oldest living college mascot in the country. A longtime star performer, she jumped through hoops and playfully interacted with trainers and spectators at Marinelands dolphin shows.

Nellies showmanship made her a national celebrity. She appeared in a Timex watch commercial, and a Frank Sinatra special.

She touched the lives of people who walked through the doors of Marineland. She gave them the gift of awareness, education and conservation while paving the way to help protect marine mammals in the worlds oceans. While an unfortunate loss for Marineland Dolphin Adventure and the Georgia Aquarium family, Nellies legacy continues through the memories created and inspiration she left behind, her human colleagues said on the Georgia Aquarium blog.

Teresa Stepzinski: (904) 359-4075

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Nellie the dolphin dies at Marineland Dolphin Adventure

With the news Tuesday night that Fox has canceled the robot cop drama Almost Human after one season, the bubble watch that time of year when underperforming TV shows wait anxiously to hear their fate has officially begun.

As the networks look to pick up new shows for next season, some existing shows will have to go. First-year series that never quite took off and veterans aging gracelessly are both in peril.

While the renewal of some shows is a no-brainer (hello, Scandal), the return of others, such as CBS Hostages, is far from certain. With decisions set to come down in the next week or two, here are our picks for the top 10 bubble shows.

That the Robin Williams comedy was left off the list when CBS renewed 18 shows last monthdoesnt bode well for its future. Its season finale two weeks ago drew less than 6 million viewers, meaning the top-rated network will likely choose to move on.

This 6-year-old drama was likewise left out of the bulk renewal, putting it in danger of being canceled. If that happens, theres a chance it could see a second life on cable Deadline.com reported last week that the studio was shopping the Simon Baker procedural to other networks.

After 15 seasons, SVU still draws an impressively loyal fan base, but that longevity equals a pricey drama that draws only modest ratings. With creator Dick Wolf now having successfully spawned another franchise in Chicago Fire and Chicago PD, NBC could opt to focus his attention there and finally close the book on the L&O franchise.

No bubble list would be complete without this perennially endangered cult comedy. Communitys saving grace for the past five seasons has been that, while its ratings are low, so are those of every other NBC comedy. With both Michael J. Foxs and Sean Hayes series tanking on Thursdays, Community is likely to get halfway to its six seasons and a movie goal.

With fellow Tuesday comedy About a Boy having found a respectable audience, this comedy about a boy with a blind father could see itself getting the ax. But averaging 5.7 million viewers in its last episode is no slouch for NBC depending on how the network feels about its new comedy development, it could squeak out another season.

This multi-camera comedy from Family Guy creator Seth MacFarlane was reviled by critics for its one-note jokes and stereotypical characters, and finished out its first season last February without a renewal. Its unlikely even the mighty MacFarlane can save this one from cancellation.

American Idol aint the launch pad it once was, as this Chris Meloni comedy discovered when it premiered last month. Airing after the half-hour results show on Thursdays, Surviving Jack drew just under 4 million viewers last week likely not enough for renewal.

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Going going gone? These TV shows face the ax

2 hours ago Water thick-knee (Burhinus vermiculatus) defending it nest against a monitor lizard. Credit: MPI for Ornithology Seewiesen/ Wolfgang Goymann

(Phys.org) Ageing inevitably occurs both in humans and in other animals. However, life-span varies widely across species. Researchers of the Max Planck Institute for Ornithology in Seewiesen have now found a possible general mechanism explaining differences in longevity. They investigated life history data of nearly 1400 bird species and found that avian life span varies considerably across the entire Earth, and that much of this variation can be explained by the species' body mass and clutch size and by the local diversity of predator species. With their data the researchers were able to confirm a key prediction of the classical evolutionary theory of ageing that had been proposed more than 50 years ago.

It is well-known that organisms vary widely in life-span. Whereas some fish, turtles or even invertebrates can become hundreds of years old, the neon pygmy goby a small fish - reaches ripe old age at only 60 days. In birds, variation in life-span extends from parrots such as the Sulphur-crested cockatoo that can become more than 100 years old, to the small Allen's hummingbird with a maximum life-span of only 4 years, a 25 fold difference. How can this variation be explained?

The classical evolutionary theory of ageing, first proposed by the famous evolutionary biologist George C. Williams over 50 years ago, gives an answer. The theory predicts that high mortality rates in adult animals due to predation, exposure to parasites and other randomly occurring events will be associated with shorter maximum life-spans. This is because under high external mortality most individuals will already be dead (eaten or succumbed to disease) before natural selection can act on rare mutations that cause healthier ageing. The theory has since been further developed and tested in a number of experimental and comparative studies. Yet contradictory results have caused scientists to cast doubt on its validity.

Mihai Valcu and Bart Kempenaers from the Max Planck Institute for Ornithology in Seewiesen together with colleagues from New Zealand and Switzerland have now tested this theory using a comprehensive database on estimates of maximum life-span of 1396 bird species, 1128 from free-living species and 268 from birds kept in captivity. The researchers used a global distribution map of these species, included data on their morphology and reproductive rate, and estimated predation rate.

By means of complex statistical analysis methods they found that in the investigated bird species maximum longevity is negatively related to the number of predator species occurring within the same geographical area. This means that the more predator species are present in the same habitat and the more evenly they are distributed, the lower is the life span of the respective species. This relationship supports the classical theory of ageing, and remains valid when other life history traits known to influence longevity such as body mass and clutch size are included into the statistical model. Indeed, larger species live longer, and those that reproduce fast (lay more eggs) live shorter lives.

Remarkably, the observed pattern showing longer life-spans when fewer predators are present emerges no matter how the analysis was done: at the species level, at a finer regional scale (groups of species within a certain area) or even when comparing entire bioregions. "With our results of a negative relationship between predation pressure and longevity that is largely independent of other key life history traits we were able to confirm the universality of the 50 year old evolutionary theory of ageing on a broad geographical scale" concludes Mihai Valcu, first author of the study. At least in birds, where the necessary data are available for many species, the theory seems to hold.

Explore further: Why do fruit flies live so long?

More information: M. Valcu, J.Dale, M. Griesser, S. Nakagawa, B. Kempenaers. "Global gradients of avian longevity support the classic evolutionary theory of ageing." Ecography, article first published online: 25 April 2014 DOI: 10.1111/ecog.00929

Journal reference: Ecography

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Predators predict longevity of birds