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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 | Scoop.it

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 | Scoop.it
How tech billionaires are using money and data to solve for death. http://wapo.st/humanupgrade
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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 | Scoop.it

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 | Scoop.it

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 | Scoop.it

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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Mortality Gap: Have Women Always Lived Longer than Men?

Mortality Gap: Have Women Always Lived Longer than Men? | Amazing Science | Scoop.it

In every single country on the planet, women live longer than men. In response to this unpleasant fact, men are fond of replying, "That's because we have to put up with women." Humorous though it may be, that's not the actual reason women live longer than men. In fact, it wasn't until the beginning of the 20th Century that the "mortality gap" between men and women became so striking.


To investigate the underlying reason for the gender gap in life expectancy, a team of researchers examined mortality data for people born between 1800 and 1935 in 13 developed countries. Using this data, they were able to determine changes in the male-female mortality ratio, as well as determine when and why women began to outlive men.


In the figure above, each birth cohort is represented by a single colored line. For example, people born between 1800 and 1819 are represented by 20 different lines, each of which is colored black; people born between 1920 and 1935 are represented by 16 colored lines, each of which is colored red. The chart plots age on the X-axis (i.e., "age at time of death") against the male-female mortality rate ratio on the Y-axis.


The figure shows that the relative mortality rate for men gets worse in subsequent years. Compare the mortality rates at age 60, for instance. The mortality rate ratio for people born between 1800 and 1839 (black and gray lines) hovers roughly around 1.2; that means that about 120 men died for every 100 women who died at age 60. Just a few decades later, a dramatic shift occurs: the male-female mortality rate ratio for people born between 1880 and 1899 (green lines) skyrockets to 1.6, meaning that 160 men died for every 100 women who died at age 60. Then it goes from bad to worse. For the 1920-1935 birth cohort, the ratio is a shocking 2.1 at age 60, meaning that 210 men died for every 100 women.


Why is this the case? The authors' analysis suggests two major factors: The first is smoking, which is more common among men. (With smoking factored out, the pattern of an increasing male-female mortality ratio still persists but to a lesser extent, as shown above.) The second is cardiovascular disease, a condition to which men seem to be more vulnerable than women. This may be due to gender differences in diet, lifestyle, and even genetics. Indeed, the researchers found that cardiovascular disease was the major factor causing excess deaths among men as compared to women.

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It's old blood, not old bones, that makes fracture healing difficult among the elderly

It's old blood, not old bones, that makes fracture healing difficult among the elderly | Amazing Science | Scoop.it

A recent finding by scientists from the Hospital for Sick Children, Toronto, and Duke University challenges long-held ideas about why our bones have a harder time healing as we age. Their research discovered that old mouse bones mend like youthful bones do when they're exposed to young blood after a fracture.


“The traditional concept is that as you get older, your bone cells kind of wear out so they can't heal as well, and we thought we'd find that during this study as well,” explains study co-author Benjamin Alman, of the Hospital for Sick Children. “But it turns out that it's not the bone cells, it's the blood cells. As you get older, the blood cells change the way they behave when you have an injury, and as a result the cells that heal bone aren't able to work as efficiently.”


The researchers paired lab mice, one old and one young, and subjected them to bone fractures, but that wasn't all they had in common. The living animals' circulatory systems were also joined together by a 150-year-old surgical technique known as parabiosis. Scientists removed a layer of skin from each mouse and stitched the exposed surfaces together. As the animals healed their capillaries joined, enabling their two hearts to pump the same blood throughout the two bodies as a single system. Parabiosis, which has been gaining new popularity in aging research, allowed Alman and colleagues to see what impacts the circulating factors of the younger mouse's blood had when introduced into the body of an older mouse.


The experiment, published this week in Nature Communications, suggests that young blood cells secrete some as-yet-unknown molecule, likely a protein or possibly some other chemical, that speeds up the healing of fractured bone. The molecule apparently does so by regulating levels of beta-catenin in bone cells known as osteoblasts. Keeping beta-catenin at the proper levels appears crucial for the formation of new high-density bone.


This ability is greatly diminished in older animals' blood because it no longer secretes the molecule, whose exact chemical nature remains a mystery at this point. “My guess is that there are a number of proteins involved that are made differently as we get older, and that they are responsible for the difficulty in healing bone,” Alman says.


The findings could prove good news for aging humans, but healing our bones won’t require the type of transfusions used in the experiment—nor will it borrow the synthesized “True Blood” variety that may soon enter clinical trials. Sharing human blood in this manner raises a number of red flags ranging from practicality to possible medical complications.

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The #1 reason people die early, in each country

The #1 reason people die early, in each country | Amazing Science | Scoop.it

You're probably aware that heart disease and cancer are far and away the leading causes of death in America. But globally the picture is more complicated: The above map shows the leading cause of lost years of life by country (click to see a larger version). The data comes from the Global Burden of Disease study, whose 2013 installment was released just a few weeks ago. It's worth stressing that "cause of lost years of life" and "cause of death" aren't identical. For example, deaths from preterm births may cause more lost years of life in a country than deaths from heart disease even if heart disease is the leading cause of death. Deaths from preterm births amount to many decades of lost life, whereas heart disease tends to develop much later on.


But that makes the fact that heart disease is the leading cause of lost life in so many countries all the more striking, and indicative of those countries' successes in reducing childhood mortality. By contrast, in many lower-income countries, the leading cause is something like malaria, diarrhea, preterm birth, HIV/AIDS, or violence, which all typically afflict people earlier in life than heart disease or stroke. We've made considerable progress in fighting childhood mortality across the globe in recent decades, but there's still much work left to be done.

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A step toward a potential anti-aging drug

A step toward a potential anti-aging drug | Amazing Science | Scoop.it

According to a new study published in Science Translational Medicine, researchers have tested a potential anti-aging drug called everolimus (AKA RAD001) — an analog (version) of the drug rapamycin (sirolimus)*. In previous research, rapamycin extended the life span of mice by 9 to 14%, even when treatment was initiated late in life, and it improved a variety of aging-related conditions in old mice, including tendon stiffening, cardiac dysfunction, cognitive decline, and decreased mobility. These findings raise the possibility that “mTOR inhibitors”* (like rapamycin and RAD001) may have beneficial effects on aging and aging-related conditions in humans.


Since it would take decades to test the effect of a drug on life span in humans, the researchers at Novartis Institutes for BioMedical Research and affiliates used a proxy: the decline in immune function in seniors’ (age 65 and older) during aging, as assessed by their response to a flu vaccine. Immune-system aging is a major cause of disease and death, making older people more susceptible to infections — and to have a weaker response to vaccines. In the research, the scientists found that R001 boosted immune systems response to a flu vaccine by 20 percent.


“The immune-enhancing effects of mTOR inhibitors need to be verified with additional studies,” the authors say. Although some scientists are reportedly already self-medicating, “the toxicity of RAD001 at doses used in oncology or organ transplantation results in adverse effects such as stomatitis, diarrhea, nausea, cytopenias, hyperlipidemia, and hyperglycemia.”


*Rapamycin and RAD001 belong to a class of drugs known as “mTOR inhibitors.” Inhibition of the mTOR (Mammalian target orapamycin) pathway extends life span in all species studied to date, the scientists note, and in mice it also delays the onset of age-related diseases and co-morbidities (unrelated pathological or disease processes involved at the same time).

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The Fountain of Youth is Closer Than We Think

The Fountain of Youth is Closer Than We Think | Amazing Science | Scoop.it


In a recent TEDx talk Human Longevity Inc.'s Dr. Robert Hariri tells how stem cells may be the secret scientific ingredient that enables humans to live younger longer. Human Longevity Inc, which was recently formed with J. Craig Venter and Peter Diamandis will use both genomics and stem cell therapies to find treatments that allow aging adults to stay healthy and functional for as long as possible. "I believe that aging is a stem cell problem, related to a shift in the balance of undifferentiated, versatile to differentiated, specialized cells," says Hariri. 

He talks of how bone marrow recipients and plastic surgery patients that have had adipose tissue injections can  achieve more youthful characteristics thanks to the introduction of stem cells into the affected areas, and the important proteins that they produce. "I think the solution here is to recharge the regenerative engine by replenishing the reservoir of stem cells that can restore that synthetic versatility," he claims.

Hariri concludes his talk by saying that, "The future use of stem cells can benefit from a new model describing functional similarities to computers." In this conception, the biological software resides in the DNA of the cell's nucleus; the cytosolic organelles that produce the proteins are the processor and the cell membrane with it's numerous receptors, serves as the keyboard. "Reprogramming the biological software of stem cells is already happening and provides a platform for controlling their fate and behavior for biomedical purposes including longevity," concludes Hariri. He is a surgeon, biomedical scientist and highly successful serial entrepreneur in two technology sectors: biomedicine and aerospace. The Chairman, Founder, Chief Scientific Officer, and former Chief Executive Officer of Celgene Cellular Therapeutics, one of the world’s largest human cellular therapeutics companies, Dr. Hariri has pioneered the use of stem cells to treat a range of life threatening diseases and has made transformative contributions in the field of tissue engineering.

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Flies live 30 percent longer when AMPK is activated

Flies live 30 percent longer when AMPK is activated | Amazing Science | Scoop.it

Activating a specific gene in the intestines of a fruit fly made it live 30 percent longer, a team of biologists has reported.


The gene in question, AMPK, detects and reacts to fluctuations in the body to help modulate energy levels. The gene is also found in humans in low levels, leading the UCLA team to postulate in the open source journal Cell Reports that we could use it to learn about potentially delaying the ageing process.


Key to this statement is the fact that in the experiment on the Drosophila melanogaster fruit fly, the ageing process slowed throughout the insect's organs -- not just in the intestine where AMPK was activated.


The team behind the study is taking an approach similar to that ofbiogerontologist and SENS Foundation co-founder Aubrey de Grey, who argues that instead of attempting to modify our cells to combat disease, we must repair the molecular damage that happens as cells degrade. Among the cell death, cell divisions and mitochondria mutations that he cites as being cellular problems to combat, is "molecular garbage", a problem also flagged up by the UCLA team. In the body, we naturally discard of this molecular garbage through a process known as autophagy.


Autophagy allows any cells that are old or degrading to be shed, and AMPK is known to help activate that system. "However, the tissue-specific mechanisms involved are poorly understood," writes the UCLA team in Cell Reports. If we could better understand and harness its capabilities, they argue, we could go some way in slowing the aging process by tackling the molecular garbage problem prevalent in old age. It is molecular garbage and protein buildups that contribute to some of the biggest killer diseases in later years.

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Immortal jellyfish: Does it really live forever?

Immortal jellyfish: Does it really live forever? | Amazing Science | Scoop.it
The Turritopsis nutricula jellyfish has displayed a remarkable ability to regenerate its cells in times of crisis.


While it is often joked that cats have nine lives, a certain species of jellyfish has been deemed “immortal” by scientists who have observed its ability to, when in crisis, revert its cells to their earliest form and grow anew. That means that these tiny creatures, 4 mm to 5 mm long, potentially have infinite lives.
 
The creature, known scientifically as Turritopsis nutricula, was discovered in the Mediterranean Sea in 1883, but its unique regeneration was not known until the mid-1990s. How does the process work? If a mature Turritopsis is threatened — injured or starving, for example — it attaches itself to a surface in warm ocean waters and converts into a blob. From that state, its cells undergo transdifferentiation, in which the cells essentially transform into different types of cells. Muscle cells can become sperm or eggs, or nerve cells can change into muscle cells, “revealing a transformation potential unparalleled in the animal kingdom,” according to the original study of the species published in 1996.


But Turritopsis can — and do — die. Their regeneration only occurs after sexual maturation, therefore they can succumb to predators or disease in the polyp stage. But because the jellyfish are the only known animal with this “immortality,” scientists are studying them closely, with the hopes of applying what they learn to issues such as human aging and illness.

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Oxytocin helps old muscle work like new, study finds

Oxytocin helps old muscle work like new, study finds | Amazing Science | Scoop.it
UC Berkeley researchers have discovered that oxytocin — a hormone associated with maternal nurturing, social attachments, childbirth and sex — is indispensable for healthy muscle maintenance and repair. It is the latest target for development into a potential treatment for age-related muscle wasting.


A few other biochemical factors in blood have been connected to aging and disease in recent years, but oxytocin is the first anti-aging molecule identified that is approved by the Food and Drug Administration for clinical use in humans, the researchers said. Pitocin, a synthetic form of oxytocin, is already used to help with labor and to control bleeding after childbirth. Clinical trials of an oxytocin nasal spray are also underway to alleviate symptoms associated with mental disorders such as autism, schizophrenia and dementia.


“Unfortunately, most of the molecules discovered so far to boost tissue regeneration are also associated with cancer, limiting their potential as treatments for humans,” said study principal investigator Irina Conboy, associate professor of bioengineering. “Our quest is to find a molecule that not only rejuvenates old muscle and other tissue, but that can do so sustainably long-term without increasing the risk of cancer.”


Conboy and her research team say that oxytocin, secreted into the blood by the brain’s pituitary gland, is a good candidate because it is a broad range hormone that reaches every organ, and it is not known to be associated with tumors or to interfere with the immune system.


The new study determined that in mice, blood levels of oxytocin declined with age. They also showed that there are fewer receptors for oxytocin in muscle stem cells in old versus young mice.


To tease out oxytocin’s role in muscle repair, the researchers injected the hormone under the skin of old mice for four days, and then for five days more after the muscles were injured. After the nine-day treatment, they found that the muscles of the mice that had received oxytocin injections healed far better than those of a control group of mice without oxytocin.


“The action of oxytocin was fast,” said Elabd. “The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice.”


Interestingly, giving young mice an extra boost of oxytocin did not seem to cause a significant change in muscle regeneration.

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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 | Scoop.it
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 | Scoop.it

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 | Scoop.it

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 | Scoop.it
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 | Scoop.it

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."

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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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Why human egg cells don't age well

Why human egg cells don't age well | Amazing Science | Scoop.it
When egg cells form with an incorrect number of chromosomes--a problem that increases with age--the result is usually a miscarriage or a genetic disease such as Down syndrome. Now, researchers at the RIKEN Center for Developmental Biology in Japan have used a novel imaging technique to pinpoint a significant event that leads to these types of age-related chromosomal errors. Published in Nature Communications, the study shows that as egg cells mature in older women, paired copies of matching chromosomes often separate from each other at the wrong time, leading to early division of chromosomes and their incorrect segregation into mature egg cells.

Most cells have two copies of each chromosome--one from each parent. Immature egg cells begin this way, but are transformed through a process called meiosis into mature egg cells that only have one copy of each chromosome. At the beginning of meiosis each chromosome copies itself and joins with its matching pair to form a group of four chromosomes that swap genetic material.

These groups of four chromosomes--called bivalents--then split apart into single pairs, and the cell divides. One part continues as the egg cell and the other part degrades. In the second stage of meiosis, the single pairs of chromosomes--two sister chromatids joined in the middle--separate and the egg cell divides again in the same way, leaving a single mature egg cell with one copy of each chromosome.

"What we found," explains team leader Tomoya Kitajima, "is that in older cells, the bivalents sometimes separate early, and this leads to division of sister chromatids in the first stage of meiosis, rather than in the second stage."

To determine the most common type of age-related segregation errors, the researchers first used a novel high resolution imaging technique to visualize chromosomes in live mouse egg cells throughout the whole first stage of meiosis. They found that chromosomes were always distributed correctly in young egg cells, but that a little less than 10% of older cells suffered from segregation errors. Closer examination of the chromosome-tracking data showed that the dominant type of error was predivision of sister chromatids, and not movement of intact chromosome pairs to only one of the new cells.

The tracking data also allowed researchers to go back in time and look at what was happening to chromosomes that eventually segregated incorrectly. They found that a large majority of them had been part of bivalents whose connection between paired chromosome copies had become hyperstretched and then snapped earlier in meiosis, leaving single pairs.
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Clonal Expansion of Early to Mid-Life Mitochondrial DNA Mutations Drives Mitochondrial Dysfunction during Human Aging

Clonal Expansion of Early to Mid-Life Mitochondrial DNA Mutations Drives Mitochondrial Dysfunction during Human Aging | Amazing Science | Scoop.it

Age-related decline in the integrity of mitochondria is an important contributor to the human aging process. In a number of ageing stem cell populations, this decline in mitochondrial function is due to clonal expansion of individual mitochondrial DNA (mtDNA) point mutations within single cells. However the dynamics of this process and when these mtDNA mutations occur initially are poorly understood. Using human colorectal epithelium as an exemplar tissue with a well-defined stem cell population, researchers have now analyzed samples from 207 healthy participants aged 17–78 years using a combination of techniques (Random Mutation Capture, Next Generation Sequencing and mitochondrial enzyme histochemistry), and show that: 1) non-pathogenic mtDNA mutations are present from early embryogenesis or may be transmitted through the germline, whereas pathogenic mtDNA mutations are detected in the somatic cells, providing evidence for purifying selection in humans, 2) pathogenic mtDNA mutations are present from early adulthood (<20 years of age), at both low levels and as clonal expansions, 3) low level mtDNA mutation frequency does not change significantly with age, suggesting that mtDNA mutation rate does not increase significantly with age, and 4) clonally expanded mtDNA mutations increase dramatically with age. These data confirm that clonal expansion of mtDNA mutations, some of which are generated very early in life, is the major driving force behind the mitochondrial dysfunction associated with ageing of the human colorectal epithelium.

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Lin28A Accelerates Wound Healing, Hair Regrowth, and Turns Back The Aging Clock A Little

Lin28A Accelerates Wound Healing, Hair Regrowth, and Turns Back The Aging Clock A Little | Amazing Science | Scoop.it

For centuries, biologists have wondered why an organism’s capacity for tissue repair and wound healing tends to decline as it gets older. The new study, which is published in the journal Cell, submits that this strange phenomenon may be the result of Lin28a – a gene whose protein product plays a crucial role in the early growth and development of a wide variety of animals. According to senior author George Daley, our gradual loss of regenerative powers may be symptomatic of a decline in Lin28a protein levels.


"It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals," he said in a press release.


To investigate the “fountain-of-youth” gene, the researchers reactivated it in adult mice. They found that the Lin28a protein accelerated the regeneration of cartilage, bone, and mesenchyme in a variety of injury models. Intriguingly, the gene also promoted faster regrowth of hair by stimulating anagen in the test subject’s hair follicles. Daley and his colleagues believe that Lin28a achieves these rejuvenating effects by stimulating metabolic processes otherwise associated with an organism’s embryo stage.


Study author Shyh-Chang Ng believes that the “fountain-of-youth” gene could be integrated into a number of different therapies. "We were surprised that what was previously believed to be a mundane cellular 'housekeeping' function would be so important for tissue repair," he told reporters. "One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans."


The current study is the latest in a growing series of inquiries into regeneration – a fascinating biological phenomenon that is observed across the entire evolutionary spectrum of organisms. Earlier this year, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics showed that a single knocked-out gene allows planarian flatworms to regenerate their head and brain. A more recent study describes a so-called bio patch thatpromotes and sustains local bone growth in weakened and damaged areas. Like the current study, these research efforts remind us that when it comes to biotechnology and medicine, the line between science fiction and reality is not always clear.  

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Elixir of Youth: Factors Within the Blood of Young Mice Have the Ability to Restore Aspects of Youth in Old Mice

Elixir of Youth: Factors Within the Blood of Young Mice Have the Ability to Restore Aspects of Youth in Old Mice | Amazing Science | Scoop.it

Emerging evidence indicates that there are factors within the blood of young animals that have the ability to restore youthful characteristics to a number of organ systems in older animals. Recent work regarding age-related cardiac hypertrophy identified growth/differentiation factor 11 (GDF11) as one such factor with rejuvenating powers. As animals become older, levels of circulating GDF11 normally decline.


Remarkably, injecting GDF11 into aged mice recapitulates the effects of heterochronic parabiosis, reversing cardiac hypertrophy7. However, it remained unclear whether the effects of GDF11 were unique to the heart.


Sinha et al.8 have now shown that increasing the systemic levels of GDF11 in aged mice also has rejuvenating effects on skeletal muscle. Aged mice injected daily with recombinant GDF11 (rGDF11) for four weeks have greater numbers of satellite cells, the local muscle stem cell population. Moreover, these satellite cells have less DNA damage and generate more myogenic cells in culture. rGDF11 supplementation also improves the in vivo regenerative capacity of satellite cells, resulting in the growth of larger muscle fibers after injury. Treatment with rGDF11 even increases exercise endurance and grip strength, demonstrating that the improvements seen in satellite cells relate to a functional enhancement in muscle performance. While it remains unclear whether these results are due primarily to effects on skeletal muscle, particularly given the known enhancement of cardiac function observed with rGDF11 treatment, this work demonstrates that a single systemic factor can help restore physiological properties of youth.


Studies regarding the rejuvenating capacity of young blood and rGDF11 have also been extended to the aged brain by Katsimpardi et al.9. The authors focused on the adult neural stem cells (NSCs) of the subventricular zone (SVZ) and found that heterochronic parabiosis enhances proliferation of Sox2+ NSCs in the aged mice. SVZ NSCs differentiate into neuroblasts that migrate to the olfactory bulb, and heterochronic parabiosis almost doubles the number of new neurons in the olfactory bulb of aged mice. Interestingly, these mice exhibit improved olfactory discrimination, but whether this behavioral change results directly from the enhanced neurogenesis or more generally to the whole-animal effects of heterochronic parabiosis is not yet known.

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Whole-genome sequences of 17 of the world’s oldest living people published

Whole-genome sequences of 17 of the world’s oldest living people published | Amazing Science | Scoop.it

Using 17 genomes, researchers were unable to find rare protein-altering variants significantly associated with extreme longevity, according to a study published November 12, 2014 in the open-access journal PLOS ONE by Hinco Gierman from Stanford University and colleagues.


Supercentenarians are the world’s oldest people, living beyond 110 years of age. Seventy-four are alive worldwide; 22 live in the U.S. The authors of this study performed whole-genome sequencing on 17 supercentenarians to explore the genetic basis underlying extreme human longevity.


From this small sample size, the researchers were unable to find rare protein-altering variants significantly associated with extreme longevity compared to control genomes. However, they did find that one supercentenarian carries a variant associated with a heart condition, which had little or no effect on his/her health, as this person lived over 110 years.


Although the authors didn’t find significant association with extreme longevity, the authors have publicly published the genomes, making them available as a resource for future studies on the genetic basis of extreme longevity.


Reference:

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TRAP-1 knock-out mice show signs of longer lives with fewer age-related diseases

TRAP-1 knock-out mice show signs of longer lives with fewer age-related diseases | Amazing Science | Scoop.it

While developing a new cancer drug, researchers at The Wistar Institute discovered that mice lacking a specific protein live longer lives with fewer age-related illnesses. The mice, which lack the TRAP-1 protein, demonstrated less age-related tissue degeneration, obesity, and spontaneous tumor formation when compared with normal mice. Their findings could change how scientists view the metabolic networks within cells.


In healthy cells, TRAP-1 is an important regulator of metabolism and has been shown to regulate energy production in mitochondria, organelles that generate chemically useful energy for the cell. In the mitochondria of cancer cells, TRAP-1 is universally overproduced.  


The Wistar team’s report, which appears in the journal Cell Reports (available online now), shows how “knockout” mice bred to lack the TRAP-1 protein compensate for this loss by switching to alternative cellular mechanisms for making energy.


“We see this astounding change in TRAP-1 knockout mice, where they show fewer signs of aging and are less likely to develop cancers,” said Dario C. Altieri. M.D., Robert and Penny Fox Distinguished Professor and director of The Wistar Institute’s National Cancer Institute-designated Cancer Center. “Our findings provide an unexpected explanation for how TRAP-1 and related proteins regulate metabolism within our cells.”


“We usually link the reprogramming of metabolic pathways with human diseases, such as cancer,” Altieri said. “What we didn’t expect to see were healthier mice with fewer tumors.”


Altieri and his colleagues created the TRAP-1 knockout mice as part of their ongoing investigation into their novel drug, Gamitrinib, which targets the protein in the mitochondria of tumor cells. TRAP-1 is a member of the heat shock protein 90 (HSP90) family, which are “chaperone” proteins that guide the physical formation of other proteins and serve a regulatory function within mitochondria. Tumors use HSP90 proteins, like TRAP-1, to help survive therapeutic attack. 

“In tumors, the loss of TRAP-1 is devastating, triggering a host of catastrophic defects, including metabolic problems that ultimately result in the death of the tumor cells,” Altieri said.  “Mice that lack TRAP-1 from the start, however, have three weeks in the womb to compensate for the loss of the protein.”


The researchers found that in their knockout mice, the loss of TRAP-1 causes mitochondrial proteins to misfold, which then triggers a compensatory response that causes cells to consume more oxygen and metabolize more sugar. This causes mitochondria in knockout mice to produce deregulated levels of ATP, the chemical used as an energy source to power all the everyday molecular reactions that allow a cell to function.

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Diet restriction suspends development in nematode worms and doubles lifespan

Diet restriction suspends development in nematode worms and doubles lifespan | Amazing Science | Scoop.it

Researchers at Duke University have found that taking food away from the C. elegans nematode worm triggers a state of arrested development: while the organism continues to wriggle about, foraging for food, its cells and organs are suspended in an ageless, quiescent state. When food becomes plentiful again, the worm develops as planned, but can live twice as long as normal.


The study found that C. elegans could be starved for at least two weeks and still develop normally once feeding resumed. Because the meter isn’t running while the worm is in its arrested state, this starvation essentially doubles the two-week lifespan of the worm. “It is possible that low-nutrient diets set off the same pathways in us to put our cells in a quiescent state,” said David R. Sherwood, an associate professor of biology at Duke University. “The trick is to find a way to pharmacologically manipulate this process so that we can get the anti-aging benefits without the pain of diet restriction.”


Over the last 80 years, researchers have put a menagerie of model organisms on a diet, and they’ve seen that nutrient deprivation can extend the lifespan of rats, mice, yeast, flies, spiders, fish, monkeys and worms anywhere from 30 percent to 200 percent longer than their free-fed counterparts.


Outside the laboratory and in the real world, organisms like C. elegans can experience bouts of feast or famine that no doubt affect their development and longevity. Sherwood’s colleague Ryan Baugh, an assistant professor of medicine at Duke, showed that hatching C. elegans eggs in a nutrient-free environment shut down their development completely. He asked Sherwood to investigate whether restricting diet to the point of starvation later in life would have the same effect.


Sherwood and his postdoctoral fellow Adam Schindler decided to focus on the last two stages of C. elegans larval development — known as L3 and L4 — when critical tissues and organs like the vulva are still developing. During these stages, the worm vulva develops from a speck of three cells to a slightly larger ball of 22 cells. The researchers found that when they took away food at various times throughout L3 and L4, development paused when the vulva was either at the three-cell stage or the 22-cell stage, but not in between.


When they investigated further, the researchers found that not just the vulva, but all the tissues and cells in the organism seemed to get stuck at two main checkpoints. These checkpoints are like toll booths along the developmental interstate. If the organism has enough nutrients, its development can pass through to the next toll booth. If it doesn’t have enough, it stays at the toll booth until it has built up the nutrients necessary to get it the rest of the way.


“Development isn’t a continuous nonstop process,” said Schindler, who is lead author of the study. “Organisms have to monitor their environment and decide whether or not it is amenable to their development. If it isn’t, they stop, if it is, they go. Those checkpoints seem to exist to allow the animal to make that decision. And the decision has implications, because the resources either go to development or to survival.”

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