Category Archives: Human Longevity

Human Longevity Inc., the J. Craig Venter-backed outfit that recently raised $70 million in Series A to help extend the human lifespan through genomics and informatics, has a trio of new hires to help steer its C-suite.

It has hired Bradley Perkins as its chief medical officer, Yaron Turpaz as its chief information officer, and Felix Frueh as its chief scientific officer.

Perkins will oversee all clinical and therapeutic operations at the company, which includes developing the consumer clinics business and stem cell therapeutics.

Perkins was previously chief transformation officer at Vanguard Health Systems, overseeing the 46,000-employee health services providers strategy and innovation initiatives. Among his many roles at the system, Perkins started a $167 million venture capital fund at Vanguard.

He has worked at the Centers for Disease Control, and co-discovered a bacteria that causes cat scratch disease which led to several new bacterial meningitis and pneumonia vaccines, according to Human Longevity.

Working closely with the CDC director, he built a $2 billion state-of-the-art emergency response capability and positioned the improvement of population health as a focus of the health care reform movement within the White House at that time, Human Longevity said.

Turpaz will build the companys genomic and phenotypic databases, and will lead the bioinformatics and software engineering efforts at Human Longevity, the company said. He worked recently at AstraZeneca as the vice president of research and development information technology. Hes worked extensively with big data analytics, Human Longevity said.

Frueh, as chief scientific officer, will lead all genomic operations and will help partner with both academia and the pharmaceutical industry. He most recently was an executive partner at Opus Three LLC, a consulting group that provides strategic advice for the pharmaceutical, diagnostics and venture capital arenas.

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Human Longevity Inc. Fills Leadership Roles

If youre lucky, you inherited a longevity gene that will up your chances of living to a ripe old age. Better yet, scientists at the University of California San Francisco have shown that people who have a variant of a longevity gene called KLOTHO are blessed with superior brain skills such as thinking, learning, and memory regardless of their age, sex, or even whether they have a genetic risk factor for Alzheimer's disease. Klotho is the name of a Greek mythological goddess of fate, "who spins the thread of life." The study was funded in part by by the National Institutes of Health and published in May 2014 in the journal Cell Reports.

A release from NIF quotes lead author Dena Dubal, M.D., Ph.D. as saying, "This could be a major step toward helping millions around the world who are suffering from Alzheimer's disease and other dementias. If we could boost the brain's ability to function, we may be able to counter dementias."

The release notes that as people live longer, the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing.

People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer's disease. "This study shows the importance of genes that regulate the multiple aging processes involved in the maintenance of cognitive function," said Suzana Petanceska, Ph.D., program director in NIA's Division of Neuroscience. "Understanding the factors that control the levels and activity of KLOTHO across multiple organ systems may open new therapeutic avenues for prevention of age-related cognitive decline and dementia." The investigators tested a variety of cognitive skills, including learning, memory, and attention. More than 700 subjects, 52 to 85 years old were tested as part of three studies. None had any sign of dementia. Consistent with previous studies, 20 to 25 percent of the subjects had one copy of the KL-VS variant and performed better on the tests than those who had no copies. Performance on the tests decreased with age regardless of whether a subject had one or no copies of the KL-VS gene variant.

The KLOTHO gene provides the blueprint for a protein made primarily by the cells of the kidney, placenta, small intestine, and prostate. A shortened version of the protein can circulate through the blood system. Blood tests showed that subjects who had one copy of the KL-VS variant also had higher levels of circulating klotho protein. The levels decreased with age as others have observed. The researchers speculate that the age-related decrease in circulating levels of klotho protein may have caused some of the decline in performance on the cognitive tests. "These surprising results pave a promising new avenue of research," said Roderick Corriveau, Ph.D., program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS). "Although preliminary, they suggest that a form of klotho could be used to enhance cognition for people suffering from dementia." To test this idea the researchers genetically engineered mice to overproduce klotho protein. The klotho-enhanced mice lived longer and had higher levels of klotho in the blood and in a brain area known as the hippocampus, which controls some types of learning and memory. Similar to human studies, the klotho-enhanced mice performed better on a variety of learning and memory tests, regardless of age. In one test, the mice remembered the location of a hidden target in a maze better, which allowed them to find it twice as fast as control mice.

Learning is thought to strengthen communication between nerve cells in the brain at structures called synapses. In the hippocampus, many synapses use a chemical called glutamate to communicate. Electrical recordings suggested that klotho makes it more likely these synapses will be strengthened during learning and memory. NMDA receptors control communication at many glutamate synapses. GluN2B subunits are components of some NMDA receptors. Previous studies have shown that the presence of GluN2B at synapses is associated with changes in synaptic strength and learning and memory. In this study, the researchers found that synapses in the brains of klotho-enhanced mice had more GluN2B subunits than control mice. Treating klotho mice with a drug that selectively blocks GluN2B-containing NMDA receptors reduced their ability to perform on learning and memory tests. The results suggest that increasing the presence of GluN2B-containing NMDA receptors may be one way that klotho could enhance cognitive skills. "Overall our results suggest that klotho may increase cognitive reserve or the brain's capacity to perform everyday intellectual tasks," said senior author Lennart Mucke, M.D., director of the Gladstone Institute of Neurological Disease, San Francisco, CA, and the Joseph B. Martin Distinguished Professor of Neuroscience, and professor of neurology at UCSF.

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Longevity Gene May Be a Brain Booster

PUBLIC RELEASE DATE:

9-May-2014

Contact: Christopher G. Thomas thomaschr@ninds.nih.gov 301-496-5751 NIH/National Institute of Neurological Disorders and Stroke

Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer's disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain. The study was partly funded by the National Institutes of Health.

"This could be a major step toward helping millions around the world who are suffering from Alzheimer's disease and other dementias," said Dena Dubal, M.D., Ph.D., an assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at the University of California San Francisco (UCSF) and the lead author of the study published in Cell Reports. "If we could boost the brain's ability to function, we may be able to counter dementias."

As people live longer the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing.

Klotho is the name of a Greek mythological goddess of fate, "who spins the thread of life." People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer's disease.

"This study shows the importance of genes that regulate the multiple aging processes involved in the maintenance of cognitive function," said Suzana Petanceska, Ph.D., program director in NIA's Division of Neuroscience. "Understanding the factors that control the levels and activity of KLOTHO across multiple organ systems may open new therapeutic avenues for prevention of age-related cognitive decline and dementia."

The investigators tested a variety of cognitive skills, including learning, memory, and attention. More than 700 subjects, 52 to 85 years old were tested as part of three studies. None had any sign of dementia. Consistent with previous studies, 20 to 25 percent of the subjects had one copy of the KL-VS variant and performed better on the tests than those who had no copies. Performance on the tests decreased with age regardless of whether a subject had one or no copies of the KL-VS gene variant.

The KLOTHO gene provides the blueprint for a protein made primarily by the cells of the kidney, placenta, small intestine, and prostate. A shortened version of the protein can circulate through the blood system. Blood tests showed that subjects who had one copy of the KL-VS variant also had higher levels of circulating klotho protein. The levels decreased with age as others have observed. The researchers speculate that the age-related decrease in circulating levels of klotho protein may have caused some of the decline in performance on the cognitive tests.

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Longevity gene may boost brain power

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.

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'Vampire therapy' reverses ageing

San Francisco, CA (PRWEB) May 02, 2014

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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