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Showing posts with label longevity. Show all posts
Showing posts with label longevity. Show all posts

Monday, September 11, 2017

New Major Genetic Study Reveals How Humans Are Evolving


A massive genetic study that aimed to find out how the human genome is evolving suggests that natural selection is getting rid of harmful genetic mutations that shorten people’s lives. The study analysed DNA from over two hundred thousand people and is one of the first attempts to probe directly how humans are evolving over one or two generations.


The major new study has analysed DNA from 215,000 people and is one of the first attempts to probe directly how humans are evolving over one or two generations.

The work, which was recently published in PLoS Biology, aimed to identify which bits of the human genome might be evolving, researchers scoured large US and UK genetic databases for mutations whose prevalence changed across different age groups.

Related articles
In the study, each person, the parents’ age of death was recorded as a measure of longevity, or their own age in some cases. People carrying a harmful genetic variant die at a higher rate, so the variant becomes rarer in the older portion of the population.

“If a genetic variant influences survival, its frequency should change with the age of the surviving individuals,” says Hakhamanesh Mostafavi, an evolutionary biologist at Columbia University who led the study.

Mostafavi and his research team tested more than eight million common mutations, and found two that seemed to become less prevalent with age. A variant of the APOE gene, which is strongly linked to Alzheimer’s disease, was rarely found in women over 70. And a mutation in the CHRNA3 gene associated with heavy smoking in men fell off in the population starting in middle age.

Individuals without these mutations have a survival edge and are more likely to live longer, the researchers suggest. Why such mutations might lower a person’s genetic fitness — their ability to reproduce and spread their genes — remains an open question for the researchers.

They suggest that for men, it could be that those who live longer can have more children, but this is not conclusive. They are also considering two other explanations for why longevity is important.

Number one, parents surviving into old age in good health can care for their children and grandchildren, increasing the later generations’ chances of surviving and reproducing. This is sometimes known as the ‘grandmother hypothesis’, and may explain why humans tend to live long after they can have children.

Second, it’s possible that genetic variants that are explicitly bad in old age are also detrimental — but not as obviously — earlier in life.

Moving forward, the researchers intend to broaden their study into the millions of people. They conclude:
These analyses will provide a comprehensive answer to the question of which loci affect survival, helping to address long-standing open questions such as the relative importance of viability selection in shaping genetic variation and the extent to which genetic variation is maintained by fitness trade-offs between sexes or across ages.

SOURCE  Nature


By  33rd SquareEmbed





Thursday, July 13, 2017

3 Mindful Nutritional Ways To Increase Your Longevity


Research into longevity indicates that changes in your diet can have a dramatic effect on your ability to resist disease and live a longer, more active life. Moreover, the way you think about and interact with the foods you eat can also improve your health and increase your ability to function more effectively.




When you give more thought to the way you eat, you change your relationship with food in a broader sense. Here are 3 ways you can be more mindful in your eating habits, to improve your health and longevity.

1 – Eat A Plant-Based Diet

Research into longevity has discovered “blue zones” in the world where people seem to live the longest number of years. In these areas of the world, cultures rely on heavily on plants to make up the bulk of their diets. These individuals have less heart disease, less diabetes, lower blood pressure and generally live longer than those in areas of the world where high meat consumption is the norm. The use of high-quality vitamin and mineral supplements can be used to provide that additional nutrients needed when foregoing meat in your diet.

2 – Eat More Slowly

Too often, people gulp down their meals while sitting at their desks at work, or grab a bite from the local fast food establishment. This habit can affect your digestion, making it difficult for your body to absorb the nutrients it needs from the food that is consumed. When you slow down your eating, you taste the food more completely. You chew the food into smaller bits, which makes it easier for your gastrointestinal system to function. You will feel fuller sooner, which can help to manage your weight more effectively. Slower eating has a number of benefits that can help you to live a longer and healthier life. If you’re concerned that your foods aren’t providing the necessary nutrients that you need, you could try adding supplements, like those at AlgaeCal, to your diet.

Related articles

3 - Eat Mindfully

Mindfulness is a mental state of being “in the moment.” This condition means you have to let go of your busy thoughts and make a conscious of feeling your existence, moment by moment. This mental habit is somewhat contrary to what people normally do, thinking about what they will do next and remembering what happened the day before. Mindful eating means you put all other thoughts aside for a period of time and focus on the experience of taking nutrition into your body. This action helps you to enjoy your food more, and allows you to get the greatest benefit from your nutrition.

Healthy eating habits are more than just the foods you choose. These habits also involve making the experience of eating a more beneficial action. Although, people now engage in more hectic lifestyles, the act of eating remains a critical part of maintaining good health. When you eat more mindfully, you learn to value both the food itself and its power in allowing you to live a long and healthy life.


By  Emma SturgisEmbed

Emma is a freelance writer currently living in Boston. When not writing, she enjoys baking and indoor rock climbing. Find her on Google +



Tuesday, April 26, 2016

Woman Gets Biologically Younger After Gene Therapy


Gene Therapy

If early data is accurate, the world’s first successful example of telomere lengthening via gene therapy in a human individual has been undertaken. The gene therapy was completed on BioViva CEO Elizabeth Parrish.


Elizabeth Parrish, CEO of BioViva USA Inc. has become the first human being to be successfully rejuvenated by gene therapy, after her own company’s experimental therapies reversed 20 years of normal telomere shortening.

Related articles
Telomere score is calculated according to telomere length of white blood cells (T-lymphocytes). This result is based on the average T-lymphocyte telomere length compared to the American population at the same age range. The higher the telomere score, the “younger” the cells.

In September 2015, then 44 year-old Parrish received two of her own company’s experimental gene therapies: one to protect against loss of muscle mass with age, another to battle stem cell depletion responsible for diverse age-related diseases and infirmities.

The treatment was originally intended to demonstrate the safety of the latest generation of the therapies. But if early data is accurate, it is already the world’s first successful example of telomere lengthening via gene therapy in a human individual. Gene therapy has been used to lengthen telomeres before in cultured cells and in mice, but never in a human patient.

Telomeres are short segments of DNA which cap the ends of every chromosome, acting as ‘buffers’ against wear and tear. They shorten with every cell division, eventually getting too short to protect the chromosome, causing the cell to malfunction and the body to age.

In September 2015, telomere data taken from Parrish’s white blood cells by SpectraCell‘s specialised clinical testing laboratory in Houston, Texas, immediately before therapies were administered, revealed that Parrish’s telomeres were unusually short for her age, leaving her vulnerable to age-associated diseases earlier in life.

Elizabeth Parrish


In March 2016, the same tests were taken again by SpectraCell revealed that her telomeres had lengthened by approximately 20 years, from 6.71kb to 7.33kb. This implies that Parrish’s white blood cells (leukocytes) have become biologically younger. These findings were independently verified by the Brussels-based non-profit HEALES (HEalthy Life Extension Company), and the Biogerontology Research Foundation, a UK-based charity committed to combating age-related diseases.

"BioViva has the potential to create breakthroughs in human gene therapy research, while leapfrogging companies in the biotech market."
Parrish’s reaction: “Current therapeutics offer only marginal benefits for people suffering from diseases of aging. Additionally, lifestyle modification has limited impact for treating these diseases. Advances in biotechnology is the best solution, and if these results are anywhere near accurate, we’ve made history”, Parrish said.

Bioviva will continue to monitor Parrish’s blood for months and years to come. Meanwhile, BioViva will be testing new gene therapies and combination gene therapies to restore age related damage. It remains to be seen whether the success in leukocytes can expanded to other tissues and organs, and repeated in future patients. For now all the answers lie in the cells of Elizabeth Parrish, ‘patient zero’ of restorative gene therapy.

Since her first gene therapy injections BioViva has received global interest from both the scientific and investment communities. Earlier this month BioViva became a portfolio company of Deep Knowledge Life Sciences (DKLS), a London-based investment fund which aims to accelerate the development of biotechnologies for healthy longevity.

Dmitry Kaminskiy, founding partner of DKLS, said “BioViva has the potential to create breakthroughs in human gene therapy research, while leapfrogging companies in the biotech market.”




SOURCE  Bioviva


By 33rd SquareEmbed


Sunday, February 7, 2016



Anti-Aging

Harvard genetics professor David Sinclair takes his research personally. Through the lens of his own mother's battle with cancer, Dr. Sinclair shares the endless potential of his age-reversing discoveries and the potential future for us all.


David Sinclair, Ph.D. is a tenured professor of Genetics at Harvard Medical School and a professor at the University of New South Wales. He is co-director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging at Harvard.

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He is known for his work on understanding why we age and how to slow its effects, including co-discovering that the red wine molecule resveratrol can slow aspects of aging. He has founded a number of biotechnology companies in areas of aging, diabetes, vaccines and bioinformatics. He co-founded and serves as co-chief editor of the scientific journal Aging and is a regular guest and contributor to media and his work is featured in four books and two documentary movies.




SOURCE  Future Thinking


By 33rd SquareEmbed


Thursday, December 3, 2015

An Accidental Path to Extended Lifespan


Life Extension

Scientists have made an accidental discovery of how to stay young for longer. They succeeded in extending young adulthood in nematode worms and discovered new metric to track aging.


Longevity for people typically means an extended period of being frail, and elderly.  Now new research offers the promise of extending young adulthood instead. The scientists who are announcing success with initial work towards this aim in roundworms are keen to be clear they are a long way from achieving it in humans.

"We don't want people to get the impression they can take the drug we used in our study to extend their own teens or early twenties," says lead author Michael Petrascheck from The Scripps Research Institute (TSRI), California.

"Having a new tool to study aging could help us make new discoveries, for example to treat genetic predispositions where aging starts earlier, such as Hutchinson-Gilford progeria syndrome"
"We may have done this in worms, but there are millions of years of evolution between worms and humans.

"We think it is exciting to see that extending lifespan by extending young adulthood can be done at all," he says.

In the study published in the journal eLife, the team administered an antidepressant called mianserin to Caenorhabditis elegans, a type of roundworm used frequently in research. In 2007, they discovered that the drug increases the lifespan of roundworms by 30-40 per cent. Their new goal was to investigate how.

mianserin


The researchers treated thousands of the worms with either water or mianserin and looked at the activity of genes as the worms aged. First, they measured the activity of genes in young adults as a reference point against which to monitor the aging process. Reproductive maturity begins in day-old roundworms and they live for 2-3 weeks on average.

As the worms aged, the team observed dramatic changes in gene expression. However, the changes occurred in a way that came as a complete surprise. Groups of genes that together play a role in the same function were found to change expression in opposing directions.

They have called this newly-discovered phenomenon 'transcriptional drift'. By examining data from mice and from 32 human brains aged 26 to 106 years, they confirmed that it also occurs in mammals.

Michael Petrascheck and Sunitha Rangaraju


Related articles
"The orchestration of gene expression no longer seemed coordinated as the organism aged and the results were confusing because genes related to the same function were going up and down at the same time," says Petrascheck.

"Transcriptional drift can be used as a new metric for measuring age-associated changes that start in young adulthood," says first author Sunitha Rangaraju.

"Until now we have been dependent on measuring death rates, which are too low in young adults to provide much data. Having a new tool to study aging could help us make new discoveries, for example to treat genetic predispositions where aging starts earlier, such as Hutchinson-Gilford progeria syndrome," she says.

“If you add the drug early, you preserve a youthful gene expression pattern,” said Petrascheck. “But if you add it too late, the damage is already done.”

Using this new metric revealed that treatment with mianserin can suppress transcriptional drift, but only when administered at the right time of life. By 10 days old, treated worms still had the gene expression characteristics of a three-day-old -- physiologically they were seven days younger. But by 12 days, the physiological changes required to extend lifespan were complete and lifelong exposure to the drug had no additional effect. Mortality rates were shifted parallel by 7-8 days across the treated worms' lifespan, confirming the finding.

Mianserin blocked signals related to the regulation of serotonin and this delayed physiological changes associated with age, including the newly-identified transcriptional drift and degenerative processes that lead to death. The effect only occurred during young adulthood and the duration of this period of life was significantly extended.

"How much of our findings with regards to lifespan extension will spill over to mammals is anyone's guess, for example the extension of lifespan might not be as dramatic," says Petrascheck.

"However, we are already excited about the fact that we observed the phenomenon of transcriptional drift in species ranging from worms, mice to humans."


SOURCE  The Scripps Research Institute


By 33rd SquareEmbed


Tuesday, December 1, 2015


Diabetes Drug Could Substantially Increase Life Expectancy

Life Extension

The diabetes drug metformin could significantly increase life expectancy and health in old age according to recent research. Now human trials are planned starting next year.


Metformin, the diabetes drug may increase life expectancy and improve the health of older people according to new research. Although the drug's anti-aging properties have so far only been tested on animals, human trials are planned for 2016.

"If you target an aging process and you slow down aging then you slow down all the diseases and pathology of aging as well."
If the effects are the same in humans as they have been in animal studies, it may very well be possible for people to live healthily into their 120s. Metformin could also be used to slow or prevent the development of diseases related to aging, such as some cases of type 2 diabetes and Alzheimer's disease, which is associated with diabetes.

"If you target an aging process and you slow down aging then you slow down all the diseases and pathology of aging as well," said Professor Gordon Lithgow, of the Buck Institute for Research on Aging in California, one of the study's advisors.

"I have been doing research into aging for 25 years and the idea that we would be talking about a clinical trial in humans for an anti-aging drug would have been thought inconceivable.

"But there is every reason to believe it's possible," Lithgow continued. "The future is taking the biology that we've now developed an applying it to humans. 20 years ago aging was a biological mystery. Now we are starting to understand what is going on."

Several studies have indicated that the lifespan of animals increases when they are given metformin. Belgian researchers tested metformin on the roundworm C.elegans. The worms aged at a slower rate, and stayed healthier for longer. When metformin was given to mice, they lived almost 40 per cent longer than they would naturally; their bone strength also increased.

Related articles
Last year, researchers from Cardiff University found that diabetes patients who were given metformin tended to live longer than those who were not given metformin. This was not just because they had better blood glucose control - their life expectancy improved in comparison to other people with diabetes who were given other diabetes drugs; blood glucose control did not affect the improvements in lifespan noted in the metformin group.
"Twenty years ago aging was a biological mystery. Now we are starting to understand what is going on."

Dr. Jay Olshanksy, of the University of Illinois, Chicago, said: "If we can slow aging in humans, even by just a little bit it would be monumental. People could be older, and feel young.

"Enough advancements in aging science have been made to lead us to believe it's plausible, it's possible, it's been done for other species and there is every reason to believe it could be done in us.

"This would be the most important medical intervention in the modern era, an ability to slow aging."

The trial, which is called Targeting Aging with Metformin, or TAME, is scheduled for next winter. Participants are currently being recruited, with the researchers aiming to test metformin on around 3,000 70 to 80 years olds who have or at high risk of cancer, dementia and heart disease.

Dr. Lithgow believes that, should the metformin trial be successful, it would be a more significant medical breakthrough than a cure for cancer.

"If we were to cure all cancers it would only raise life expectancy by around three years, because something else is coming behind the cancer, but if we could slow down the aging process you could dramatically improve how long people can live," said Lithgow.

"We know that it is possible for handfuls of people to very old age and still be physically and socially active, so clearly they carry some kind of protection in their bodies. They are essentially not aging as quickly. If we can harness that, then everyone can achieve those lifespans."


SOURCE  Diabetes.co.uk


By 33rd SquareEmbed


Tuesday, November 3, 2015

Aerobic Exercise Found To Prevent Age-Related Brain Changes


Life Extension


New research suggests that aerobic exercise may be especially helpful in mid-life, preventing deterioration of the blood-brain barrier and corresponding neurodegenerative effects.
 


Structural deterioration associated with old age can be prevented by long-term aerobic exercise starting in mid-life, according to Jackson Laboratory researchers.

In a paper in the journal PLOS Biology, JAX Assistant Professor Gareth Howell, Ph.D., Associate Research Scientist Ileana Soto, Ph.D., and their colleagues found that structural changes that make the blood–brain barrier leaky and result in inflammation of brain tissues in old mice can be mitigated by allowing the animals to run regularly, so providing a potential explanation for the beneficial effects of exercise on dementia in humans.

Old age is the major risk factor for Alzheimer's disease, like many other diseases. Age-related cognitive deficits are due partly to changes in neuronal function, but also correlate with deficiencies in the blood supply to the brain and with low-level inflammation.

Related articles

In the study, the researchers set out to investigate the changes in the brains of normal young and aged laboratory mice by comparing by their gene expression profiles using a technique called RNA sequencing, and by comparing their structures at high-resolution by using fluorescence microscopy and electron microscopy.

The gene expression analysis indicated age-related changes in the expression of genes relevant to vascular function (including focal adhesion, vascular smooth muscle and ECM-receptor interactions), and inflammation (especially related to the complement system, which clears foreign particles) in the brain cortex. These changes were accompanied by a decline in the function of astrocytes (key support cells in brain) and loss of pericytes (the contractile cells that surround small capillaries and venules and maintain the blood–brain barrier), and of major components of the basement membrane, which forms an integral part of the blood–brain barrier. The researchers also noted an increase in the density and functional activation of the immune cells known as microglia/monocytes, which scavenge the brain for infectious agents and damaged cells.

Aerobic Exercise Found To Prevent Age-Related Brain Changes


Soto says, "Collectively, our data suggest that normal aging causes significant dysfunction to the cortical neurovascular unit, including basement membrane reduction and pericyte loss. These changes correlate strongly with an increase in microglia/monocytes in the aged cortex.”

Physical activity is already known to ameliorate the cognitive decline and sensorimotor deficits seen in old age in humans as well as in mice. To investigate the impact of long-term physical exercise on the brain changes seen in the aging mice, the researchers provided the animals with a running wheel from 12 months old (equivalent to middle aged in humans) and assessed their brains at 18 months (equivalent to about 60 years in humans, when the risk of Alzheimer's disease is greatly increased).

Young and old mice alike ran about two miles per night, and this physical activity improved the ability and motivation of the old mice to engage in the typical spontaneous behaviors that seem to be affected by aging. This exercise significantly reduced age-related pericyte loss in the brain cortex and improved other indicators of dysfunction of the vascular system and blood–brain barrier. Exercise also decreased the numbers of microglia/monocytes expressing a crucial initiating component of the complement pathway that others have shown previously to play are role in age-related cognitive decline.

Interestingly, these beneficial effects of exercise were not seen in mice deficient in a gene called Apoe, variants of which are a major genetic risk factor for Alzheimer's disease. The authors also report that Apoe expression in the brain cortex declines in aged mice and this decline can also be prevented by exercise.

"I hope our study helps in encouraging a healthy lifestyle that includes exercise."


The authors conclude, "Our data, supported by data from human studies, point towards focusing efforts on understanding the impact of aging and lifestyle choices on neurovascular unit decline and neuroinflammation, particularly astrocyte and pericyte dysfunction.”

Howell believes as a society we need to work hard to ensure we maintain an active lifestyle wherever possible. “In this day and age, with so many distractions and conveniences, it is easy to fall into a lifestyle that does not include enough exercise. With an aging population, I hope our study helps in encouraging a healthy lifestyle that includes exercise.

“For those that are unfortunately unable to exercise,” Howell adds, “Our study provides insight into a possible mechanism by which exercise may benefit the aging brain and may one day lead to improved treatments for age-related cognitive decline, Alzheimer's disease and other neurodegenerative disorders."


SOURCE  The Jackson Laboratory


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Tuesday, July 28, 2015

Genetic Link Found Between Intelligence and Longevity


Longevity


For the first time, research has pointed to a genetic link between intelligence and longevity. The finding have important implications for public health, and for those interested in the genetics of intelligence, lifespan or inequalities in health outcomes including lifespan.
 


The tendency of more intelligent people to live longer has been shown, for the first time, to be mainly down to their genes by new research published in the International Journal of Epidemiology.

By analyzing data from twins, researchers found that 95 per cent of the link between intelligence and lifespan is genetic. The researchers found that, within twin pairs, the brighter twin tends to live longer than the less bright twin and this was much more pronounced in fraternal (non identical) twins than in identical twins.

This is the first study to test for a genetic association between intelligence and lifespan.

Studies that compare genetically identical twins with fraternal twins –  who only share half of their twin’s DNA –   help distinguish the effects of genes from the effects of shared environmental factors such as housing, schooling and childhood nutrition.

"Our research shows that the link between intelligence and longer life is mostly genetic."


Rosalind Arden, a research associate at the London School of Economics and Political Science (LSE), said: “We know that children who score higher in IQ-type tests are prone to living longer. Also, people at the top of an employment hierarchy, such as senior civil servants, tend to be long-lived. But, in both cases, we have not understood why.

Related articles

“Our research shows that the link between intelligence and longer life is mostly genetic. So, to the extent that being smarter plays a role in doing a top job, the association between top jobs and longer lifespans is more a result of genes than having a big desk.

“However, it’s important to emphasize that the association between intelligence and lifespan is small. So you can’t, for example, deduce your child’s likely lifespan from how he or she does in their exams this summer.”

The researchers looked at three different twin studies from Sweden, the United States and Denmark where both intelligence and age of death was recorded, and where at least one twin in each pair had died.  Only twins of the same sex were included in the analysis.

On the reasons for the findings, Rosalind Arden said: “It could be that people whose genes make them brighter also have genes for a healthy body.  Or intelligence and lifespan may both be sensitive to overall mutations, with people with fewer genetic mutations being more intelligent and living longer. We need to continue to test these ideas to understand what processes are in play.”


SOURCE  London School of Economics and Political Science


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Thursday, July 23, 2015

Aging Found To Be A Quick Start Process As Sexual Maturity Reached, Not A Slow Process


Aging


Researchers have discovered that adult cells abruptly begin their downhill slide when an animal reaches reproductive maturity. They believe this genetic switch provides a target for future study.
 


Northwestern University researchers now have a molecular clue that pinpoints the start of aging in animals. In a study of the transparent roundworm C. elegans, they found that adult cells abruptly begin their downhill slide when an animal reaches reproductive maturity.

A genetic switch starts the aging process by turning off cell stress responses that protect the cell by keeping important proteins folded and functional. The switch is thrown by germline stem cells in early adulthood, after the animal starts to reproduce, ensuring its line will live on.

Related articles


While the studies were conducted in worms, the findings have implications for humans, the researchers report. The genetic switch and other components identified by the scientists as playing a role in aging are conserved in all animals, including humans, offering targets for future study.

Knowing more about how the quality control system works in cells could help researchers one day figure out how to provide humans with a better cellular quality of life and therefore delay degenerative diseases related to aging, such as neurodegenerative diseases.

"Wouldn't it be better for society if people could be healthy and productive for a longer period during their lifetime?" said Richard I. Morimoto, the senior author of the study. "I am very interested in keeping the quality control systems optimal as long as we can, and now we have a target. Our findings suggest there should be a way to turn this genetic switch back on and protect our aging cells by increasing their ability to resist stress."

Aging Found To Be A Quick Start Process As Sexual Maturity Reached, Not A Slow Process


The study, built on a decade of research, has been published in the journal Molecular Cell. Johnathan Labbadia, a postdoctoral fellow in Morimoto's lab, is the first author of the paper.

In C. elegans, the decline begins eight hours into adulthood -- all the switches get thrown to shut off an animal's cell stress protective mechanisms. Morimoto and Labbadia found it is the germline stem cells responsible for making eggs and sperm that control the switch.

In animals, including C. elegans and humans, the heat shock response is essential for proper protein folding and cellular health. Aging is associated with a decline in quality control, so Morimoto and Labbadia looked specifically at the heat shock response in the life of the roundworm.

"Our findings suggest there should be a way to turn this genetic switch back on and protect our aging cells by increasing their ability to resist stress."


"We saw a dramatic collapse of the protective heat shock response beginning in early adulthood," Morimoto said.

Morimoto and Labbadia found the genetic switch occurs between two major tissues in an organism that determine the future of the species: the germline and the soma (the body tissues of the animal, such as muscle cells and neurons). Once the germline has completed its job and produced eggs and sperm -- necessary for the next generation of animals -- it sends a signal to cell tissues to turn off protective mechanisms, starting the decline of the adult animal.

"C. elegans has told us that aging is not a continuum of various events, which a lot of people thought it was," Morimoto said.

"In a system where we can actually do the experiments, we discover a switch that is very precise for aging," he said. "All these stress pathways that insure robustness of tissue function are essential for life, so it was unexpected that a genetic switch is literally thrown eight hours into adulthood, leading to the simultaneous repression of the heat shock response and other cell stress responses."

Using a combination of genetic and biochemical approaches, Morimoto and Labbadia found the protective heat shock response declines steeply over a four-hour period in early adulthood, precisely at the onset of reproductive maturity. The animals still appear normal in behavior, but the scientists can see molecular changes and the decline of protein quality control.

"This was fascinating to see," Morimoto said. "We had, in a sense, a super stress-resistant animal that is robust against all kinds of cellular stress and protein damage. This genetic switch gives us a target for future research."

SOURCE  Nortwestern University


By 33rd SquareEmbed


Thursday, June 4, 2015

One Secret to a Longer Life—Be a Female

Aging
Human supercentenarians share at least one thing in common--over 95 percent are women. Scientists have long observed differences between the sexes when it comes to aging, but there is no clear explanation for why females live longer. 





Human supercentenarians share at least one trait in common—over 95 percent are women. Scientists have long noticed the differences between the sexes in aging, but there is still no clear explanation for why females live longer.

Related articles
Now, in a discussion paper of what we know about stem cell behavior and sex, Stanford University researchers Ben Dulken and Anne Brunet argue that it's time to look at differences in regenerative decline between men and women. This line of research could open up new explanations for how the sex hormones estrogen and testosterone, or other factors, affect lifespan.

It's known that estrogen has direct effects on stem cell populations in female mice, from increasing the number of blood stem cells (which is very helpful during pregnancy) to enhancing the regenerative capacity of brain stem cells at the height of estrus. Whether these changes have a direct impact on lifespan is what's yet to be explored. Recent studies have already found that estrogen supplements increase the lifespan of male mice, and that human eunuchs live about 14 years longer than non-castrated males.

the effect of sex on the aging of stem cells

"As the search continues for ways to ameliorate the aging process and maintain the regenerative capacity of stem cells, let us not forget one of the most effective aging modifiers: sex."


Though interactions between stem cells, aging, and sex have been topics of great interest, the intersection of all three—the effect of sex on the aging of stem cells—has not been well studied. However, several mechanisms could be involved in establishing and perpetuating sexual dimorphism during the aging of stem cells.

More work is also needed to understand how genetics impacts stem cell aging between the sexes. Scientists have seen that knocking out different genes in mice can add longevity benefits to one sex but not the other, and that males in twin studies have shorter telomeres—a sign of shorter cellular lifespan—compared to females.

"It is likely that sex plays a role in defining both lifespan and healthspan, and the effects of sex may not be identical for these two variables," the authors write. "As the search continues for ways to ameliorate the aging process and maintain the regenerative capacity of stem cells, let us not forget one of the most effective aging modifiers: sex."

SOURCE  EurekAlert

By 33rd SquareEmbed

Tuesday, May 26, 2015

Scientists Reverse Aging in Human Cell Lines

 Aging
Scientists have effectively reversed aging in human cell lines. They found that, contrary to the mitochondrial theory of aging, epigenetic regulation controls age-associated defects.





Research led by Jun-Ichi Hayashi from the University of Tsukuba in Japan has shown that, in human cell lines at least, aging can be reversed.

The scientists also found that the regulation of two genes involved
with the production of glycine, the smallest and simplest amino acid, is partly responsible
for some of the characteristics of aging.

Professor Hayashi and his team made this exciting discovery while in the process of addressing some controversial issues surrounding a popular theory of aging.

This theory, the mitochondrial theory of aging, proposes that age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA.

Abnormal mitochondrial function is one of the hallmarks of aging in many species, including humans. This is mostly due to the fact that the mitochondrion is the so-called powerhouse of the cell as it produces energy in a process called cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence. Accumulation of these changes is associated with a reduced lifespan and early onset of aging-related characteristics such as weight and hair loss, curvature of the spine and osteoporosis.

mitochondrion

There is a growing body of conflicting evidence that has raised doubts about the validity of this theory though. The Tsukuba team in particular has performed some compelling research that has led them to propose that age-associated mitochondrial defects are not controlled by the accumulation of mutations in the mitochondrial DNA but by another form of genetic regulation.

The research examined the function of the mitochondria in human fibroblast cell lines derived from young people (ranging in age from a fetus to a 12 year old) and elderly people (ranging in age from 80-97 years old). They compared the mitochondrial respiration and the amount of DNA damage in the mitochondria of the two groups, expecting respiration to be reduced and DNA damage to be increased in the cells from the elderly group. While the elderly group had reduced respiration, in accordance with the current theory, there was, however, no difference in the amount of DNA damage between the elderly and young groups of cells. This led the researchers to propose that another form
of genetic regulation, epigenetic regulation, may be responsible for the age-associated effects seen in the mitochondria.

The work has been published in Nature Scientific Reports.

Related articles
Epigenetic regulation refers to changes, such as the addition of chemical structures or proteins, which alter the physical structure of the DNA, resulting in genes turning on or off. Unlike mutations, these changes do not affect the DNA sequence itself. If this theory is correct, then genetically reprogramming the cells to an embryonic stem cell–like state would remove any epigenetic changes associated with the mitochondrial DNA.

In order to test this theory, the researchers reprogrammed human fibroblast cell lines derived from young and elderly people to an embryonic stem cell-like state. These cells were then turned back into fibroblasts and their mitochondrial respiratory function examined. Incredibly, the age-associated defects had been reversed - all of the fibroblasts had respiration rates comparable to those of the fetal fibroblast cell line, irrespective of whether they were derived from young or elderly people. This indicates that the aging process in the mitochondrion is controlled by epigenetic regulation, not by mutations.

The researchers then looked for genes that might be controlled epigenetically resulting in these age-associated mitochondrial defects. Two genes that regulate glycine production in mitochondria, CGAT and SHMT2, were found. The researchers showed that by changing the regulation of these genes, they could induce defects or restore mitochondrial function in the fibroblast cell lines. In a compelling finding, the addition of glycine for 10 days to the culture medium of the 97 year old fibroblast cell line restored its respiratory function. This suggests that glycine treatment can reverse the age-associated respiration defects in the elderly human fibroblasts.

These findings reveal that, contrary to the mitochondrial theory of aging, epigenetic regulation controls age-associated respiration defects in human fibroblast cell lines. Can epigenetic regulation also control aging in humans? That theory remains to be tested, and if proven, could result in glycine supplements giving our older population a new lease of life.



SOURCE  University of Tsukuba via AlphaGalileo

By 33rd SquareEmbed

Wednesday, May 13, 2015


 Anti-Aging
Aubrey de Grey appeared recently on the Joe Rogan Experience podcast and shared his thoughts on combating aging and his work at the SENS Research Foundation.





A slightly under-the-weather Aubrey de Grey appeared recently on the Joe Rogan Experience podcast. Despite his cold, de Grey captures the audience with his ideas about anti-aging research.

Well known to 33rd Square readers, de Grey is an English author and theoretician in the field of gerontology and the Chief Science Officer of the SENS Research Foundation.

de Grey and Rogan discuss anti-aging research, how aging is like a disease; how we will stop aging, repairing the body by regenerative medicine and other means, diet and aging, life expectancy around the world.

Aubrey de Grey on Joe Rogan

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"I would say there is a really good chance, say a 50/50 chance, that we will be able to say 10 years from now, Parkinson's disease has genuinely been cured with stem cell therapy."


The difference between longevity in the USA and Japan is really only four years points out de Grey. So despite the widespread belief that certain things have a dramatic effect on aging, de Grey shows that they are really not significant anti-aging factors.

According to de Grey, there are seven main types of damage that need to be addressed by regenerative medicine in order to solve the aging problem:
1. Cell loss / cell atrophy
2. Division-obsessed cells (cancer)
3. Death-resistant cells
4. Mitochondrial mutations
5. Intracellular junk
6. Extracellular junk
7. Extracellular cross-links
Stem cells therapy holds some of best promise for counteracting the effects of aging, says de Grey. Discussing work done on Parkinson's disease he states, "I would say there is a really good chance, say a 50/50 chance, that we will be able to say 10 years from now, Parkinson's disease has genuinely been cured with stem cell therapy."

Rogan and de Grey also discuss downloading consciousness, living forever, the population, and natural resources; how bad could it be living forever; philosophy of living forever. Check it out!

SOURCE  Joe Rogan Experience

By 33rd SquareEmbed