Posts Tagged ‘aging’


By Alex Horton

At 117, Nabi Tajima was older than modern-day Australia, and everyone else known to live on the planet.

Tajima, born Aug. 4, 1900, in Araki, Japan, and recognized as the world’s oldest person, has passed on that mantle. She died Saturday, having been hospitalized since January, the Associated Press reported, and was the last known person born in the 19th century.

She was living in the small island town of Kikai, the AP reported.

The title of “world’s oldest living person” is a remarkable, if fleeting, one. Tajima claimed the distinction in September, when fellow 117-year-old Violet Brown died in Jamaica. Brown was the oldest person in the world for about five months.

Tajima was in the exclusive group of supercentenarians, people who have crossed the 110-year threshold. The U.S.-based Gerontology Research Group, which tracks certified people who become supercentenarians, reports 36 worldwide. All but one of them are women, and 18 of them are Japanese. Good diets and supportive family structure have been linked to Japan’s world-leading life expectancy.

Tajima straddled the 19th, 20th and 21st centuries and is one of the few people who could recall a time before World War I. Two days after her 45th birthday, the United States dropped the first of two atomic bombs northeast of her home island.

Her legacy is similarly expansive; she had nine children and 160 descendants, including great-great-great grandchildren, the Gerontology Research Group said.

Tajima’s secret to longevity was “eating delicious things and sleeping well,” the group said. She danced with her hands at the sound of a samisen, a traditional three-string instrument.

Chiyo Miyako, also in Japan, has become the world’s oldest person, according to the group. At 116 years and 355 days, she has about nine months to reach her countrywoman’s mark of 117 years and 260 days.

Miyako would not have to travel far to visit her male compatriot. Japan’s Masazo Nonaka, at 112 years and 271 days old, was confirmed to be the world’s oldest man by Guinness World Records this month. The organization had been set to recognize Tajima before she died, the AP reported.

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by Diana Kwon

Findings from a randomized, controlled trial finds that reducing food intake decreases metabolism and reduces oxidative damage to tissues and cells.

Studies in various animals, including rodents and monkeys, have reported that caloric restriction can extend their lifespans. Findings from a two-year, randomized, controlled trial with human participants, published last week (March 22) in Cell Metabolism, suggest that cutting down on calories may also be able to prolong the lives of people.

To investigate the effects of reducing food intake, Leanne Redman, an endocrinologist at the Pennington Biomedical Research Center at Louisiana State University, and her colleagues enrolled 53 healthy men and women between the ages of 21 and 50 and split them into two groups—one group reduced their caloric intake by 15 percent over two years, and the other remained on a regular diet.

The team found that the people who ate a restricted diet lost an average of around 9 kilograms and experienced a 10-percent drop in their resting metabolic rates. When the researchers examined the participants’ blood, they also found a reduction in markers of oxidative stress in those who cut down on calories. “After two years, the lower rate of metabolism and level of calorie restriction was linked to a reduction in oxidative damage to cells and tissues,” Redman tells Wired.

“[I]f by-products of metabolism accelerate aging processes, calorie restriction sustained over several years may help to decrease risk for chronic disease and prolong life,” Redman says in a statement.

This study was part of a larger, multi-center investigation of caloric restriction in humans, the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy (CALERIE) trial. Luigi Fontana, an internist who ran a CALERIE investigation at Washington University in St. Louis, says that a slower metabolism and reduced oxidative stress will not necessarily lead to a longer life. “You can have a low resting metabolic rate because you’re dying of starvation,” he tells Wired. “Does that make it a biomarker of longevity? No. You can be calorie restricted by eating half a hamburger and a few fries each day but will you live longer? No, you will die of malnutrition.”

https://www.the-scientist.com/?articles.view/articleNo/52141/title/Caloric-Restriction-Slows-Signs-of-Aging-in-Humans/

A group of genes and genetic switches involved in age-related brain deterioration have been identified by scientists at the Babraham Institute, Cambridge and Sapienza University, Rome. The research, published online today (5th March) in Aging Cell, found that changes to one of these genes, called Dbx2, could prematurely age brain stem cells, causing them to grow more slowly. The study was led jointly by Giuseppe Lupo and Emanuele Cacci in Italy and Peter Rugg-Gunn in the UK.

Cells in the brain are constantly dying and being replaced with new ones produced by brain stem cells. As we age, it becomes harder for these stem cells to produce new brain cells and so the brain slowly deteriorates. By comparing the genetic activity in brain cells from old and young mice, the scientists identified over 250 genes that changed their level of activity with age. Older cells turn some genes, including Dbx2, on and they turn other genes off.

By increasing the activity of Dbx2 in young brain stem cells, the team were able to make them behave more like older cells. Changes to the activity of this one gene slowed the growth of brain stem cells. These prematurely aged stem cells are not the same as old stem cells but have many key similarities. This means that many of the genes identified in this study are likely to have important roles in brain ageing.

The research also identified changes in several epigenetic marks – a type of genetic switch – in the older stem cells that might contribute to their deterioration with age. Epigenetic marks are chemical tags attached to the genome that affect the activity of certain genes. The placement of these marks in the genome change as we age and this alters how the cells behave. The researchers think that some of these changes that happen in the brain may alter causing brain stem cells to grow more slowly.

First author on the paper, Dr Giuseppe Lupo, Assistant Professor at Sapienza University said: “The genes and gene regulators that we identified are corrupted in neural stem cells from older mice. By studying the Dbx2 gene we have shown that these changes may contribute to ageing in the brain by slowing the growth of brain stem cells and by switching on the activity of other age-associated genes.”

Co-lead scientist Dr Peter Rugg-Gunn at the Babraham Institute said: “Ageing ultimately affects all of us and the societal and healthcare burden of neurodegenerative diseases is enormous. By understanding how ageing affects the brain, at least in mice, we hope to identify ways to spot neural stem cell decline. Eventually, we may find ways to slow or even reverse brain deterioration – potentially by resetting the epigenetic switches – helping more of us to stay mentally agile for longer into old age.”

Co-lead scientist Dr Emanuele Cacci at Sapienza University said: “We hope this research will lead to benefits for human health. We have succeeded in accelerating parts of the ageing process in neural stem cells. By studying these genes more closely, we now plan to try turning back the clock for older cells. If we can do this in mice, then the same thing could also be possible for humans.”

This article has been republished from materials provided by the Babraham Institute. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference: Lupo, G., Nisi, P. S., Esteve, P., Paul, Y.-L., Novo, C. L., Sidders, B., … Rugg-Gunn, P. J. (n.d.). Molecular profiling of aged neural progenitors identifies Dbx2 as a candidate regulator of age-associated neurogenic decline. Aging Cell, n/a-n/a. https://doi.org/10.1111/acel.12745

https://www.technologynetworks.com/genomics/news/these-genes-are-involved-in-age-linked-brain-deterioration-298221?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=61138279&_hsenc=p2ANqtz-_FeiFbqi-SP5EqlFOOosvK1dViRCt4fG_ztTzGnpct1WLd4sY0BUbdkcuE7-2clIdZwQsKU1fdtv-8HDaJoh76WD9KwA&_hsmi=61138279


Illustration by Paweł Jońca

by Helen Thomson

In March 2015, Li-Huei Tsai set up a tiny disco for some of the mice in her laboratory. For an hour each day, she placed them in a box lit only by a flickering strobe. The mice — which had been engineered to produce plaques of the peptide amyloid-β in the brain, a hallmark of Alzheimer’s disease — crawled about curiously. When Tsai later dissected them, those that had been to the mini dance parties had significantly lower levels of plaque than mice that had spent the same time in the dark.

Tsai, a neuroscientist at Massachusetts Institute of Technology (MIT) in Cambridge, says she checked the result; then checked it again. “For the longest time, I didn’t believe it,” she says. Her team had managed to clear amyloid from part of the brain with a flickering light. The strobe was tuned to 40 hertz and was designed to manipulate the rodents’ brainwaves, triggering a host of biological effects that eliminated the plaque-forming proteins. Although promising findings in mouse models of Alzheimer’s disease have been notoriously difficult to replicate in humans, the experiment offered some tantalizing possibilities. “The result was so mind-boggling and so robust, it took a while for the idea to sink in, but we knew we needed to work out a way of trying out the same thing in humans,” Tsai says.

Scientists identified the waves of electrical activity that constantly ripple through the brain almost 100 years ago, but they have struggled to assign these oscillations a definitive role in behaviour or brain function. Studies have strongly linked brainwaves to memory consolidation during sleep, and implicated them in processing sensory inputs and even coordinating consciousness. Yet not everyone is convinced that brainwaves are all that meaningful. “Right now we really don’t know what they do,” says Michael Shadlen, a neuroscientist at Columbia University in New York City.

Now, a growing body of evidence, including Tsai’s findings, hint at a meaningful connection to neurological disorders such as Alzheimer’s and Parkinson’s diseases. The work offers the possibility of forestalling or even reversing the damage caused by such conditions without using a drug. More than two dozen clinical trials are aiming to modulate brainwaves in some way — some with flickering lights or rhythmic sounds, but most through the direct application of electrical currents to the brain or scalp. They aim to treat everything from insomnia to schizophrenia and premenstrual dysphoric disorder.

Tsai’s study was the first glimpse of a cellular response to brainwave manipulation. “Her results were a really big surprise,” says Walter Koroshetz, director of the US National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “It’s a novel observation that would be really interesting to pursue.”


A powerful wave

Brainwaves were first noticed by German psychiatrist Hans Berger. In 1929, he published a paper describing the repeating waves of current he observed when he placed electrodes on people’s scalps. It was the world’s first electroencephalogram (EEG) recording — but nobody took much notice. Berger was a controversial figure who had spent much of his career trying to identify the physiological basis of psychic phenomena. It was only after his colleagues began to confirm the results several years later that Berger’s invention was recognized as a window into brain activity.

Neurons communicate using electrical impulses created by the flow of ions into and out of each cell. Although a single firing neuron cannot be picked up through the electrodes of an EEG, when a group of neurons fires again and again in synchrony, it shows up as oscillating electrical ripples that sweep through the brain.

Those of the highest frequency are gamma waves, which range from 25 to 140 hertz. People often show a lot of this kind of activity when they are at peak concentration. At the other end of the scale are delta waves, which have the lowest frequency — around 0.5 to 4 hertz. These tend to occur in deep sleep (see ‘Rhythms of the mind’).

At any point in time, one type of brainwave tends to dominate, although other bands are always present to some extent. Scientists have long wondered what purpose, if any, this hum of activity serves, and some clues have emerged over the past three decades. For instance, in 1994, discoveries in mice indicated that the distinct patterns of oscillatory activity during sleep mirrored those during a previous learning exercise. Scientists suggested that these waves could be helping to solidify memories.

Brainwaves also seem to influence conscious perception. Randolph Helfrich at the University of California, Berkeley, and his colleagues devised a way to enhance or reduce gamma oscillations of around 40 hertz using a non-invasive technique called transcranial alternating current stimulation (tACS). By tweaking these oscillations, they were able to influence whether a person perceived a video of moving dots as travelling vertically or horizontally.

The oscillations also provide a potential mechanism for how the brain creates a coherent experience from the chaotic symphony of stimuli hitting the senses at any one time, a puzzle known as the ‘binding problem’. By synchronizing the firing rates of neurons responding to the same event, brainwaves might ensure that the all of the relevant information relating to one object arrives at the correct area of the brain at exactly the right time. Coordinating these signals is the key to perception, says Robert Knight, a cognitive neuroscientist at the University of California, Berkeley, “You can’t just pray that they will self-organize.”


Healthy oscillations

But these oscillations can become disrupted in certain disorders. In Parkinson’s disease, for example, the brain generally starts to show an increase in beta waves in the motor regions as body movement becomes impaired. In a healthy brain, beta waves are suppressed just before a body movement. But in Parkinson’s disease, neurons seem to get stuck in a synchronized pattern of activity. This leads to rigidity and movement difficulties. Peter Brown, who studies Parkinson’s disease at the University of Oxford, UK, says that current treatments for the symptoms of the disease — deep-brain stimulation and the drug levodopa — might work by reducing beta waves.

People with Alzheimer’s disease show a reduction in gamma oscillations5. So Tsai and others wondered whether gamma-wave activity could be restored, and whether this would have any effect on the disease.

They started by using optogenetics, in which brain cells are engineered to respond directly to a flash of light. In 2009, Tsai’s team, in collaboration with Christopher Moore, also at MIT at the time, demonstrated for the first time that it is possible to use the technique to drive gamma oscillations in a specific part of the mouse brain6.

Tsai and her colleagues subsequently found that tinkering with the oscillations sets in motion a host of biological events. It initiates changes in gene expression that cause microglia — immune cells in the brain — to change shape. The cells essentially go into scavenger mode, enabling them to better dispose of harmful clutter in the brain, such as amyloid-β. Koroshetz says that the link to neuroimmunity is new and striking. “The role of immune cells like microglia in the brain is incredibly important and poorly understood, and is one of the hottest areas for research now,” he says.

If the technique was to have any therapeutic relevance, however, Tsai and her colleagues had to find a less-invasive way of manipulating brainwaves. Flashing lights at specific frequencies has been shown to influence oscillations in some parts of the brain, so the researchers turned to strobe lights. They started by exposing young mice with a propensity for amyloid build-up to flickering LED lights for one hour. This created a drop in free-floating amyloid, but it was temporary, lasting less than 24 hours, and restricted to the visual cortex.

To achieve a longer-lasting effect on animals with amyloid plaques, they repeated the experiment for an hour a day over the course of a week, this time using older mice in which plaques had begun to form. Twenty-four hours after the end of the experiment, these animals showed a 67% reduction in plaque in the visual cortex compared with controls. The team also found that the technique reduced tau protein, another hallmark of Alzheimer’s disease.

Alzheimer’s plaques tend to have their earliest negative impacts on the hippocampus, however, not the visual cortex. To elicit oscillations where they are needed, Tsai and her colleagues are investigating other techniques. Playing rodents a 40-hertz noise, for example, seems to cause a decrease in amyloid in the hippocampus — perhaps because the hippo-campus sits closer to the auditory cortex than to the visual cortex.

Tsai and her colleague Ed Boyden, a neuro-scientist at MIT, have now formed a company, Cognito Therapeutics in Cambridge, to test similar treatments in humans. Last year, they started a safety trial, which involves testing a flickering light device, worn like a pair of glasses, on 12 people with Alzheimer’s.

Caveats abound. The mouse model of Alzheimer’s disease is not a perfect reflection of the disorder, and many therapies that have shown promise in rodents have failed in humans. “I used to tell people — if you’re going to get Alzheimer’s, first become a mouse,” says Thomas Insel, a neuroscientist and psychiatrist who led the US National Institute of Mental Health in Bethesda, Maryland, from 2002 until 2015.

Others are also looking to test how manipulating brainwaves might help people with Alzheimer’s disease. “We thought Tsai’s study was outstanding,” says Emiliano Santarnecchi at Harvard Medical School in Boston, Massachusetts. His team had already been using tACS to stimulate the brain, and he wondered whether it might elicit stronger effects than a flashing strobe. “This kind of stimulation can target areas of the brain more specifically than sensory stimulation can — after seeing Tsai’s results, it was a no-brainer that we should try it in Alzheimer’s patients.”

His team has begun an early clinical trial in which ten people with Alzheimer’s disease receive tACS for one hour daily for two weeks. A second trial, in collaboration with Boyden and Tsai, will look for signals of activated microglia and levels of tau protein. Results are expected from both trials by the end of the year.

Knight says that Tsai’s animal studies clearly show that oscillations have an effect on cellular metabolism — but whether the same effect will be seen in humans is another matter. “In the end, it’s data that will win out,” he says.

The studies may reveal risks, too. Gamma oscillations are the type most likely to induce seizures in people with photosensitive epilepsy, says Dora Hermes, a neuroscientist at Stanford University in California. She recalls a famous episode of a Japanese cartoon that featured flickering red and blue lights, which induced seizures in some viewers. “So many people watched that episode that there were almost 700 extra visits to the emergency department that day.”

A brain boost

Nevertheless, there is clearly a growing excitement around treating neurological diseases using neuromodulation, rather than pharmaceuticals. “There’s pretty good evidence that by changing neural-circuit activity we can get improvements in Parkinson’s, chronic pain, obsessive–compulsive disorder and depression,” says Insel. This is important, he says, because so far, pharmaceutical treatments for neurological disease have suffered from a lack of specificity. Koroshetz adds that funding institutes are eager for treatments that are innovative, non-invasive and quickly translatable to people.

Since publishing their mouse paper, Boyden says, he has had a deluge of requests from researchers wanting to use the same technique to treat other conditions. But there are a lot of details to work out. “We need to figure out what is the most effective, non-invasive way of manipulating oscillations in different parts of the brain,” he says. “Perhaps it is using light, but maybe it’s a smart pillow or a headband that could target these oscillations using electricity or sound.” One of the simplest methods that scientists have found is neurofeedback, which has shown some success in treating a range of conditions, including anxiety, depression and attention-deficit hyperactivity disorder. People who use this technique are taught to control their brainwaves by measuring them with an EEG and getting feedback in the form of visual or audio cues.

Phyllis Zee, a neurologist at Northwestern University in Chicago, Illinois, and her colleagues delivered pulses of ‘pink noise’ — audio frequencies that together sound a bit like a waterfall — to healthy older adults while they slept. They were particularly interested in eliciting the delta oscillations that characterize deep sleep. This aspect of sleep decreases with age, and is associated with a decreased ability to consolidate memories.

So far, her team has found that stimulation increased the amplitude of the slow waves, and was associated with a 25–30% improvement in recall of word pairs learnt the night before, compared with a fake treatment7. Her team is midway through a clinical trial to see whether longer-term acoustic stimulation might help people with mild cognitive impairment.

Although relatively safe, these kinds of technologies do have limitations. Neurofeedback is easy to learn, for instance, but it can take time to have an effect, and the results are often short-lived. In experiments that use magnetic or acoustic stimulation, it is difficult to know precisely what area of the brain is being affected. “The field of external brain stimulation is a little weak at the moment,” says Knight. Many approaches, he says, are open loop, meaning that they don’t track the effect of the modulation using an EEG. Closed loop, he says, would be more practical. Some experiments, such as Zee’s and those involving neuro-feedback, already do this. “I think the field is turning a corner,” Knight says. “It’s attracting some serious research.”

In addition to potentially leading to treatments, these studies could break open the field of neural oscillations in general, helping to link them more firmly to behaviour and how the brain works as a whole.

Shadlen says he is open to the idea that oscillations play a part in human behaviour and consciousness. But for now, he remains unconvinced that they are directly responsible for these phenomena — referring to the many roles people ascribe to them as “magical incantations”. He says he fully accepts that these brain rhythms are signatures of important brain processes, “but to posit the idea that synchronous spikes of activity are meaningful, that by suddenly wiggling inputs at a specific frequency, it suddenly elevates activity onto our conscious awareness? That requires more explanation.”

Whatever their role, Tsai mostly wants to discipline brainwaves and harness them against disease. Cognito Therapeutics has just received approval for a second, larger trial, which will look at whether the therapy has any effect on Alzheimer’s disease symptoms. Meanwhile, Tsai’s team is focusing on understanding more about the downstream biological effects and how to better target the hippocampus with non-invasive technologies.

For Tsai, the work is personal. Her grandmother, who raised her, was affected by dementia. “Her confused face made a deep imprint in my mind,” Tsai says. “This is the biggest challenge of our lifetime, and I will give it all I have.”

https://www.nature.com/articles/d41586-018-02391-6

If you’re between 55 and 75 years old, you may want to try playing 3D platform games like Super Mario 64 to stave off mild cognitive impairment and perhaps even prevent Alzheimer’s disease.

That’s the finding of a new Canadian study by Université de Montréal psychology professors Gregory West, Sylvie Belleville and Isabelle Peretz. Published in PLOS One, it was done in cooperation with the Institut universitaire de gériatrie de Montréal (IUGM), Benjamin Rich Zendel of Memorial University in Newfoundland, and Véronique Bohbot of Montreal’s Douglas Hospital Research Centre.

In two separate studies, in 2014 and 2017, young adults in their twenties were asked to play 3D video games of logic and puzzles on platforms like Super Mario 64. Findings showed that the gray matter in their hippocampus increased after training.

The hippocampus is the region of the brain primarily associated with spatial and episodic memory, a key factor in long-term cognitive health. The gray matter it contains acts as a marker for neurological disorders that can occur over time, including mild cognitive impairment and Alzheimer’s.

West and his colleagues wanted to see if the results could be replicated among healthy seniors.

The research team recruited 33 people, ages 55 to 75, who were randomly assigned to three separate groups. Participants were instructed to play Super Mario 64 for 30 minutes a day, five days a week, take piano lessons (for the first time in their life) with the same frequency and in the same sequence, or not perform any particular task.

The experiment lasted six months and was conducted in the participants’ homes, where the consoles and pianos, provided by West’s team, were installed.

The researchers evaluated the effects of the experiment at the beginning and at the end of the exercise, six months later, using two different measurements: cognitive performance tests and magnetic resonance imaging (MRI) to measure variations in the volume of gray matter. This enabled them to observe brain activity and any changes in three areas:

the dorsolateral prefrontal cortex that controls planning, decision-making and inhibition;
the cerebellum that plays a major role in motor control and balance; and
the hippocampus, the centre of spatial and episodic memory.
According to the MRI test results, only the participants in the video-game cohort saw increases in gray matter volume in the hippocampus and cerebellum. Their short-term memory also improved.

The tests also revealed gray matter increases in the dorsolateral prefrontal cortex and cerebellum of the participants who took piano lessons, whereas some degree of atrophy was noted in all three areas of the brain among those in the passive control group.

What mechanism triggers increases in gray matter, especially in the hippocampus, after playing video games? “3-D video games engage the hippocampus into creating a cognitive map, or a mental representation, of the virtual environment that the brain is exploring.,” said West. “Several studies suggest stimulation of the hippocampus increases both functional activity and gray matter within this region.”

Conversely, when the brain is not learning new things, gray matter atrophies as people age. “The good news is that we can reverse those effects and increase volume by learning something new, and games like Super Mario 64, which activate the hippocampus, seem to hold some potential in that respect,” said West. Added Belleville: “These findings can also be used to drive future research on Alzheimer’s, since there is a link between the volume of the hippocampus and the risk of developing the disease.”

“It remains to be seen,” concluded West, “whether it is specifically brain activity associated with spatial memory that affects plasticity, or whether it’s simply a matter of learning something new.”

http://nouvelles.umontreal.ca/en/article/2017/12/06/some-video-games-are-good-for-older-adults-brains/

Every hour you run extends your life span by seven hours, a new study has revealed.

Scientists say that running just one hour a week is the most effective exercise to increase life expectancy.

This holds true no matter how many miles or how fast you run, the researchers claim.
For those that take this advice to heart and run regularly, they say you can extend your life span by up to three years.

The study, conducted at Iowa State University, reanalyzed data from The Cooper Institute, in Texas, and also examined results from a number of other recent studies that looked at the link between exercise and mortality.

Scientists found that the new review reinforced the findings of earlier research.
At whatever pace or mileage, a person’s risk of premature death dropped by 40 percent when he or she took up running.

This applied even when researchers controlled for smoking, drinking or a history of health problems such as obesity.

Three years ago, the same team conducted a study that analyzed more than 55,000 adults, and determined that running for just seven minutes a day could help slash the risk of dying from heart disease.

They followed participants over a period of 15 years, and found that of the more than 3,000 who died, only one-third of deaths were from heart disease.

Co-author Dr Duck-chul High-mileage runners also questioned if they were overperforming and if, at some point, running would actually contribute to premature mortality.
After analyzing the data in the new study, scientists determined that hour for hour, running statistically returns more time to people’s lives than it consumes.
In The Cooper Institute study, participants reported an average of two hours running per week.
The amount ran over the course of 40 years would add up to fewer than six months, but it could increase life expectancy by more than three years.

The researchers also determined that if every non-runner who had been part of the reviewed studies took up the sport, there would have been 16 percent fewer deaths over all, and 25 percent fewer fatal heart attacks.

Other types of exercise were also found to be beneficial. Walking and cycling dropped the risk of premature death by about 12 percent.

Dr Lee says scientists remain uncertain as to why running helps with longevity.

But he says it’s likely because the sport combats many common risk factors for early death, including high blood pressure and extra body fat, especially around the middle.

It also raises aerobic fitness, one of the best-known indicators for long-term health.
Running, however, does not make you immortal and the life expectancy rates don’t increase beyond three years.

Improvements in life expectancy generally plateaued at about four hours of running per week, Dr Lee said. But they did not decline.

Read more: http://www.dailymail.co.uk/health/article-4405252/Every-hour-run-adds-7-hours-lifespan.html#ixzz4e5eSXAzj

by Philip Perry

Researchers at the Salk Institute in La Jolla, California have discovered a way to turn back the hands of time. Juan Carlos Izpisua Belmonte led this study, published in the journal Cell. Here, elderly mice underwent a new sort of gene therapy for six weeks. Afterward, their injuries healed, their heart health improved, and even their spines were straighter. The mice also lived longer, 30% longer.

Today, we target individual age-related diseases when they spring up. But this study could help us develop a therapy to attack aging itself, and perhaps even target it before it begins taking shape. But such a therapy is at least ten years away, according to Izpisua Belmonte.

Many biologists now believe that the body, specifically the telomeres—the structures at the end of chromosomes, after a certain time simply wear out. Once degradation overtakes us, it’s the beginning of the end. This study strengthens another theory. Over the course of a cell’s life, epigenetic changes occur. This is the activation or depression of certain genes in order to allow the organism to respond better to its environment. Methylation tags are added to activate genes. These changes build up over time, slowing us down, and making us vulnerable to disease.


Chromosomes with telomeres in red.

Though we may add life to years, don’t consider immortality an option, at least not in the near-term. “There are probably still limits that we will face in terms of complete reversal of aging,” Izpisua Belmonte said. “Our focus is not only extension of lifespan but most importantly health-span.” That means adding more healthy years to life, a noble prospect indeed.

The technique employs induced pluripotent stem cells (iPS). These are similar to those which are present in developing embryos. They are important as they can turn into any type of cell in the body. The technique was first used to turn back time on human skin cells, successfully.

By switching around four essential genes, all active inside the womb, scientists were able to turn skin cells into iPS cells. These four genes are known as Yamanaka factors. Scientists have been aware of their potential in anti-aging medicine for some time. In the next leg, researchers used genetically engineered mice who could have their Yamanaka factors manipulated easily, once they were exposed to a certain agent, present in their drinking water.

Since Yamanaka factors reset genes to where they were before regulators came and changed them, researchers believe this strengthens the notion that aging is an accumulation of epigenetic changes. What’s really exciting is that this procedure alters the epigenome itself, rather than having the change the genes of each individual cell.


The mechanics of epigenetics.

In another leg of the experiment, mice with progeria underwent this therapy. Progeria is a disease that causes accelerated aging. Those who have seen children who look like seniors know the condition. It leads to organ damage and early death. But after six months of treatment, the mice looked younger. They had better muscle tone and younger looking skin, and even lived around 30% longer than those who did not undergo the treatment.

Luckily for the mice, time was turned back the appropriate amount. If turned back too far, stem cells can proliferate in an uncontrolled fashion, which could lead to tumor formation. This is why researchers have been reticent to activate the Yamanaka factors directly. However, these scientists figured out that by intermittently stimulating the factors, they could reverse the aging process, without causing cancer. The next decade will concentrate on perfecting this technique.

Since the threat of cancer is great, terminally ill patients would be the first to take part in a human trial, most likely those with progeria. Unfortunately, the method used in this study could not directly be applied to a fully functioning human. But researchers believe a drug could do the job, and they are actively developing one.

“This study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought,” Izpisua Belmonte said. Of course, mouse systems and human one’s are far different. This only gives us an indication of whether or not it might work. And even if it does, scientists will have to figure out how far to turn back the clock. But as Izpisua Belmonte said, “With careful modulation, aging might be reversed.”