Brooke Greenberg (born January 8, 1993), is a now 20 year old girl from Reisterstown, Maryland, who has remained physically and cognitively similar to a toddler. She is about 30 inches (76 cm) tall, weighs about 16 pounds (7.3 kg), and has an estimated mental age of 9 months to 1 year. Brooke’s doctors have termed her condition Syndrome X.
Brooke was born on January 8, 1993 at Sinai Hospital in Baltimore, Maryland, one month prior to her due date, weighing just four pounds (1.8 kg). She was born with anterior hip dislocation, a condition which caused her legs to be swiveled upwards, awkwardly, toward her shoulders; this was corrected surgically. Otherwise, Brooke appeared to be a normal infant.
In her first six years, Brooke Greenberg went through a series of unexplained medical emergencies from which she recovered. She had seven perforated stomach ulcers. She also suffered a seizure. This was followed by what was later diagnosed as a stroke; weeks later, no damage was detected. At age five, Brooke had a mass in her brain that caused her to sleep for 14 days. The doctors diagnosed the mass as a brain tumor. However, Brooke later awoke, and physicians found no tumor present. Brooke’s pediatrician, Dr. Lawrence Pakula, states that the source of her sudden illness remains a mystery.
Over the past several years, the Greenbergs visited many specialists, looking for an explanation for their daughter’s strange condition, and found she has a mutation in Chromosome 1. In 2001, when Dateline documented Brooke, she was still the size of a six-month-old infant, weighing just 13 lb (5.9 kg) at 27 inches (69 cm) tall. The family still had no explanation. Brooke Greenberg’s mother Melanie said: “They [the specialists] just said she’ll catch up. Then we went to the nutritionist, the endocrinologist. We tried the growth hormone…”. The growth hormone treatment had no effect. Howard, Brooke’s father, said: “I mean she did not put on an ounce or she did not grow an inch … That’s when I knew there was a problem.” After the growth hormone administration failed, the doctors, unable to diagnose a known condition, named her condition Syndrome X.
The Greenbergs made many visits to nearby Johns Hopkins Children’s Center, and even took Brooke to New York’s Mount Sinai Hospital, searching for information about their daughter’s condition. When geneticists sequenced Greenberg’s DNA, they found that the genes associated with the premature aging diseases were normal, unlike the mutated versions in patients with Werner syndrome and progeria.
In 2006, Dr. Richard Walker of the University of South Florida College of Medicine, said that Brooke’s body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic disorder or chromosomal abnormality that would help explain why.
In 2009, Walker said: “There’ve been very minimal changes in Brooke’s brain … Various parts of her body, rather than all being at the same stage, seem to be disconnected.” Walker noted that Greenberg’s brain, for example, is not much more mature than that of a newborn infant. He estimates her mental age at around 9 months to a year old. Brooke can make gestures and recognize sounds, but cannot speak. Her bones are like those of a ten-year-old, and she still has her baby teeth, which have an estimated developmental age of about 8 years. Said Walker, “We think that Brooke’s condition presents us with a unique opportunity to understand the process of aging.” Her telomeres seem to be shortening at the normal rate.
Yesterday, Brooke Greenberg and her family appeared on the Katie Couric Show as part of a show focused on medical mysteries. Greenberg, who is 20 years old, appears to be the age of a toddler. While the family does not know the root of Greenberg's apparent inability to age, Mount Sinai's Eric Schadt, who also appeared on the show with host Katie Couric, has been studying her genome. As Schadt notes in the clip below, in addition to figuring out the source of her disorder, Greenberg's genome could also help researchers learn more about the aging process.
A new study indicates that scientists have found a new way of delaying the aging process in mice, and they hope to replicate the finding in people. The research was built upon an earlier study that shed light on progeria, a rare genetic disease that prematurely ages one in four million babies.
A mutation was found in the Lamin A protein, which lines the nucleus in human cells, disrupting the repair process and accelerating aging. They also found that normal and healthy Lamin A binds to and activates the gene SIRT1, which has been long associated with longevity. If scientists can develop drugs that mimic Lamin A or increase the binding between Lamin A and SIRT1, this may lead to anti-aging drugs.
The team also examined if the binding efficiency was boosted with resveratrol, a compound found in the skin of red grapes. Mice fed with concentrated resveratrol fared significantly better than healthy mice that weren’t given it and the onset of aging was delayed and the life expectancy was extended. Mice with progeria lived 30% longer when fed with resveratrol compared with progerial mice not given the compound.
Inducing cells to express telomerase, the enzyme which is supposed to slow down the metabolic clock, has enabled researchers boost the lifespan of mouse by 24% with a single treatment.
The gene therapy acts on specific genes and is applied in adult life, not from the embryonic stage. Researchers at the Spanish National Cancer Research Center (CNIO) have demonstrated that the mouse lifespan can be extended by the application of one treatment acting directly on the animal’s genes in adult life. The therapy has been found to be safe and effective in mice.
Adult and aged mice were treated with the gene therapy, delivering a rejuvenating effect. On average, the mice lived 24% longer. The older mice lived 13% longer. The therapy produces an appreciable improvement on the animal’s health and delayed the onset of age-related diseases.
The genes were treated with a DNA-modified virus. The viral genes were replaced by those of the telomerase enzyme, which plays a key role in aging. Telomerase repairs the extreme ends of chromosomes, and slows the cells and therefore the body’s biological clock.
There is a potential to develop a telomerase-based anti-aging gene therapy that won’t increase the risk of cancer. Telomeres are the caps that protect the end of chromosomes, but each time the cell divides, the telomeres get shorter until they lose all functionality. The cell then stops dividing or dies. Telomerase prevents telomeres from shortening or even rebuilding them.
In most cells, telomerase is only active before birth. The cells of adult organisms contain no telomerase. There are some exceptions such as adult stem cells and cancer cells, which divide limitlessly and could be immortal.
The risk of cancer tumor promotion is a risk that has set back telomerase-based anti-aging therapies. The kind of virus employed to carry the telomerase gene to the cells is very important. The viruses used is in this study have been successfully used in gene therapy treatment of hemophilia and eye disease. They are non-replicating viruses derived from others that are non-pathogenic in humans.
Christian Sommer, a German marine-biology student in his early 20s, was conducting research on hydrozoans, small invertebrates that, depending on their stage in the life cycle, resemble either a jellyfish or a soft coral. Every morning, Sommer went snorkeling in the turquoise water off the cliffs of Portofino, Italy. He scanned the ocean floor for hydrozoans, gathering them with plankton nets. Among the hundreds of organisms he collected was a tiny, relatively obscure species known to biologists as Turritopsis dohrnii. Today it is more commonly known as the immortal jellyfish. Sommer kept his hydrozoans in petri dishes and observed their reproduction habits. After several days he noticed that his Turritopsis dohrnii was behaving in a very peculiar manner, for which he could hypothesize no earthly explanation. Plainly speaking, it refused to die. It appeared to age in reverse, growing younger and younger until it reached its earliest stage of development, at which point it began its life cycle anew.
Sommer was baffled by this development but didn’t immediately grasp its significance. (It was nearly a decade before the word “immortal” was first used to describe the species.) But several biologists in Genoa, fascinated by Sommer’s finding, continued to study the species, and in 1996 they published a paper called “Reversing the Life Cycle.” The scientists described how the species — at any stage of its development — could transform itself back to a polyp, the organism’s earliest stage of life, “thus escaping death and achieving potential immortality.” This finding appeared to debunk the most fundamental law of the natural world — you are born, and then you die. One of the paper’s authors, Ferdinando Boero, likened the Turritopsis to a butterfly that, instead of dying, turns back into a caterpillar. Another metaphor is a chicken that transforms into an egg, which gives birth to another chicken. The anthropomorphic analogy is that of an old man who grows younger and younger until he is again a fetus. For this reason Turritopsis dohrnii is often referred to as the Benjamin Button jellyfish.
Some progress has been made, however, in the quarter-century since Christian Sommer’s discovery. We now know, for instance, that the rejuvenation of Turritopsis dohrnii and some other members of the genus is caused by environmental stress or physical assault. We know that, during rejuvenation, it undergoes cellular transdifferentiation, an unusual process by which one type of cell is converted into another — a skin cell into a nerve cell, for instance. (The same process occurs in human stem cells.) But we still don’t understand how it ages in reverse.
Immortality is, to a certain degree, a question of semantics. “That word ‘immortal’ is distracting,” says James Carlton, the professor of marine sciences at Williams. “If by ‘immortal’ you mean passing on your genes, then yes, it’s immortal. But those are not the same cells anymore. The cells are immortal, but not necessarily the organism itself.” To complete the Benjamin Button analogy, imagine the man, after returning to a fetus, being born again. The cells would be recycled, but the old Benjamin would be gone; in his place would be a different man with a new brain, a new heart, a new body. He would be a clone.
Unraveling the mystery of why the inhabitants of Ikaria, an island of 99 square miles that is home to almost 10,000 Greek nationals, live so long and so well. In 2000, another island of longevity has been identified - a region of Sardinia’s Nuoro province is a place with the highest concentration of male centenarians in the world.
Social structure might turn out to be more important. In Sardinia, a cultural attitude that celebrated the elderly kept them engaged in the community and in extended-family homes until they were in their 100s. Studies have linked early retirement among some workers in industrialized economies to reduced life expectancy.
The human immune system weakens with the passing of time, thus making us more susceptible to cancer and infectious diseases. This aging also affects the ability of our organism to take advantage of vaccination. A new study conducted by scientists at the Stanford University School of Medicine shows that if a certain protein is blocked, the response of the cells to vaccines and other atingens like cancer or microbial antigens can be restored. The levels of this particular protein increase with age.
Doctor Jorg Goronzy, a professor of rheumatology and the lead author of the paper says that this discovery is very important for long-term therapies. He added that in the near future the possibility of countering the effects of aging on our immune system might be achievable through pharmacology.
The research team discovered a protein, named DUSP6 (Dual specificity phosphatase 6), that impedes the capacity of an entire class of immune cells, thus preventing them from interacting with foreign bodies or substances. These substances include pathogens and vaccines. Another finding was that of a possible compound that is able to restore the responsiveness of the immune cells back to normal, once the DUSP6 protein is inhibited.
Dr Goronzy says that the human immune system decades with aging, starting from around the age of 40. Goronzy added that even though almost 90% of adults below the age of 40 respond to vaccines, the rate of responsiveness drops to almost 40% after the age of 60. An example of poor responsiveness in older patients is that of influenza deaths, most of which are registered in patients older than 65.
In a long-running study, rhesus monkeys whose caloric intake was restricted by 30 percent didn’t live any longer than their normal-weight peers. For 25 years, the rhesus monkeys were kept semi-starved, lean and hungry. The males’ weights were so low they were the equivalent of a 6-foot-tall man who tipped the scales at just 120 to 133 pounds. The hope was that if the monkeys lived longer, healthier lives by eating a lot less, then maybe people, their evolutionary cousins, would too. Some scientists, anticipating such benefits, began severely restricting their own diets.
The results of this major, long-awaited study, which began in 1987, are finally in. But it did not bring the vindication calorie restriction enthusiasts had anticipated. It turns out the skinny monkeys did not live any longer than those kept at more normal weights. Some lab test results improved, but only in monkeys that were put on the diet when they were old. The causes of death — cancer, heart disease — were the same in both the underfed and the normally fed monkeys.
Lab test results showed lower levels of cholesterol and blood sugar in the male monkeys that started eating 30 percent fewer calories in old age, but not in the females. Males and females that were put on the diet when they were old had lower levels of triglycerides, which are linked to heart disease risk. Monkeys put on the diet when they were young or middle-aged did not get the same benefits, though they had less cancer. But the bottom line was that the monkeys that ate less did not live any longer than those that ate normally. Rafael de Cabo, lead author of the diet study, published online on Wednesday in the journal Nature, said he was surprised and disappointed that the underfed monkeys did not live longer. Like many other researchers on aging, he had expected an outcome similar to that of a 2009 study from the University of Wisconsin that concluded that caloric restriction did extend monkeys’ life spans.
The study was led by Justin Denney, PhD, assistant professor of sociology at Rice University. Researchers collected data from the Human Mortality Database for 1930-2000 to predict future life expectancy in 2055. Based on this research, not only has life expectancy stagnated in America, it trails several developed countries.
For an American born today, life expectancy is around 78.49 years of age. Compared to countries with the highest life expectancies, Americans may be missing out on five to 10 years of life. Monaco has the highest life expectancy at 89.68 years while Macau at 84.43 and Japan at 83.91 are close behind. Imagine getting an extra decade to experience life and that's what many Americans are missing out on.
Human aging cannot be fully understood in terms of the constrained genetic setting. Epigenetic drift is an alternative means of explaining age-associated alterations. To address this issue, whole-genome bisulfite sequencing (WGBS) of newborn and centenarian genomes was performed. The centenarian DNA had a lower DNA methylation content and a reduced correlation in the methylation status of neighboring cytosine—phosphate—guanine (CpGs) throughout the genome in comparison with the more homogeneously methylated newborn DNA. The more hypomethylated CpGs observed in the centenarian DNA compared with the neonate covered all genomic compartments, such as promoters, exonic, intronic, and intergenic regions. For regulatory regions, the most hypomethylated sequences in the centenarian DNA were present mainly at CpG-poor promoters and in tissue-specific genes, whereas a greater level of DNA methylation was observed in CpG island promoters. An extended the study to a larger cohort of newborn and nonagenarian samples using a 450,000 CpG-site DNA methylation microarray reinforced the observation of more hypomethylated DNA sequences in the advanced age group. WGBS and 450,000 analyses of middle-age individuals demonstrated DNA methylomes in the crossroad between the newborn and the nonagenarian/centenarian groups. This is the first study of a unique detailed DNA methylation analysis at extreme points of human life with a sensitivity level downt to a single-nucleotide.
Researchers from The University of Nottingham have discovered how planarian flatworms overcome the aging process to be potentially immortal: they can rejuvenate their telomeres. The discovery, funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC), may eventually lead to alleviating aging and age-related characteristics in human cells. Planarian worms have amazed scientists with their apparently limitless ability to regenerate. Researchers have been studying their ability to replace aged or damaged tissues and cells in a bid to understand the mechanisms underlying their longevity.
Supercentenarians are persons who have lived beyond the age of 110. Currently there are only about 80 such known individuals in the world whose age is verified. The world record holder is Jeanne Calment, who survived until age 122. Amyloidosis is a disease state hallmarked by the deposition of fibers of abnormally clumped masses of the protein ransthyretin, which normally acts to carry thyroid and other hormones. Mutations in the gene make the fibers abnormally sticky and they tend to clump into long fibers that are deposited in multiple organs.
These persons have already escaped the typical causes of death, but the normally innocuous amounts of amyloid that increase with age may actually become toxic to them because they have lived so many years. However, experimental drugs (such as Tapamidis meglumine, approved in Europe under the trade name Vyndaqel) exist that may eliminate amyloid. These drugs are being studied for young persons with pathological amyloidosis. Could they become the first drugs to extend human lifespan beyond current theoretical limits?
Mouse lifespan was extended up to 24 percent with a single gene treatment in research at the Spanish National Cancer Research Centre (CNIO), using gene...
New research from the University of Glasgow suggests that lifespan is affected by the rate at which bodies grow early in life.
A team from the University’s Institute of Biodiversity, Animal Health and Comparative Medicine altered the growth rate of 240 fish by exposing them to brief cold or warm spells, which put them behind or ahead their normal growth schedule. Once the environmental temperature was returned to normal, the fish got back on track by accelerating or slowing their growth accordingly. However, the change in growth rate also affected their rate of aging.
While the normal lifespan of sticklebacks is around two years, the slow-growth fish lived for more than 30 percent longer, with an average lifespan of nearly 1000 days. In contrast, the accelerated-growth fish had a lifespan that was 15% shorter than normal.
they should check if this is statistically in confirmation with Einstein's Relativity which says "more enegy automatically means ime runs faster and less energy means time runs slower" hence having less energy spent per unit time allows this energy to be spent over a longer period time and hence aging slower. Slowe metabolic activites should entail longer ife span and even Einstein had said so "bilogical aging and the rate at which physical processes are governed by Relativity" b/cos they are to be governed by physical laws and Einstein's law is a physical law as well.
Studying the DNA of two distant bat species, the scientists discovered how genes dealing with the bats' immune system had undergone the most rapid change. This may explain why they are relatively free of disease and live exceptionally long lives compared with other mammals of similar size, such as the rat, said Professor Lin-Fa Wang, an infectious disease expert at the Duke-NUS Graduate Medical School in Singapore who led the multi-centre study.
"We are not saying bats never get sick or never get infections. What we are saying is they handle infections a lot better," Wang said. What was missing from both species of bats was a gene segment known to trigger extreme, and potentially fatal, immune reactions to infections, called the cytokine storm.
Cytokine storms end up killing not only offending viruses in the body, but the host's own cells and tissues too.
"Viruses rarely kill the host. The killing comes from the host's immune response. So it looks like what bats are doing is depress the inflammation (cytokine storm). If we can learn that, we can design drugs to minimize the inflammation damage and control viral infection," Wang said.
Compared with other mammals of similar size, bats live a long time, with lifespans of between 20 and 40 years. Rats live between 2 and 3 years, on average.
Interestingly, Wang and his colleagues found that the highly evolved genes that give bats their superior immune system also enable them to fly. Out of more than 5,000 types of mammals on the planet, bats are the only one capable of sustained flight and some species can fly more than 1,000 km in a single night.
Such intense physical exertion is known to produce toxic "free radicals" that cause tissue damage and it is these same genes that give the bat the ability to repair itself, Wang said. "What we found was the genes that evolved fastest were genes involved in repairing DNA damage. That makes sense ... because when you fly, metabolism goes up and it generates free radicals that are toxic to cells," Wang said.
"Because bats fly, they (would have had) to evolve and adapt ... to get genes that can repair DNA damage." Wang said we have much to learn from the bat, which has evolved to avoid disease and live exceptionally long lives. "Cancer, ageing and infectious disease, these are the three major areas of concern for people," he said.
"We have studied rats for 150 years to understand how to do better in these three areas. Now we have a system, the bat, that has done very well in evolution. We can learn from the bat. With modern techniques, we can design new drugs to slow down the ageing process, treat cancer, fight infections."
Cancer biologist Jan van Deursen at the Mayo Clinic in Rochester, Minnesota, and his colleagues were initially interested in studying a common feature of cancers, called aneuploidy. Aneuploid cells have too few or too many chromosomes. Nearly all cancer cells fall into this category, but it's not clear whether aneuploidy actually causes cancer. van Deursen, along with a then-graduate student, Darren Baker, engineered mice to produce less BubR1, a protein that helps cells segregate their chromosomes when they divide. When BubR1 is reduced, chromosomes can't properly separate into identical daughter cells, leaving some daughters with the wrong number of chromosomes. van Deursen, Baker, and their colleagues wanted to see whether these mice would develop cancer.
To their surprise, instead of tumor-filled mice, they wound up with animals that aged very quickly. "These mice were clearly very, very different than a normal mouse," says Baker, who now studies the biology of aging at the Mayo Clinic. Last year, they reported that removing old cells—that is, cells with a genetic marker indicating senescence—from these mice could help them stay healthier longer. Adding intrigue is an extremely rare human condition caused by mutations in the BubR1 gene. Patients with the disease, mosaic variegated aneuploidy syndrome, age prematurely and have an elevated risk of cancer. Too little BubR1 seems to be bad news.
Too much, on the other hand, might be a good thing. In work published today in Nature Cell Biology, the biologists report that genetically engineered mice that make extra BubR1 are less prone to cancer. For example, they found that when they exposed normal mice to a chemical that causes lung and skin tumors, all of them got cancer. But only 33% of those overexpressing BubR1 at high levels did. They also found that these animals developed fatal cancers much later than normal mice—after about 2 years, only 15% of the engineered mice had died of cancer, compared with roughly 40% of normal mice. The animals that overexpressed BubR1 at high levels also lived 15% longer than controls, on average. And the mice looked veritably Olympian on a treadmill, running about twice as far—200 meters rather than 100 meters—as control animals. All of this left Baker, van Deursen, and their colleagues thinking that BuBR1's life-extending effects aren't due to only its ability to prevent cancer, although that's not yet certain.
To survey previously uncharted territory, a team of researchers at UW-Madison has created an “atlas” that maps more than 1,500 unique landmarks within mitochondria that could provide clues to the metabolic connections between caloric restriction and aging.
The map, as well as the techniques used to create it, could lead to a better understanding of how cell metabolism is rewired in some cancers, age-related diseases and metabolic conditions such as diabetes.
The hydra is a unique multicellular organism. What make it so special is that it is essentially immortal and shows no signs of aging either at the cellular or organism level. It preferentially reproduces asexually, rather than mating it forms buds which break off into progeny. The animal is able to do this by maintaining a continuous robust and unending supply of stem cells.
One theory as to the cause of human aging is the progressive loss of stem cells. Tissue in the body can recover from damage, be it internal or external, through the generation of fresh new cells from division of stem cells residing in niches in those tissues. However with advancing age, eventually these stem cell niches become depleted and the organism, in this case people, reach the end of life.
In the current landmark study, researchers looked to find which genes in hydra are responsible for a never ending supply of stem cells. They discovered this characteristic depends specifically on a gene called FoxO, a fork-head box O transcription factor. This gene is a master genetic switch that when active allows for the expression of many genes involved in cell cycling. When FoxO activity was reduced in hydra they shows signs of aging and cell senescence.
These findings are quite interesting because is has already been shon that a FoxO gene is involved in human aging as well. There is a specific variant of the FoxO3, a human gene that has been linked to extreme human lifespan. It is more commonly found in centenarians.
Life after death, for most people, is a faithful belief in a spiritual hereafter, a transfer to a higher, non-bodily consciousness. For cryonics enthusiasts, however, a “second life” – or more accurately, a resuscitated life with a little help from freezer storage – here on Earth is the goal.
The Prospect of Immortality is a six-year study by UK photographer Murray Ballard, who has traveled the world pulling back the curtain on the amateurs, optimists, businesses and apparatuses of cryonics. “It’s not a large industry,” says Ballard, who visited the Alcor Life Extension Foundation in Phoenix, Arizona; the Cryonics Institute in Detroit, Michigan; KrioRus in Moscow, Russia; and Suspended Animation Inc in Boytan Beach, Florida; among others.
Cryonics is the preservation of deceased humans in liquid nitrogen at temperatures just shy of its boiling point of −196°C/77 Kelvin. Cryopreservation of humans is not reversible with current science, but cryonicists hypothesize that people who are considered dead by current medical definitions may someday be recovered by using advanced future technologies.
Stats are hard to come by, but it is estimated there are about 2,000 people signed up for cryonics and approximately 250 people currently cryopreserved. Over 100 pets have also been placed in vats of liquid nitrogen with the hopes of a future recovery.
Ballard’s project began in 2006 after he read a news article, “Freezer Failure Ends Couple’s Hopes of Life After Death,” about a French couple who had been kept in industrial freezers beneath their chateau in the Loire valley. He phoned up a small group of UK cryonicists and attended their meetings and training sessions. Later, funding from an arts organization paid for two trips to the U.S.
A chance meeting with one of the founders of KrioRus, a Russian cryonics organization, at a UK conference set up a memorable week-long trip to Moscow, St. Petersburg, and Vorenzh. There he photographed the two resting places of the first Russian cryonics neuro-patient.
“I photographed her grave in a cemetery just outside St. Petersburg and the cryostat containing her head at the facility in Moscow.”
Heads take up less storage space than whole bodies. They’re cheaper to store.
Researchers at King’s College London, Harvard University and Massachusetts General Hospital have identified for the first time a key factor responsible for declining muscle repair during ageing, and discovered how to halt the process in mice with a common drug. Although an early study, the finding provides clues as to how muscles lose mass with age, which can result in weakness that affects mobility and may cause falls.
Published today in the journal Nature, and funded by the Biotechnology, and Biological Sciences Research Council, Harvard Stem Cell Institute and National Institutes of Health (US), the study looked at stem cells found inside muscle - which are responsible for repairing injury - to find out why the ability of muscles to regenerate declines with age. A dormant reservoir of stem cells is present inside every muscle, ready to be activated by exercise and injury to repair any damage. When needed, these cells divide into hundreds of new muscle fibres that repair the muscle. At the end of the repairing process some of these cells also replenish the pool of dormant stem cells so that the muscle retains the ability to repair itself again and again.
The researchers carried out a study on old mice and found the number of dormant stem cells present in the pool reduces with age, which could explain the decline in the muscle’s ability to repair and regenerate as it gets older. When these old muscles were screened the team found high levels of FGF2, a protein that has the ability to stimulate cells to divide. While encouraging stem cells to divide and repair muscle is a normal and crucial process, they found that FGF2 could also awaken the dormant pool of stem cells even when they were not needed. The continued activation of dormant stem cells meant the pool was depleted over time, so when the muscle really needed stem cells to repair itself the muscle was unable to respond properly.
Following this finding, the researchers attempted to inhibit FGF2 in old muscles to prevent the stem cell pool from being kick-started into action unnecessarily. By administering a common FGF2 inhibitor drug they were able to inhibit the decline in the number of muscle stem cells in the mice.
However, preventing or reversing muscle waste during old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is an extremely important finding.
Thomas Rando and Anne Brunet provide a general overview on the process and potential prevention of aging. The topics they cover vary from symptoms of aging to unusual characteristics that seem to prolong longevity.
At first glance, the inaugural 1812 issue of the New England Journal of Medicine and Surgery, and the Collateral Branches of Science seems reassuringly familiar: a review of angina pectoris, articles on infant diarrhea and burns. The apparent similarity to today's Journal, however, obscures a fundamental discontinuity (1812a, b, c; see Historical Journal Articles Cited). Disease has changed since 1812. People have different diseases, doctors hold different ideas about those diseases, and diseases carry different meanings in society. To understand the material and conceptual transformations of disease over the past 200 years, one must explore the incontrovertibly social nature of disease.
Disease is always generated, experienced, defined, and ameliorated within a social world. Patients need notions of disease that explicate their suffering. Doctors need theories of etiology and pathophysiology that account for the burden of disease and inform therapeutic practice. Policymakers need realistic understandings of determinants of disease and medicine's impact in order to design systems that foster health. The history of disease offers crucial insights into the intersections of these interests and the ways they can inform medical practice and health policy.
Each cell in the human body is programmed to die. Death is their default state. It is only by behaving, by obeying outside orders and carrying out the processes it’s meant to, that the cell is able to inhibit its own destruction. This is a good thing for the body as a whole, because cells that do manage to escape the tight death-regulation control are cancerous cells, and cause havoc within the body.
A new study confirms that people, like many animals, easily recognize a unique—but not unpleasant—eau de elderly. The unique scent of the elderly lingers wherever they live and in any confined spaces they have recently occupied, such as taxis and elevators. Many different cultures have recognized the phenomenon—the Japanese even have a word for it, kareishuu—but the biological truth of old person smell remains uncertain. In a new study, blindfolded volunteers reliably recognized the aroma of the elderly by sniffing sweat-soaked armpit pads, although they had a much harder time correctly matching pads to the young and middle-aged, and they were not able to make fine distinctions about age based on scent alone. Contrary to the popular notion that old person smell is disagreeable, volunteers in the new study rated the odors of the elderly as much less unpleasant and intense than those of the middle-aged and young. Combined with earlier research, the new findings suggest that people retain a latent ability to gauge someone's age based on their odor, a talent inherited from evolutionary ancestors that might be linked to the ways animals recognize the sick and dying.
For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connection between them has remained largely a mystery, Dr. Schneider said. What was known, due in part to past studies by Schneider and his team, was that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer.
When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. Now, more than a decade in the making, the mystery surrounding the connection between inflammation, advanced aging and cancer is finally being unraveled.
The current study reveals that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer
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