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Alison Abbott Redouan Bshary well remembers the moment he realized that fish were smarter than they are given credit for. It was 1998, and Bshary was a young behavioural ecologist with a dream project: snorkelling in Egypt's Red Sea to observe the behaviour of coral-reef fish. That day, he was watching a grumpy-looking grouper fish as it approached a giant moray eel. As two of the region's top predators, groupers and morays might be expected to compete for their food and even avoid each other — but Bshary saw them team up to hunt. First, the grouper signalled to the eel with its head, and then the two swam side by side, with the eel dipping into crevices, flushing out fish beyond the grouper's reach and getting a chance to feed alongside. Bshary was astonished by the unexpected cooperation; if he hadn't had a snorkel in his mouth, he would have gasped. This underwater observation was the first in a series of surprising discoveries that Bshary has gone on to make about the social behaviour of fish. Not only can they signal to each other and cooperate across species, but they can also cheat, deceive, console or punish one another — even show concern about their personal reputations. “I have always had a lot of respect for fish,” says Bshary. “But one after the other, these behaviours took me by surprise.” His investigations have led him to take a crash course in scuba diving, go beach camping in Egypt and build fake coral reefs in Australia. The work has also destroyed the stereotypical idea that fish are dumb creatures, capable of only the simplest behaviours — and it has presented a challenge to behavioural ecologists in a different field. Scientists who study primates have claimed that human-like behaviours such as cooperation are the sole privilege of animals such as monkeys and apes, and that they helped to drive the evolution of primates' large brains. Bshary — quiet, but afraid of neither adventure nor of contesting others' ideas — has given those scientists reason to think again. © 2015 Nature Publishing Grou
Steve Connor Having children can permanently affect the brain of women because the surge in female sex hormones during pregnancy can influence the development of key parts of the central nervous system, a series of studies has shown. The findings suggest that childbirth can affect the female brain, but they could also shed light on the controversy over whether hormone replacement therapy in menopausal women affects the risk of developing Alzheimer’s disease in later life, scientists said. The research looked at two of the oestrogen hormones used to treat the symptoms of menopausal women and found that they could have a complex effect depending on the age of the women and whether or not they had previously given birth. Although the work was mostly carried out on laboratory rats, the scientists said that the findings are more widely applicable to humans because the same hormones and brain cells are involved. The scientists found that the surge in oestrogen hormones during pregnancy, where levels can soar to several hundred times normal levels, can alter “neuroplasticity” or the re-growth of nerve cells in a part of the brain called the hippocampus, which is responsible for aspects of memory and spatial awareness. “Our most recent research show that previous motherhood alters cognition and neuroplasticity in response to hormone therapy, demonstrating that motherhood permanently alters the brain,” said Liisa Galea of the University of British Columbia in Vancouver, Canada.
Mo Costandi Being unable to feel pain may sound appealing, but it would be extremely hazardous to your health. Pain is, for most of us, a very unpleasant feeling, but it serves the important evolutionary purpose of alerting us to potentially life-threatening injuries. Without it, people are more prone to hurting themselves and so, because they can be completely oblivious to serious injuries, a life without pain is often cut short. Take 16-year-old Ashlyn Blocker from Patterson, Georgia, who has been completely unable to sense any kind of physical pain since the day she was born. As a newborn, she barely made a sound, and when her milk teeth started coming out, she nearly chewed off part of her tongue. Growing up, she burnt the skin off the palm of her hands on a pressure washer that her father had left running, and once ran around on a broken ankle for two whole days before her parents noticed the injury. She was once swarmed and bitten by hundreds of fire ants, has dipped her hands into boiling water, and injured herself in countless other ways, without ever feeling a thing. Ashlyn is one of a tiny number of people with congenital insensitivity to pain. The condition is so rare, in fact, that the doctor who diagnosed her in 2006 told her parents that she may be the only one in the world who has it. But later that year, a research team led by Geoffrey Woods of the University of Cambridge, identified three distinct mutations in the SCN9A gene, all of which cause the same condition in members of three large families in northern Pakistan, and in 2013, Ashlyn’s doctor Roland Staud and his colleagues reported that her condition is the result of two other mutations in the same gene. Now, Woods and his colleagues have discovered yet more mutations that cause congenital insensitivity to pain. © 2015 Guardian News and Media Limited
By John Horgan The New York Times "Sunday Review" section has anointed Richard Friedman its go-to guy for touting behavioral genetics--or "gene-whiz science," as I prefer to call it. In March, Friedman, professor of clinical psychiatry at Weill Cornell Medical College, proclaimed that researchers had discovered a "feel-good gene," which "makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences." As I pointed out on this blog, Friedman's claim—like virtually all reported linkages of complex human traits and disorders to specific genes (see Further Reading)--is based on flimsy, contradictory evidence. I'm so naïve, or arrogant, that I actually thought my critique might dissuade the Times from further hype of gene-whiz science. Times editors must care more about traffic than accuracy, because they devoted almost the entire front page of yesterday’s "Sunday Review" to Friedman's latest travesty, "Infidelity Lurks in Your Genes." The core of Friedman's essay is his assertion that some women are "biologically inclined to wander." More specifically, women who carry variants of the gene AVPR1A—which encodes the receptor for the hormone arginine vasopressin--are "much more likely to engage in 'extra-pair bonding,' the scientific euphemism for sexual infidelity." In support of this claim, Friedman cites a study of Finnish twins and non-twin siblings by a team led by Australian psychologist Brendan Zietsch. The team surveyed the Finnish subjects and found that 9.8 percent of the men and 6.4 percent of the women reported engaging in at least one "extra-pair mating." The researchers found an association between five AVPR1A markers and extra-pair mating in women but not in men.
By BENEDICT CAREY and PAM BELLUCK He was a graduate student who seemingly had it all: drive, a big idea and the financial backing to pay for a sprawling study to test it. In 2012, as same-sex marriage advocates were working to build support in California, Michael LaCour, a political science researcher at the University of California, Los Angeles, asked a critical question: Can canvassers with a personal stake in an issue — in this case, gay men and women — actually sway voters’ opinions in a lasting way? He would need an influential partner to help frame, interpret and place into context his findings — to produce an authoritative scientific answer. And he went to one of the giants in the field, Donald P. Green, a Columbia University professor and co-author of a widely used text on field experiments. “I thought it was a very ambitious idea, so ambitious that it might not be suitable for a graduate student,” said Dr. Green, who signed on as a co-author of Mr. LaCour’s study in 2013. “But it’s such an important question, and he was very passionate about it.” Last week, their finding that gay canvassers were in fact powerfully persuasive with people who had voted against same-sex marriage — published in December in Science, one of the world’s leading scientific journals — collapsed amid accusations that Mr. LaCour had misrepresented his study methods and lacked the evidence to back up his findings. On Tuesday, Dr. Green asked the journal to retract the study because of Mr. LaCour’s failure to produce his original data. Mr. LaCour declined to be interviewed, but has said in statements that he stands by the findings. © 2015 The New York Times Company
Keyword: Sexual Behavior
Link ID: 20979 - Posted: 05.26.2015
Michael C. Corbalis In the quest to identify what might be unique to the human mind, one might well ask whether non-human animals have a theory of mind. In fiction, perhaps, they do. Eeyore, the morose donkey in Winnie-the-Pooh, at one point complains: ‘A little consideration, a little thought for others, makes all the difference.’ In real life, some animals do seem to show empathy toward others in distress. The primatologist Frans de Waal photographed a juvenile chimpanzee placing a consoling arm around an adult chimpanzee in distress after losing a fight, but suggests that monkeys do not do this. However, one study shows that monkeys won’t pull a chain to receive food if doing so causes a painful stimulus to be delivered to another monkey, evidently understanding that it will cause distress. Even mice, according to another study, react more intensely to pain if they perceive other mice in pain. It is often claimed that dogs show empathy toward their human owners, whereas cats do not. Cats don’t empathise—they exploit. Understanding what others are thinking, or what they believe, can be complicated, but perceiving emotion in others is much more basic to survival, and no doubt has ancient roots in evolution. Different emotions usually give different outward signs. In Shakespeare’s “Henry V,” the King recognises the signs of rage, urging his troops to . . . imitate the action of the tiger; Stiffen the sinews, summon up the blood, Disguise fair nature with hard-favour’d rage; Then lend the eye a terrible aspect . . . The human enemy will read the emotion of Henry’s troops, just as the antelope will read the emotion of the marauding tiger. Perhaps the best treatise on the outward signs of emotion is Charles Darwin’s “The Expression of the Emotions in Man and Animals,” which details the way fear and anger are expressed in cats and dogs, although he does not neglect the positive emotions: © 2015 Salon Media Group, Inc.
By Esther Hsieh Imagine you are enjoying your golden years, driving to your daily appointment for some painless brain zapping that is helping to stave off memory loss. That's the hope of a new study, in which people who learned associations (such as a random word and an image) after transcranial magnetic stimulation (TMS) were better able to learn more pairings days and weeks later—with no further stimulation needed. TMS uses a magnetic coil placed on the head to increase electrical signaling a few centimeters into the brain. Past studies have found that TMS can boost cognition and memory during stimulation, but this is the first to show that such gains can last even after the TMS regimen is completed. In the new study, which was published in Science, neuroscientists first used brain imaging to identify the associative memory network of 16 young, healthy participants. This network, based around the hippocampus, glues together things such as sights, places, sounds and time to form a memory, explains neuroscientist Joel Voss of Northwestern University, a senior author of the paper. Next, the researchers applied TMS behind the left ear of each participant for 20 minutes for five consecutive days to stimulate this memory network. To see if participants' associative memory improved, one day after the stimulation regimen finished they were tested for their ability to learn random words paired with faces. Subjects who had had TMS performed 33 percent better, compared with those who received placebo treatments, such as sham stimulation. © 2015 Scientific American
by Clare Wilson A new study has discredited the theory that dyslexia is caused by visual problems. So what does cause the condition and how can it be treated? What kind of visual problems are claimed to cause dyslexia? A huge variety. They include difficulties in merging information from both eyes, problems with glare from white pages or the text blurring or "dancing" on the page. A host of products claim to relieve this so-called visual stress, especially products that change the background colour of the page, such as tinted glasses and coloured overlays. Others advise eye exercises that supposedly help people with dyslexia track words on the page. Despite lack of evidence that these approaches work, some people with dyslexia say they help – more than half of university students with dyslexia have used such products. What are the new findings? That there's no evidence visual stress is linked with dyslexia. Nearly 6000 UK children aged between 7 and 9 had their reading abilities tested as well as performing a battery of visual tests. About 3 per cent of them had serious dyslexia, in line with the national average. But in the visual tests, the differences between the students with and without dyslexia were minimal. In two of the 11 tests, about 16 per cent of the children with dyslexia scored poorly, compared with 10 per cent for children with normal reading abilities. But that small difference could be caused by the fact that they read less, says author Alexandra Creavin of the University of Bristol, UK. And more importantly, the 16 per cent figure is so low, it can't be the main explanation for dyslexia. © Copyright Reed Business Information Ltd.
By Tara Haelle Thousands of infants each year die in their cribs from sudden infant death syndrome (SIDS) for reasons that have remained largely a mystery. A study published May 25 provides strong evidence that oxygen deprivation plays a big role. One reason the cause of SIDS has been so difficult to study is the sheer number of variables researchers have had to account for: whether the infant sleeps face down, breathes secondhand smoke or has an illness as well as whether the child has an unidentified underlying susceptibility. To isolate the effects of oxygen concentration, researchers from the University of Colorado compared the rate of SIDS in infants living at high altitudes, where the air is thin, to those living closer to sea level. Infants at high altitudes, they found, were more than twice as likely to die from SIDS. It was “very clever of the authors,” says Michael Goodstein, a pediatrician and member of the 2010–2011 Task Force on Sudden Infant Death Syndrome who was not involved in the study. “The authors did a good job controlling for other variables,” he adds. Beyond the risk of living at high altitudes, the study suggests a common link among different risk factors about the causes of SIDS. For example, the authors note that sleeping on the stomach and exposure to tobacco smoke can also contribute to hypoxia—insufficient oxygen reaching the tissues. Similarly, past research has suggested that sleeping on soft surfaces may shift the chin down, partly obstructing the airway, which might cause an infant to breathe in less oxygen. It’s unclear how hypoxia might contribute to SIDS but it could have to do with a buildup of carbon dioxide in the tissues when a child does not wake up. © 2015 Scientific American
By FRANCES ROBLES MIAMI — A hazardous new synthetic drug originating in China is being blamed for 18 recent deaths in a single South Florida county, as police grapple with an inexpensive narcotic that causes exaggerated strength and dangerous paranoid hallucinations. On Thursday, the Fort Lauderdale police killed a man, reportedly high on the man-made street drug, alpha-PVP, known more commonly as flakka, who had held a woman hostage with a knife to her throat. The shooting of Javoris Washington, 29, was the latest in a series of volatile episodes that the police in South Florida have faced with highly aggressive drug users. Law enforcement agencies have had difficulty tamping down a surge in synthetic drugs, which were banned after becoming popular in clubs five years ago only to re-emerge deadlier than ever under new formulations. As soon as legislation catches up with the latest craze, manufacturers design a new drug to take its place, federal and local law enforcement agencies say. In Broward County, which includes Fort Lauderdale and is considered ground zero for the new drug, there have been 18 flakka-related fatalities since September, the chief medical examiner there said. “I have never seen such a rash of cases, all associated with the same substance,” said James N. Hall, an epidemiologist at Nova Southeastern University who has studied the Florida drug market for decades. “It’s probably the worst I have seen since the peak of crack cocaine. Rather than a drug, it’s really a poison.” © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 20974 - Posted: 05.25.2015
Richard Harris American medicine is heading into new terrain, a place where a year's supply of drugs can come with a price tag that exceeds what an average family earns. Pharmacy benefit manager Express Scripts says last year more than half a million Americans racked up prescription drug bills exceeding $50,000. Barbara Haedtke of Portland, Ore., knows this all too well. When she was diagnosed with multiple sclerosis in 2001 at the age of 35, she was prescribed Avonex, at a cost of around $10,000 a year. Her health insurance paid most of that until she and her husband found themselves without jobs during an economic downturn. "We were in the hole, and so $10,000 was a lot of money," she says. "Under the best circumstances it's a lot of money, but then particularly it was really difficult." Barbara Haedtke says she's grateful for a drug-company program that helps cover copays, but doesn't know how long she'll get that benefit. The drug company gave her the medication at no charge until she once again had a job with insurance, and for that, she says, she's really grateful. But the story doesn't end there. Haedtke used Avonex for about a decade and watched with disbelief as the price more than tripled. She's now taking a new drug, Tecfidera, that's priced even higher — $66,000 a year, according to her pharmacy receipt. The drug is supposed to help reduce the number of episodes that characterize multiple sclerosis, a disease in which nerve fibers gradually degenerate, causing muscle weakness, numbness, loss of balance and even paralysis. © 2015 NPR
by Helen Thomson A brain implant that can decode what someone wants to do has allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity – and enjoy a beer at his own pace. Erik Sorto was left unable to move any of his limbs after an accident severed his spinal cord 12 years ago. People with similar injuries have previously controlled prosthetic limbs using implants placed in their motor cortex – an area of the brain responsible for the mechanics of movement. This is far from ideal because it results in delayed, jerky motions as the person thinks about all the individual aspects of the movement. When reaching for a drink, for example, they would have to think about moving their arm forward, then left, then opening their hand, then closing their hand around the cup and so on. Richard Andersen at the California Institute of Technology in Pasadena and his colleagues hoped they could achieve a more fluid movement by placing an implant in the posterior parietal cortex – a part of the brain involved in planning motor movements. "We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, 'I want to pick up that cup', rather than the individual components," said Anderson at the NeuroGaming Conference in San Francisco, California, where he presented the work this month. © Copyright Reed Business Information Ltd.
Link ID: 20972 - Posted: 05.23.2015
Nala Rogers Alzheimer’s disease may have evolved alongside human intelligence, researchers report in a paper posted this month on BioRxiv1. The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development. This may have helped to increase the connectivity of neurons, making modern humans smarter as they evolved from their hominin ancestors. But that new intellectual capacity was not without cost: the same genes are implicated in Alzheimer's disease. Kun Tang, a population geneticist at the Shanghai Institutes for Biological Sciences in China who led the research, speculates that the memory disorder developed as ageing brains struggled with new metabolic demands imposed by increasing intelligence. Humans are the only species known to develop Alzheimer's; the disease is absent even in closely related primate species such as chimpanzees. Tang and his colleagues searched modern human DNA for evidence of this ancient evolution. They examined the genomes of 90 people with African, Asian or European ancestry, looking for patterns of variation driven by changes in population size and natural selection. Marked by selection The analysis was tricky, because the two effects can mimic each other. To control for the effects of population changes ― thereby isolating the signatures of natural selection — the researchers estimated how population sizes changed over time. Then they identified genome segments that did not match up with the population history, revealing the DNA stretches that were most likely shaped by selection. © 2015 Nature Publishing Group
Richard A. Friedman AMERICANS disapprove of marital infidelity. Ninety-one percent of them find it morally wrong, more than the number that reject polygamy, human cloning or suicide, according to a 2013 Gallup poll. Yet the number of Americans who actually cheat on their partners is rather substantial: Over the past two decades, the rate of infidelity among married men has been pretty constant at around 21 percent, while the percentage of married women who admitted to cheating has mostly hovered between 10 and 15 percent, according to the General Social Survey at the University of Chicago’s independent research organization, NORC. We are accustomed to thinking of sexual infidelity as a symptom of an unhappy relationship, a moral flaw or a sign of deteriorating social values. When I was trained as a psychiatrist we were told to look for various emotional and developmental factors — like a history of unstable relationships or a philandering parent — to explain infidelity. But during my career, many of the questions we asked patients were found to be insufficient because for so much behavior, it turns out that genes, gene expression and hormones matter a lot. Now that even appears to be the case for infidelity. We have long known that men have a genetic, evolutionary impulse to cheat, because that increases the odds of having more of their offspring in the world. But now there is intriguing new research showing that some women, too, are biologically inclined to wander, although not for clear evolutionary benefits. Women who carry certain variants of the vasopressin receptor gene are much more likely to engage in “extra pair bonding,” the scientific euphemism for sexual infidelity. © 2015 The New York Times Company
By Jason G. Goldman In 1970 child welfare authorities in Los Angeles discovered that a 14-year-old girl referred to as “Genie” had been living in nearly total social isolation from birth. An unfortunate participant in an unintended experiment, Genie proved interesting to psychologists and linguists, who wondered whether she could still acquire language despite her lack of exposure to it. Genie did help researchers better define the critical period for learning speech—she quickly acquired a vocabulary but did not gain proficiency with grammar—but thankfully, that kind of case study comes along rarely. So scientists have turned to surrogates for isolation experiments. The approach is used extensively with parrots, songbirds and hummingbirds, which, like us, learn how to verbally communicate over time; those abilities are not innate. Studying most vocal-learning mammals—for example, elephants, whales, sea lions—is not practical, so Tel Aviv University zoologists Yosef Prat, Mor Taub and Yossi Yovel turned to the Egyptian fruit bat, a vocal-learning species that babbles before mastering communication, as a child does. The results of their study, the first to raise bats in a vocal vacuum, were published this spring in the journal Science Advances. Five bat pups were reared by their respective mothers in isolation, so the pups heard no adult conversations. After weaning, the juveniles were grouped together and exposed to adult bat chatter through a speaker. A second group of five bats was raised in a colony, hearing their species' vocal interactions from birth. Whereas the group-raised bats eventually swapped early babbling for adult communication, the isolated bats stuck with their immature vocalizations well into adolescence. © 2015 Scientific American
By Meeri Kim The dangers of concussions, caused by traumatic stretching and damage to nerve cells in the brain that lead to dizziness, nausea and headache, has been well documented. But ear damage that is sometimes caused by a head injury has symptoms so similar to the signs of a concussion that doctors may misdiagnose it and administer the wrong treatment. A perilymph fistula is a tear or defect in the small, thin membranes that normally separate the air-filled middle ear from the inner ear, which is filled with a fluid called perilymph. When a fistula forms, tiny amounts of this fluid leak out of the inner ear, an organ crucial not only for hearing but also for balance. Losing even a few small drops of perilymph leaves people disoriented, nauseous and often with a splitting headache, vertigo and memory loss. While most people with a concussion recover within a few days, a perilymph fistula can leave a person disabled for months. There is some controversy around perilymph fistula due to its difficulty of diagnosis — the leak is not directly observable, but rather identified by its symptoms. However, it is generally accepted as a real condition by otolaryngologists and sports physicians, and typically known to follow a traumatic event. But concussions — as well as post-concussion syndrome, which is marked by dizziness, headache and other symptoms that can last even a year after the initial blow — also occur as the result of such an injury.
I’m fairly new to San Francisco, so I’m still building my mental database of restaurants I like. But this weekend, I know exactly where I’m heading to for dinner: Nick’s Crispy Tacos. Then, when I get home, I’m kicking back to a documentary I’ve never heard of, a Mongolian drama called The Cave of the Yellow Dog. An artificially intelligent algorithm told me I’d enjoy both these things. I’d like the restaurant, the machine told me, because I prefer Mexican food and wine bars “with a casual atmosphere,” and the movie because “drama movies are in my digital DNA.” Besides, the title shows up around the web next to Boyhood, another film I like. Nara Logics, the company behind this algorithm, is the brainchild (pun intended) of its CTO and cofounder, Nathan Wilson, a former research scientist at MIT who holds a doctorate in brain and cognitive science. Wilson spent his academic career and early professional life immersed in studying neural networks—software that mimics how a human mind thinks and makes connections. Nara Logics’ brain-like platform, under development for the past five years, is the product of all that thinking.. The Cambridge, Massachusetts-based company includes on its board such bigwig neuroscientists as Sebastian Seung from Princeton, Mriganka Sur from MIT, and Emily Hueske of Harvard’s Center for Brain and Science. So what does all that neuroscience brain power have to offer the tech world, when so many Internet giants—from Google and Facebook to Microsoft and Baidu—already have specialized internal teams looking to push the boundaries of artificial intelligence? These behemoths use AI to bolster their online services, everything from on-the-fly translations to image recognition services. But to hear Wilson tell it, all that in-house work still leaves a large gap—namely, all the businesses and people who could benefit from access to an artificial brain but can’t build it themselves. “We’re building a pipeline, and taking insights out of the lab to intelligent, applied use cases,” Wilson tells WIRED. “Nara is AI for the people.”
Link ID: 20967 - Posted: 05.23.2015
Carl Zimmer Octopuses, squid and cuttlefish — a group of mollusks known as cephalopods — are the ocean’s champions of camouflage. Octopuses can mimic the color and texture of a rock or a piece of coral. Squid can give their skin a glittering sheen to match the water they are swimming in. Cuttlefish will even cloak themselves in black and white squares should a devious scientist put a checkerboard in their aquarium. Cephalopods can perform these spectacles thanks to a dense fabric of specialized cells in their skin. But before a cephalopod can take on a new disguise, it needs to perceive the background that it is going to blend into. Cephalopods have large, powerful eyes to take in their surroundings. But two new studies in The Journal Experimental Biology suggest that they have another way to perceive light: their skin. It’s possible that these animals have, in effect, evolved a body-wide eye. When light enters the eye of a cephalopod, it strikes molecules in the retina called opsins. The collision starts a biochemical reaction that sends an electric signal from the cephalopod’s eye to its brain. (We produce a related form of opsins in our eyes as well.) In 2010, Roger T. Hanlon, a biologist at the Marine Biological Laboratory in Woods Hole, Mass., and his colleagues reported that cuttlefish make opsins in their skin, as well. This discovery raised the tantalizing possibility that the animals could use their skin to sense light much as their eyes do. Dr. Hanlon teamed up with Thomas W. Cronin, a visual ecologist at the University of Maryland Baltimore County, and his colleagues to take a closer look. © 2015 The New York Times Company
Athletes who lose consciousness after concussions may be at greater risk for memory loss later in life, a small study of retired National Football League players suggests. Researchers compared memory tests and brain scans for former NFL players and a control group of people who didn't play college or pro football. After concussions that resulted in lost consciousness, the football players were more likely to have mild cognitive impairment and brain atrophy years later. "Our results do suggest that players with a history of concussion with a loss of consciousness may be at greater risk for cognitive problems later in life," senior study author Munro Cullum, chief of neuropsychology at the University of Texas Southwestern Medical Center in Dallas, said by email. "We are at the early stages of understanding who is actually at risk at the individual level." Cullum and colleagues recruited 28 retired NFL players living in Texas: eight who were diagnosed with mild cognitive impairment and 20 who didn't appear to have any memory problems. They ranged in age from 36 to 79, and were an average of about 58 years old. All but three former athletes experienced at least one concussion, and they typically had more than three. Researchers compared these men to 27 people who didn't play football but were similar in age, education, and mental capacity to the retired athletes, including six with cognitive impairment. These men were 41 to 77 years old, and about 59 on average. ©2015 CBC/Radio-Canada
Scientists at Mayo Clinic, Jacksonville, Florida created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), both of which are caused by a mutation in the a gene called C9ORF72. The study was partially funded by the National Institutes of Health and published in the journal Science. More than 30,000 Americans live with ALS, which destroys nerves that control essential movements, including speaking, walking, breathing and swallowing. After Alzheimer’s disease, FTD is the most common form of early onset dementia. It is characterized by changes in personality, behavior and language due to loss of neurons in the brain’s frontal and temporal lobes. Patients with mutations in the chromosome 9 open reading frame 72 (C9ORF72) gene have all or some symptoms associated with both disorders. “Our mouse model exhibits the pathologies and symptoms of ALS and FTD seen in patients with theC9ORF72 mutation,” said the study’s lead author, Leonard Petrucelli, Ph.D., chair and Ralph and Ruth Abrams Professor of the Department of Neuroscience at Mayo Clinic, and a senior author of the study. “These mice could greatly improve our understanding of ALS and FTD and hasten the development of effective treatments.” To create the model, Ms. Jeannie Chew, a Mayo Graduate School student and member of Dr. Petrucelli’s team, injected the brains of newborn mice with a disease-causing version of the C9ORF72 gene. As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms.