Love a sugar hit? Your sweet tooth may hail from an unlikely source: your liver. A hormone made by the organ appears to control how much carbohydrate and sugar we want to eat, and helps slow us down when we are overindulging. The hormone, called FGF21, has already been found to help obese mice lose weight and regain their sensitivity to insulin. A modified form is currently in clinical trials to test whether it has the same effect in people with diabetes. Our bodies break down carbohydrates into sugars such as sucrose, glucose and fructose. Recent genetic studies have suggested that people with altered levels of FGF21 consume more carbohydrates. To find out more, a team co-led by Matthew Potthoff at the University of Iowa observed the eating habits of mice with either abnormally high or low levels of the hormone. They found that mice genetically modified to lack the hormone chose to drink much higher levels of sugar-sweetened drinks than normal mice. Those given an extra dose of the hormone, on the other hand, reduced their sugar intake. The team also showed that the hormone is produced in response to high carbohydrate levels; it then enters the bloodstream, where it sends a signal to the brain to suppress our sugar intake. In people, blood levels of FGF21 triple 24 hours after a spike in blood sugar levels. When monkeys were given the synthetic version of the hormone being tested in clinical trials, they also opted for a diet low in sugar, according to a separate study by Steven Kliewer at the University of Texas Southwestern Medical Center at Dallas and colleagues. The team also found that these monkeys consumed less alcohol than those that weren’t given the compound. © Copyright Reed Business Information Ltd.

Keyword: Obesity; Hormones & Behavior
Link ID: 21732 - Posted: 12.29.2015

By BENEDICT CAREY SAN FRANCISCO — The idea was to go out in an emotional swan dive, a lunge for the afterlife that would stretch his 17-year-old imagination. He settled on a plan and shared the details with a Facebook friend: He would drop DMT, a powerful psychedelic, and then cut his throat. “Everyone was telling me what I could and couldn’t do — doctors, my parents,” said Frank, now a 19-year-old college student. “I was going to hurt myself, to show people, ‘Look, I am still in control of my life.’” And so, in time, he was. Frank, who eight months earlier had received a diagnosis of psychosis, the signature symptom of schizophrenia, and had been in and out of the hospital, gradually learned to take charge of his own recovery, in a new approach to treatment for people experiencing a first psychotic “break” with reality. At a time when lawmakers in Washington are debating large-scale reforms to the mental health care system, analysts are carefully watching a handful of new first-break programs like the one that treated Frank in New York as a way to potentially ease the cycle of hospitalization and lifetime disability that afflict so many mentally ill people. More than two million people in the United States have received a diagnosis of schizophrenia. Most are consigned to whatever treatment is available amid a hodgepodge of programs that often focus on antipsychotic drugs to blunt delusions and paranoia — medicines that can come with side effects so debilitating that many patients go off them and end up in a loop of hospitalization and despair. But over the past several years, a number of states have set up programs with a different approach, emphasizing supportive services, like sustained one-on-one therapy, school and work assistance, and family education, as well as medication. The therapists work to engage each patient as an equal partner in decisions — including about medication dosage, to make it as tolerable as possible. © 2015 The New York Times Company

Keyword: Schizophrenia
Link ID: 21731 - Posted: 12.29.2015

By Gary Stix A lingering question asked by neuroscientists has to do with what, if anything, makes the male and female brain distinctive, whether in mice or (wo)men. There is still no concise answer. The best evidence from the most recent research suggests that both males and females share the same neural circuitry, but use it differently. Catherine Dulac, a professor of molecular and cellular biology at Harvard, and investigator at the Howard Hughes medical Institute, is a pioneer in exploring these questions. I talked to her briefly about her research, which also extends far beyond just the neurobiology of gender. Can you tell me in broad overview about what you study? I'm interested in understanding how the brain engages in instinctive social behaviors. There are a lot of instinctive behaviors such as eating and sleeping that are essential in animals and humans, but social behavior is a very distinctive and particularly interesting set of instinctive behaviors that we would like to understand at the neuronal level. What we would like to understand in mechanistic terms is how does an individual recognize other animals of its own species, for example how does an animal identifies a male, a female, or an infant, how does the brain processes these signals in order to trigger appropriate social behaviors such as mating, aggression or parenting. Can you tell me a little bit about your work of the last few years that relates to gender identification? © 2015 Scientific American

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 21730 - Posted: 12.29.2015

By Katrina Schwartz It has become a cultural cliché that raising adolescents is the most difficult part of parenting. It’s common to joke that when kids are in their teens they are sullen, uncommunicative, more interested in their phones than in their parents and generally hard to take. But this negative trope about adolescents misses the incredible opportunity to positively shape a kid’s brain and future life course during this period of development. “[Adolescence is] a stage of life when we can really thrive, but we need to take advantage of the opportunity,” said Temple University neuroscientist Laurence Steinberg at a Learning and the Brain conference in Boston. Steinberg has spent his career studying how the adolescent brain develops and believes there is a fundamental disconnect between the popular characterizations of adolescents and what’s really going on in their brains. Because the brain is still developing during adolescence, it has incredible plasticity. It’s akin to the first five years of life, when a child’s brain is growing and developing new pathways all the time in response to experiences. Adult brains are somewhat plastic as well — otherwise they wouldn’t be able to learn new things — but “brain plasticity in adulthood involves minor changes to existing circuits, not the wholesale development of new ones or elimination of others,” Steinberg said. Adolescence is the last time in a person’s life that the brain can be so dramatically overhauled. © 2015 KQED Inc.

Keyword: Development of the Brain; Sexual Behavior
Link ID: 21729 - Posted: 12.29.2015

By Karen Weintraub Mild cognitive impairment, or M.C.I., is not a disease in itself. Rather, it is a clinical description based on performance on a test of memory and thinking skills. Depending on its cause, mild cognitive impairment is potentially reversible. Poor performance on a cognitive test could be caused by certain medications, sleep apnea, depression or other problems, said Dr. Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School and Beth Israel Deaconess Medical Center. In those cases, when the underlying disease is treated, cognitive abilities can bounce back. But in about half of people with M.C.I. – doctors are not sure of the exact number — memory problems are the first sign of impending Alzheimer’s disease. If M.C.I. progresses to Alzheimer’s, there is no recovery. Alzheimer’s is marked by an inexorable decline that is always fatal, although the path from the first signs of cognitive impairment to death may take three to 15 years, said Dr. David Knopman, a professor of neurology at the Mayo Clinic in Rochester, Minn. As many as 20 percent to 30 percent of those with M.C.I. who score below but near the cutoff for normal can cross back above in a subsequent cognitive test – perhaps because they are having a better day, he said. But someone whose score is borderline is at higher risk of developing Alzheimer’s than someone who scores higher, said Dr. Knopman, also vice chair of the medical and scientific advisory council of the Alzheimer’s Association. Doctors may be hesitant to label someone with early Alzheimer’s, which can be difficult to diagnose in the early stages, so they often call it mild cognitive impairment instead, said Dr. John C. Morris, a professor of neurology and the director of the Knight Alzheimer's Disease Research Center at Washington University School of Medicine in St. Louis. © 2015 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 21728 - Posted: 12.29.2015

by Sarah Zielinski When you get a phone call or a text from a friend or acquaintance, how fast you respond — or whether you even bother to pick up your phone — often depends on the quality of the relationship you have with that person. If it’s your best friend or mom, you probably pick up right away. If it’s that annoying coworker contacting you on Sunday morning, you might ignore it. Ring-tailed lemurs, it seems, are even pickier in who they choose to respond to. They only respond to calls from close buddies, a new study finds. These aren’t phone calls but contact calls. Ring-tailed lemurs live in female-dominated groups of 11 to 16, and up to 25, animals, and when the group is on the move, it’s common for one member to yell out a “meow!” and for other members to “meow!” back. A lemur may also make the call if it gets lost. The calls serve to keep the group together. The main way ring-tailed lemurs (and many other primates) build friendships, though, is through grooming. Grooming helps maintain health and hygiene and, more importantly, bonds between members. It’s a time-consuming endeavor, and animals have to be picky about who they bother to groom. Ipek Kulahci and colleagues at Princeton University wanted to see if there was a link between relationships built through grooming and vocal exchanges among ring-tailed lemurs. Contact calls don’t require nearly as much time or effort as grooming sessions, so it is possible that animals could be less discriminating when they respond to calls. But, the researchers reasoned, if the vocalizations were a way of maintaining the relationships built through painstaking grooming sessions, then the lemurs would be as picky in their responses as in their grooming partners. © Society for Science & the Public 2000 - 2015.

Keyword: Animal Communication; Language
Link ID: 21727 - Posted: 12.29.2015

James Bond's villain in the latest 007 film, Spectre, could use a lesson in neuroanatomy, a Toronto neurosurgeon says. In a scene recorded in a Morroccan desert, Ernst Stavro Blofeld, played by Christoph Waltz, tortures Bond using restraints and a head clamp fused with a robotic drill. The goal is to inflict pain and erase 007's memory bank of faces. But Blofeld didn't have his brain anatomy down and could have likely killed Daniel Craig's character instead, Dr. Michael Cusimano of St. Michael's Hospital, says in a letter published in this week's issue of the journal Nature. Aiming to erase Bond's memory of faces, the villain correctly intends to drill into the lateral fusiform gyrus, an area of the brain responsible for recognizing faces, Cusimano said. But in practice, the drill was placed in the wrong area, aiming for the neck instead of the brain. "Whereas the drill should have been aimed just in front of 007's ear, it was directed below the mastoid process under and behind his left ear," Cusimano wrote. It likely would have triggered a stroke or massive hemorrhage, he said. In a draft of the letter, Cusimano said he was "spellbound" watching the film in a packed theatre, but his enjoyment was somewhat marred by the blunder. "I laughed," he recalled in an interview. "I think people around me kind of looked at me and were wondering why I was laughing because it's a pretty tense part of the movie." ©2015 CBC/Radio-Canada.

Keyword: Attention
Link ID: 21726 - Posted: 12.27.2015

By BENEDICT CAREY Dr. Robert L. Spitzer, who gave psychiatry its first set of rigorous standards to describe mental disorders, providing a framework for diagnosis, research and legal judgments, as well as a lingua franca for the endless social debate over where to draw the line between normal and abnormal behavior, died on Friday. He was 83. From Our Advertisers Dr. Spitzer died from complications of heart disease at the assisted living facility where he lived in Seattle, his wife, Janet Williams, said. The couple had moved to Seattle from Princeton, N.J., this year. Dr. Spitzer’s remaking of psychiatry began with an early interest in one of the least glamorous and, historically, most ignored corners of the field: measurement. In the early 1960s, the field was fighting to sustain its credibility, in large part because diagnoses varied widely from doctor to doctor. For instance, a patient told he was depressed by one doctor might be called anxious or neurotic by another. The field’s diagnostic manual, at the time a pamphlet-like document rooted in Freudian ideas, left wide latitude for the therapist’s judgment. Dr. Spitzer, a rising star at Columbia University, was himself looking for direction, increasingly frustrated with Freudian analysis. A chance meeting with a colleague working on a new edition of the manual — the Diagnostic and Statistical Manual of Mental Disorders, or the D.S.M. for short — led to a job taking notes for the committee debating revisions. There, he became fascinated with reliable means for measuring symptoms and behavior — i.e., assessment. “At the time, there was zero interest in assessment,” said Dr. Michael First, a professor of clinical psychiatry at Columbia. “He saw how important it was, and his whole career led to assessment being taken seriously.” © 2015 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 21725 - Posted: 12.27.2015

By Diana Kwon Symptoms come and go in most cases of multiple sclerosis (MS), a chronic disease in which the immune system attacks myelin, the nonconductive sheath that surrounds neurons' axons. Yet 10 to 15 percent of cases are progressive rather than relapsing. This more severe version appears later in life and is marked by steadily worsening symptoms. No treatments are currently available, but that might be about to change. In September pharmaceutical company Hoffmann–La Roche announced positive results from three large clinical trials of ocrelizumab, an injectable antibody medication that targets B cells, for both relapsing and progressive MS. They found that the drug was more effective at treating relapsing MS than interferon beta-1a (Rebif), a top-performing drug now used to treat the disease. Even more exciting, it slowed the advance of symptoms in patients with progressive MS for the entire 12-week duration of the study. “The drug has dramatic effects on relapsing MS, and we finally have our foot in the door with the progressive form,” says Stephen Hauser, a neurologist at the University of California, San Francisco, who was involved in the trials. The fact that ocrelizumab works on both types of MS is a tantalizing clue for scientists trying to understand the root causes of the disease and figure out why the inflammation of the relapsing form eventually turns into progressive degeneration in some patients. “These results give evidence that the inflammatory and the degenerative components of MS are related,” Hauser says. “The big question now is, If we begin treatment really early, can we protect relapsing patients from developing the progressive problems later on?” © 2015 Scientific American

Keyword: Multiple Sclerosis
Link ID: 21724 - Posted: 12.27.2015

By KEN BELSON Researchers at several universities and research institutes were awarded almost $16 million Tuesday to find a way to diagnose, while victims are alive, chronic traumatic encephalopathy, a degenerative brain disease linked to repeated head hits in contact sports. The National Institutes of Health and the National Institute of Neurological Disorders and Stroke issued the seven-year grant as part of a long-term study of brain disease in former N.F.L. and college football players, many of whom sustained multiple concussions on the field. Despite the implications that the research may have on football players and the N.F.L., no league money will be used to help pay for the grant. For years, researchers have been able to diagnose C.T.E. only by examining the brains of players who died and whose families agreed to donate the organ, a limitation that has slowed efforts to determine who is susceptible to having the disease. The new study, considered among the most ambitious in the field of sports-related brain injury, aims to develop ways to spot the disease in the living and figure out why certain players get it and others do not. A more comprehensive understanding of the disease, the researchers said, may lead to ways to prevent it. “There are so many critical unanswered questions about C.T.E.,” Dr. Robert Stern, the lead principal investigator and a professor at Boston University School of Medicine, said in a statement. “We are optimistic that this project will lead to many of these answers, by developing accurate methods of detecting and diagnosing C.T.E. during life, and by examining genetic and other risk factors for this disease.” © 2015 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 21723 - Posted: 12.24.2015

By Ferris Jabr Matthew Brien has struggled with overeating for the past 20 years. At age 24, he stood at 5′10′′ and weighed a trim 135 pounds. Today the licensed massage therapist tips the scales at 230 pounds and finds it particularly difficult to resist bread, pasta, soda, cookies and ice cream—especially those dense pints stuffed with almonds and chocolate chunks. He has tried various weight-loss programs that limit food portions, but he can never keep it up for long. “It's almost subconscious,” he says. “Dinner is done? Okay, I am going to have dessert. Maybe someone else can have just two scoops of ice cream, but I am going to have the whole damn [container]. I can't shut those feelings down.” Eating for the sake of pleasure, rather than survival, is nothing new. But only in the past several years have researchers come to understand deeply how certain foods—particularly fats and sweets—actually change brain chemistry in a way that drives some people to overconsume. Scientists have a relatively new name for such cravings: hedonic hunger, a powerful desire for food in the absence of any need for it; the yearning we experience when our stomach is full but our brain is still ravenous. And a growing number of experts now argue that hedonic hunger is one of the primary contributors to surging obesity rates in developed countries worldwide, particularly in the U.S., where scrumptious desserts and mouthwatering junk foods are cheap and plentiful. “Shifting the focus to pleasure” is a new approach to understanding hunger and weight gain, says Michael Lowe, a clinical psychologist at Drexel University who coined the term “hedonic hunger” in 2007. © 2015 Scientific American

Keyword: Obesity; Attention
Link ID: 21722 - Posted: 12.24.2015

Need to remember something important? Take a break. A proper one – no TV or flicking through your phone messages. It seems that resting in a quiet room for 10 minutes without stimulation can boost our ability to remember new information. The effect is particularly strong in people with amnesia, suggesting that they may not have lost the ability to form new memories after all. “A lot of people think the brain is a muscle that needs to be continually stimulated, but perhaps that’s not the best way,” says Michaela Dewar at Heriot-Watt University in Edinburgh, UK. New memories are fragile. They need to be consolidated before being committed to long-term storage, a process thought to happen while we sleep. But at least some consolidation may occur while we’re awake, says Dewar – all you need is a timeout. In 2012, Dewar’s team showed that having a rest helps a person to remember what they were told a few minutes earlier. And the effect seems to last. People who had a 10-minute rest after hearing a story remembered 10 per cent more of it a week later than those who played a spot-the-difference game immediately afterwards. “We dim the lights and ask them to sit in an empty, quiet room, with no mobile phones,” says Dewar. When asked what they had been thinking about afterwards, most volunteers said they had let their minds wander. Now Dewar, along with Michael Craig at the University of Edinburgh and their colleagues, have found that spatial memories can also be consolidated when we rest. © Copyright Reed Business Information Ltd.

Keyword: Sleep; Learning & Memory
Link ID: 21721 - Posted: 12.24.2015

By Francine Russo Some children insist, from the moment they can speak, that they are not the gender indicated by their biological sex. So where does this knowledge reside? And is it possible to discern a genetic or anatomical basis for transgender identity? Exploration of these questions is relatively new, but there is a bit of evidence for a genetic basis. Identical twins are somewhat more likely than fraternal twins to both be trans. Male and female brains are, on average, slightly different in structure, although there is tremendous individual variability. Several studies have looked for signs that transgender people have brains more similar to their experienced gender. Spanish investigators—led by psychobiologist Antonio Guillamon of the National Distance Education University in Madrid and neuropsychologist Carme Junqué Plaja of the University of Barcelona—used MRI to examine the brains of 24 female-to-males and 18 male-to-females—both before and after treatment with cross-sex hormones. Their results, published in 2013, showed that even before treatment the brain structures of the trans people were more similar in some respects to the brains of their experienced gender than those of their natal gender. For example, the female-to-male subjects had relatively thin subcortical areas (these areas tend to be thinner in men than in women). Male-to-female subjects tended to have thinner cortical regions in the right hemisphere, which is characteristic of a female brain. (Such differences became more pronounced after treatment.) “Trans people have brains that are different from males and females, a unique kind of brain,” Guillamon says. “It is simplistic to say that a female-to-male transgender person is a female trapped in a male body. It's not because they have a male brain but a transsexual brain.” Of course, behavior and experience shape brain anatomy, so it is impossible to say if these subtle differences are inborn. © 2015 Scientific American

Keyword: Sexual Behavior; Brain imaging
Link ID: 21720 - Posted: 12.24.2015

By Elahe Izadi Tiny cameras attached to wild New Caledonian crows capture, for the first time, video footage of these elusive birds fashioning hooked stick tools, according to researchers. These South Pacific birds build tools out of twigs and leaves that they use to root out food, and they're the only non-humans that make hooked tools in the wild, write the authors of a study published Wednesday in the journal Biology Letters. Humans have previously seen the crows making the tools in artificial situations, in which scientists baited feeding sites and provided the raw tools; but researchers say the New Caledonian crows have never been filmed doing this in a completely natural setting. "New Caledonian crows are renowned for their unusually sophisticated tool behavior," the study authors write. "Despite decades of fieldwork, however, very little is known about how they make and use their foraging tools in the wild, which is largely owing to the difficulties in observing these shy forest birds." Study author Jolyon Troscianko of the University of Exeter in England described the tropical birds as "notoriously difficult to observe" because of the terrain of their habitat and their sensitivity to disturbance, he said in a press release. "By documenting their fascinating behavior with this new camera technology, we obtained valuable insights into the importance of tools in their daily search for food," he added.

Keyword: Evolution; Intelligence
Link ID: 21719 - Posted: 12.24.2015

Tim Radford British scientists believe they have made a huge step forward in the understanding of the mechanisms of human intelligence. That genetic inheritance must play some part has never been disputed. Despite occasional claims later dismissed, no-one has yet produced a single gene that controls intelligence. But Michael Johnson of Imperial College London, a consultant neurologist and colleagues report in Nature Neuroscience that they may have discovered a very different answer: two networks of genes, perhaps controlled by some master regulatory system, lie behind the human gift for lateral thinking, mental arithmetic, pub quizzes, strategic planning, cryptic crosswords and the ability to laugh at limericks. As usual, such research raises potentially politically-loaded questions about the nature of intelligence. “Intelligence is a composite measure of different cognitive abilities and how they are distributed in a population. It doesn’t measure any one thing. But it is measurable,” Dr Johnson said. About 40% of the variation in intelligence is explained by inheritance. The other factors are not yet certain. But the scientists raise the distant possibility that armed with the new information they may be able to devise ways to modify human intelligence. “The idea of ultimately using drugs to affect cognitive performance is not in any way new. We all drink coffee to improve our cognitive performance,” Dr Johnson said. “It’s about understanding the pathways that are related to cognitive ability both in health and disease, especially disease so one day we could help people with learning disabilities fulfill their potential. That is very important.” © 2015 Guardian News and Media Limited

Keyword: Intelligence; Genes & Behavior
Link ID: 21718 - Posted: 12.22.2015

Rae Ellen Bichell Ever notice the catnaps that older relatives take in the middle of the day? Or how grandparents tend to be early risers? You're not alone. Colleen McClung did, too. A neuroscientist at the University of Pittsburgh Medical Center, McClung wanted to know what was going on in the brain that changes people's daily rhythms as they age. We all have a set of so-called clock genes that keep us on a 24-hour cycle. In the morning they wind us up, and at night they help us wind down. A study out Monday in Proceedings of the National Academy of Sciences found that those genes might beat to a different rhythm in older folks. "When you think about the early bird dinner specials, it sort of fits in with their natural shift in circadian rhythms," says McClung. "There is a core set of genes that has been described in every animal — every plant all the way down from fungus to humans — and they're pretty much the same set of genes." The genes are the master controllers of a bunch of other genes that control processes ranging from metabolism to sleep. When you woke up this morning, the timekeeping genes told a gland in your brain to give a jolt of the stress hormone cortisol to wake up. Tonight, they'll tell a gland to spit out melatonin, a hormone that makes you sleepy. "You can think of them as sort of the conductor of an orchestra," says McClung. They make sure all the other genes keep time. © 2015 npr

Keyword: Sleep; Development of the Brain
Link ID: 21717 - Posted: 12.22.2015

A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease, creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of Alzheimer’s may prevent dementia and reduce damage to the brain. “This exciting research advances our understanding of the role of the proteasomes in neurodegeneration and provides a potential way to alleviate symptoms of neurodegenerative disorders,” said Roderick Corriveau, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. The proteasome is a hollow, cylindrical structure which chews up defective proteins into smaller, pieces that can be recycled into new proteins needed by a cell. To understand how neurodegenerative disorders affect proteasomes, Natura Myeku, Ph.D., a postdoctoral fellow working with Karen E. Duff, Ph.D., professor of pathology and cell biology at Columbia University, New York City, focused on tau, a structural protein that accumulates into clumps called tangles in the brain cells of patients with Alzheimer’s disease and several other neurodegenerative disorders known as tauopathies. Using a genetically engineered mouse model of tauopathy, as well as looking at cells in a dish, the scientists discovered that as levels of abnormal tau increased, the proteasome activity slowed down.

Keyword: Alzheimers
Link ID: 21716 - Posted: 12.22.2015

By John Bohannon In July 1984, a man broke into the apartment of Jennifer Thompson, a 22-year-old in North Carolina, and threatened her with a knife. She negotiated, convincing him to not kill her. Instead, he raped her and fled. Just hours later, a sketch artist worked with Thompson to create an image of the assailant's face. Then the police showed her a series of mug shots of similar-looking men. Thompson picked out 22-year-old Ronald Cotton, whose photograph was on file because of a robbery committed in his youth. When word reached Cotton that the police were looking for him, he walked into a precinct voluntarily. He was eventually sentenced to life in prison based on Thompson's testimony. Eleven years later, after DNA sequencing technology caught up, samples taken from Thomson's body matched a different man who finally confessed. Cotton was set free. When Thompson first identified Cotton by photo, she was not convinced of her choice. "I think this is the guy," she told the police after several minutes of hesitation. As time went on, she grew surer. By the time Thompson faced Cotton in court a year later, her doubts were gone. She confidently pointed to him as the man who raped her. Because of examples like these, the U.S. justice system has been changing how eyewitnesses are used in criminal cases. Juries are told to discount the value of eyewitness testimony and ignore how confident the witnesses may be about whom they think they saw. Now, a new study of robbery investigations suggests that these changes may be doing more harm than good. © 2015 American Association for the Advancement of Science

Keyword: Learning & Memory
Link ID: 21715 - Posted: 12.22.2015

By JOSEPH LEDOUX IN this age of terror, we struggle to figure out how to protect ourselves — especially, of late, from active shooters. One suggestion, promoted by the Federal Bureau of Investigation and Department of Homeland Security, and now widely disseminated, is “run, hide, fight.” The idea is: Run if you can; hide if you can’t run; and fight if all else fails. This three-step program appeals to common sense, but whether it makes scientific sense is another question. Underlying the idea of “run, hide, fight” is the presumption that volitional choices are readily available in situations of danger. But the fact is, when you are in danger, whether it is a bicyclist speeding at you or a shooter locked and loaded, you may well find yourself frozen, unable to act and think clearly. Freezing is not a choice. It is a built-in impulse controlled by ancient circuits in the brain involving the amygdala and its neural partners, and is automatically set into motion by external threats. By contrast, the kinds of intentional actions implied by “run, hide, fight” require newer circuits in the neocortex. Contemporary science has refined the old “fight or flight” concept — the idea that those are the two hard-wired options when in mortal danger — to the updated “freeze, flee, fight.” While “freeze, flee, fight” is superficially similar to “run, hide, fight,” the two expressions make fundamentally different assumptions about how and why we do what we do, when in danger. Why do we freeze? It’s part of a predatory defense system that is wired to keep the organism alive. Not only do we do it, but so do other mammals and other vertebrates. Even invertebrates — like flies — freeze. If you are freezing, you are less likely to be detected if the predator is far away, and if the predator is close by, you can postpone the attack (movement by the prey is a trigger for attack). © 2015 The New York Times Company

Keyword: Emotions; Attention
Link ID: 21714 - Posted: 12.19.2015

Bret Stetka In June of 2001 musician Peter Gabriel flew to Atlanta to make music with two apes. The jam went surprisingly well. At each session Gabriel, a known dabbler in experimental music and a founding member of the band Genesis, would riff with a small group of musicians. The bonobos – one named Panbanisha, the other Kanzi — were trained to play in response on keyboards and showed a surprising, if rudimentary, awareness of melody and rhythm. Since then Gabriel has been working with scientists to help better understand animal cognition, including musical perception. Plenty of related research has explored whether or not animals other than humans can recognize what we consider to be music – whether they can they find coherence in a series of sounds that could otherwise transmit as noise. Many do, to a degree. And it's not just apes that respond to song. Parrots reportedly demonstrate some degree of "entrainment," or the syncing up of brainwave patterns with an external rhythm; dolphins may — and I stress may — respond to Radiohead; and certain styles of music reportedly influence dog behavior (Wagner supposedly honed his operas based on the response of his Cavalier King Charles Spaniel). But most researchers agree that fully appreciating what we create and recognize as music is a primarily human phenomenon. Recent research hints at how the human brain is uniquely able to recognize and enjoy music — how we render simple ripples of vibrating air into visceral, emotional experiences. It turns out, the answer has a lot to do with timing. The work also reveals why your musician friends are sometimes more tolerant of really boring music. © 2015 npr

Keyword: Hearing; Emotions
Link ID: 21713 - Posted: 12.19.2015