Matt Kaplan By making noise that could potentially expose them to predators, young pied babblers get their parents to give them more attentions. Begging loudly has long been viewed as an offspring’s way of saying “I’m hungry”. But in predator-filled environments, these squawks can put young birds in harm's way, and may be a form of blackmail that forces parents to pay attention and feed the youngsters more than they might otherwise. The discovery comes from a three-year analysis of a well-studied community of pied babbler (Turdoides bicolor) in the Kalahari Desert of South Africa1. Alex Thompson of the University of Cape Town and colleagues from Britain and Australia, spent more than 200 hours observing the animals in the wild and recorded more than 3,000 incidents of parents feeding fledglings. Thompson and his team noted that fledglings were fed an average of 0.12 grams of food per minute when on the ground and away from cover, but just 0.03 grams per minute when begging from the safety of the trees. Furthermore, when the birds were played an audio recording of alarm calls indicating that a ground predator was in the vicinity, parents more than doubled the amount they gave to ground-based youngsters, but made no compensation for those in the trees. Fascinated, the team speculated that the young, which were slower than adults to respond to the alarm calls and cannot escape as quickly from danger, were intentionally putting themselves into a dangerous situation when hungry to force their parents to pay attention and feed them. © 2013 Nature Publishing Group,

Keyword: Sexual Behavior; Evolution
Link ID: 18008 - Posted: 04.10.2013

By KATIE HAFNER While undressing for bed one night in 2009, Susan Spencer-Wendel noticed that the muscles in her left palm had disappeared, leaving a scrawny pile of tendons and bones. Her right hand was fine. She let out a yelp and showed the hand to her husband, who told her to go to the doctor. She was 42. Ms. Spencer-Wendel then entered a protracted period of denial. Adopted as an infant in Florida, she traveled from her home in West Palm Beach to find blood relatives living in Cyprus, who confirmed that there was no family history of her worst fear: amyotrophic lateral sclerosis, or A.L.S., the relentless disease that lays waste to muscles while leaving the mind intact. In June 2011, a doctor in Miami gave her a definitive diagnosis of A.L.S., smiling “like he was inviting me to a birthday party,” she writes in “Until I Say Goodbye: My Year of Living With Joy.” Patients with A.L.S., which is also known as Lou Gehrig’s disease, typically live no more than four years after the onset of symptoms. There is no cure. Ms. Spencer-Wendel thought she had prepared herself fully — that she would burst off the starting block like a sprinter to greet her fate. Instead, when she heard the news, “I dropped my head for the start ... and began to cry.” Her heart-ripping book chronicles what she did immediately after her diagnosis: she decided to embrace life while death chased her down. Instead of letting the world close in on her, she resolved to travel as far and as wide for as long as she could. She went to the Yukon with her best friend, Budapest with her husband, and the Bahamas with her sister. © 2013 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 18007 - Posted: 04.09.2013

By Stephani Sutherland Scientists have long known that once we nod off, certain memories grow stronger. One recent theory suggests that forgetting, too, is an essential function of sleep [see “Sleep's Secret Repairs,” by Jason Castro; Scientific American Mind, May/June 2012]. Researchers now suspect that post-traumatic stress disorder (PTSD) may emerge from flaws in sleep's forgetting process. Two studies presented at the 2012 meeting of the Society for Neuroscience in New Orleans indicate that sleep might offer a window of opportunity for weakening memories and providing relief from lingering reminders of trauma. Neuroscientists believe that during sleep, a memory-elimination routine cleans out obsolete information by physically weakening synapses, the junctions between communicating neurons. Gina Poe, a neuroscientist at the University of Michigan, found in mice that for synapses to lose strength, levels of the neurotransmitter noradrenaline must drop. Noradrenaline levels typically fall during REM sleep in rodents and humans, but in people with PTSD the amount stays high throughout sleep. Normalizing noradrenaline with pharmaceuticals, Poe says, “could absolutely be a key target to actually cure PTSD through normal sleep.” In a separate experiment, researcher Asya Rolls of Stanford University hijacked memory remodeling in sleeping mice to make a traumatic association less scary. Rolls and her colleagues conditioned mice to fear the scent of jasmine flowers by pairing the smell with a foot shock. When the mice slept, they released a puff of jasmine. Under normal circumstances, the smell would reactivate and bolster the memory, a process that requires newly made structural proteins. The researchers gave some mice a drug that prevented the manufacture of these building blocks in a key fear-memory area. When these mice woke up, they no longer responded to the odor with fearful behavior, indicating that the memory had been successfully disrupted. The findings might someday translate to a new kind of sleep-based therapy in people whose traumatic experiences are tied to specific sounds and smells—such as the noise of a bomb going off—that can be presented to their sleeping brain. © 2013 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 18006 - Posted: 04.09.2013

By DENISE GRADY SAN FRANCISCO — Scientists are trained to be skeptics, and Elizabeth H. Blackburn considers herself one of the biggest. Show her the data, and be ready to defend it. But even though she relishes the give and take, Dr. Blackburn admits to impatience at times with the questions some scientists have raised about one of her ventures. “It’s just such a no-brainer, and yet people have such difficulty understanding it,” she said. At issue is a lab test that measures telomeres, stretches of DNA that cap the ends of chromosomes and help keep cells from aging too soon. Unusually short telomeres may be a sign of illness, and Dr. Blackburn, who shared the 2009 Nobel Prize in medicine for her work on telomeres (TEEL-o-meers), thinks measuring them could give doctors and patients a chance to intervene early and maybe even prevent disease. A company she helped found expects to begin offering tests to the public later this year. Other researchers have raised doubts about the usefulness of the measurement, which does not diagnose a specific disease. But Dr. Blackburn, 64, a professor of biology and physiology at the University of California, San Francisco, says she has been convinced by a decade of data from her own team and others, linking short telomeres to heart disease, diabetes, cancer and other diseases, and to chronic stress and post-traumatic stress disorder. With studies that explore the connections among emotional stress, health and telomeres, she has delved into questions that she would have shied away from earlier in her career, as a woman trying to establish herself in science. But now, she has enough confidence and autonomy to follow the leads that intrigue her. The scope of her research has expanded tremendously, from a tight focus on molecular biology to broader questions about the implications of her work for health and public policy. © 2013 The New York Times Company

Keyword: Stress; Genes & Behavior
Link ID: 18005 - Posted: 04.09.2013

By Scicurious In his State of the Union this year, President Obama referred to increasing support for science and technology, and mentioned the “Brain Activity Map”. Of course neuroscientists were instantly atwitter. It was the first we’d all heard of any Brain Activity Map. What is it? What did it mean? After a lot of speculation and some quickly formed opinions about whether or not it was a good idea…the White House has now unveiled what the project actually is: BRAIN, Brain Research through Advancing Innovative Neurotechnologies. And what is the project exactly? Will the BRAIN project end up as a BAM (Brain Activity Map)? Or a BUST (Badly Underfunded S**T)? I’d like to explore what I know, and I’d like to hear what everyone else knows as well. Am I wrong? Am I too optimistic? Too pessimistic? Have at. What is the BRAIN Project about? What are its goals? Well, nobody knows, actually. I certainly don’t know. But it appears that no one else knows either. “This working group, co-chaired by Dr. Cornelia “Cori” Bargmann (The Rockefeller University) and Dr. William Newsome (Stanford University), is being asked to articulate the scientific goals of the BRAIN initiative and develop a multi-year scientific plan for achieving these goals, including timetables, milestones, and cost estimates.” So basically, BRAIN is a very fancy initiative, with a fancy name…and so far, no goals. And of course, we’re all excited and trying to figure out what it’s going to be and whether or not it will work. Maybe it would have been in the better interest of the White House to wait until there were…you know, goals. But there is one goal that seems established here: new technologies. © 2013 Scientific American

Keyword: Brain imaging
Link ID: 18004 - Posted: 04.09.2013

By Sara Reardon and Bob Holmes, When President Obama called for $100 million in federal funding last week to map the human brain, he said he was hoping to “unlock the mystery of the three pounds of matter that sits between our ears.” Scientists hope that tracking brain activity neuron by neuron — an effort now called the Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative — will revolutionize our understanding of brain function in the same way that the Human Genome Project is transforming our understanding of our genes. But just how do you go about mapping a brain? This is a question that two projects with similar lofty goals are already grappling with. The Human Brain Project aims to do it by creating a computer simulation of the entire brain. The Human Connectome Project is using magnetic resonance imaging to track the fibers that connect different regions of the brain on the millimeter scale, giving a rough-grained road map of the brain. To succeed, researchers will need to find noninvasive ways to record the firing of individual neurons, because all current methods involve opening the skull and, often, sticking electrodes into brain tissue. “Right now, you’re literally driving posts into the brain. It’s not very sophisticated,” says neurobiologist John Ngai of the University of California at Berkeley. A few groups are working on new approaches. The MindScope project at the Allen Institute for Brain Science in Seattle aims to map the visual cortex of mice. The team identifies where neurons are firing by injecting the brain with dyes or using genetically engineered proteins that bind to calcium molecules. When a neuron fires, calcium flows into the cell and activates the dye or protein. © 1996-2013 The Washington Post

Keyword: Brain imaging
Link ID: 18003 - Posted: 04.09.2013

By DOUGLAS QUENQUA The French geneticist Jérôme Lejeune discovered more than 50 years ago that Down syndrome is caused by the presence of an extra copy of chromosome 21. But to this day it has remained a mystery why that results in impaired physical and cognitive development. Now researchers at the Sanford-Burnham Medical Research Institute think they have found a clue. The scientists, who were investigating Alzheimer’s disease, found that mice that lacked a protein known as SNX27 had many of the same learning and memory defects as mice with Down syndrome. Looking at the brains of people with the syndrome, the researchers discovered that they, too, lacked SNX27. While chromosome 21 is not directly involved in SNX27 production, it does encode a regulator — miR-155 — that inhibits production. According to the study, published in the journal Nature Medicine, levels of miR-155 in the brains of people with Down syndrome correlate almost exactly with the decrease in SNX27. “In the brain, SNX27 keeps certain receptors on the cell surface — receptors that are necessary for neurons to fire properly,” said the study’s senior author, Huaxi Xu, in a statement released by the institute. “So in Down syndrome, we believe lack of SNX27 is at least partly to blame for developmental and cognitive defects.” To test their findings, Dr. Xu’s team introduced more SNX27 to mice with Down syndrome. As they expected, the mice showed immediate improvements in cognitive function and behavior. Now the researchers are investigating molecules that might increase production of SNX27 in the human brain. © 2013 The New York Times Company

Keyword: Development of the Brain; Genes & Behavior
Link ID: 18002 - Posted: 04.09.2013

By Linda Carroll, Kate Snow and Meghan Frank, NBC News As a little girl, Bonnie Ihme had big plans. Bright and artistically talented, she dreamed of becoming an architect. But the older she got, the more distant that dream seemed. By third grade, school had become a struggle. She felt easily distracted and found it impossible to focus in class. Eventually she abandoned her plan to be an architect. Ihme got married, had two kids and began cleaning houses and helping her husband with his business. But even that simpler life felt impossibly difficult. The Michigan mom had trouble keeping track of all the threads of her life. She’d send her kids to school without sneakers on gym day. She’d forget to bring library books back. She felt more overwhelmed than ever before. “I really would try hard to pull it all together,” Ihme told NBC’s Kate Snow in an interview airing on Rock Center Friday. “But when … you’re late for a Christmas concert that your daughter was really looking forward to going to and we get there and her class is walking back to the classroom and the tears in her eyes… you try harder.” Ihme saw history repeating itself in her 10-year-old son, Jacob, who began struggling with school, just as she had. Jacob would spend hours doing his homework, only to forget to bring it to school the next morning. Ihme’s heart ached for her son. © 2013 NBCNews.com

Keyword: ADHD
Link ID: 18001 - Posted: 04.08.2013

Barry Gordon, professor of neurology and cognitive science at the Johns Hopkins University School of Medicine, replies: We are aware of a tiny fraction of the thinking that goes on in our minds, and we can control only a tiny part of our conscious thoughts. The vast majority of our thinking efforts goes on subconsciously. Only one or two of these thoughts are likely to breach into consciousness at a time. Slips of the tongue and accidental actions offer glimpses of our unfiltered subconscious mental life. The intrusive thoughts you may experience throughout the day or before bed illustrate the disconcerting fact that many of the functions of the mind are outside of conscious control. Whether we maintain true control over any mental functions is the central debate about free will. Perhaps this lack of autonomy is to be expected as the foundations for almost all the mind's labors were laid long before our ancestors evolved consciousness. Even deliberate decisions are not completely under our power. Our awareness only sets the start and the end of a goal but leaves the implementation to unconscious mental processes. Thus, a batter can decide to swing at a ball that comes into the strike zone and can delineate the boundaries of that zone. But when the ball comes sailing through, unconscious mental functions take over. The actions required to send him to first base are too complex and unfold too quickly for our comparatively slow conscious control to handle. © 2013 Scientific American

Keyword: Sleep; Consciousness
Link ID: 18000 - Posted: 04.08.2013

Steve Connor Fear may be felt in the heart as well as the head, according to a study that has found a link between the cycles of a beating heart and the likelihood of someone taking fright. Tests on healthy volunteers found that they were more likely to feel a sense of fear at the moment when their hearts are contracting and pumping blood around their bodies, compared with the point when the heartbeat is relaxed. Scientists say the results suggest that the heart is able to influence how the brain responds to a fearful event, depending on which point it is at in its regular cycle of contraction and relaxation. Sarah Garfinkel, a researcher at the Brighton and Sussex Medical School, said: “We demonstrate for the first time that the way in which we process fear is different dependent on when we see fearful images in relation to our heart.” The study, to be presented today at the British Neuroscience Association Festival in London, tested the fear response of 20 healthy volunteers as they were shown images of fearful faces while connected to heart monitors. “Our results show that if we see a fearful face during systole – when the heart is pumping – then we judge this fearful face as more intense than if we see the very same fearful face during diastole – when the heart is relaxed,” Dr Garfinkel said. “From previous research, we know that if we present images very fast then we have trouble detecting them, but if an image is particularly emotional then it can ‘pop’ out and be seen. © independent.co.uk

Keyword: Emotions
Link ID: 17999 - Posted: 04.08.2013

Scientists have identified a group of brain cells which have the power to control appetite and could be a major cause of eating disorders such as obesity. In experiments in rodents, cells called tanycytes were found to produce neurons which specifically regulate appetite. The University of East Anglia researchers say their find means appetite is not fixed at birth. Their study is published in the Journal of Neuroscience. It was previously thought that nerve cells in the brain associated with appetite regulation were generated entirely during an embryo's development in the womb and could not be altered. But the UEA study's discovery of these tanycytes, which act like stem cells, in the brains of young and adult rodents shows that appetite can be modified. Researchers looked in detail at the hypothalamus section of the brain, which is known to regulate sleep, energy expenditure, appetite, thirst and many other critical biological functions. They studied the nerve cells that regulate appetite using a 'genetic fate mapping' technique and found that some cells added neurons to the appetite-regulating circuitry of the mouse brain after birth and into adulthood. BBC © 2013

Keyword: Obesity
Link ID: 17998 - Posted: 04.08.2013

Steve Connor The rise in the number of overweight children in Britain may be as much to do with their genes as their diet and exercise levels, according to a study that has identified a handful of genetic mutations linked with childhood obesity. Scientists have discovered that children with the most severe kinds of obesity are more likely than other children to have one or more of four genetic variations in their DNA, which could influence such things as appetite and food metabolism. The discovery is part of a wider search for the genes involved in increasing a person’s risk of becoming overweight when exposed to an “obesogenic environment” of high-calorie food and inactivity – which is known to affect some people more than others. The study looked at 1,000 children with the most severe form of early-onset obesity, which is highly likely to result in obesity in adulthood. Some of the 10-year-olds in the study weighed between 80kg and 100kg (12.5st-15.7st). Some of the genetic variations revealed by the study were rare but others are relatively common, suggesting an interaction between genetics and environment, which could explain why certain children become obese while others do not even when they share a similar upbringing. Obesity among British children aged between two and ten has risen since 1995 from 10.1 per cent to 13.9 per cent in 2011. This rise cannot be due to a change in genes alone, because it takes many generations to alter the frequency of genetic mutations in the population. © independent.co.uk

Keyword: Obesity; Genes & Behavior
Link ID: 17997 - Posted: 04.08.2013

By Neuroskeptic Last year, there was quite a bit of excitement over a “Genetic Test To Predict Risk for Autism”. The test was revealed in a paper in Molecular Psychiatry, by Australian researchers Skafidas and colleagues. The claim was that a statistical classifier could spot patterns of genetic variation that differed between people with autism and healthy controls – with 70% accuracy. For a good discussion of the paper, including comments from the lead author, see here. However, a Letter to Molecular Psychiatry has just cast doubt on the whole thing. The authors write A classifier was recently reported to predict with 70% accuracy if an individual has an autism spectrum disorder using 237 single-nucleotide polymorphisms (SNPs). Biomarkers, genetic or otherwise, that would facilitate earlier autism spectrum disorder diagnosis are crucial; therefore, these results warrant careful scrutiny. So scrutinize it they do, and they find it wanting: In other words, the ‘autism’ genetic variants were indeed more common in the autism cases, compared to controls, but only because the cases and controls were from different places. The classifier worked, but it wasn’t detecting autism, it was detecting ancestry.

Keyword: Autism; Genes & Behavior
Link ID: 17996 - Posted: 04.08.2013

By Rachel Ehrenberg A computer can decode the stuff of dreams. By comparing brain activity during sleep with activity patterns collected while study participants looked at certain objects, a computer learned to identify some contents of people’s unconscious reveries. “It’s striking work,” says cognitive psychologist Frank Tong of Vanderbilt University in Nashville, who was not involved in the research. “It’s a demonstration that brain activity during dreaming is very similar to activity during wakefulness.” The work, reported April 4 in Science by Japanese researchers led by Yukiyasu Kamitani of Advanced Telecommunications Research Institute International, adds to somewhat scant knowledge of how the brain constructs dreams, says Tong. The research could lead to a better understanding of what the brain does during different states of consciousness, such as those experienced by some coma patients. Dreams are a bit of a black box and difficult to study. Experiments with mice have revealed aspects of sleep and dreaming, such as how the experiences contribute to forming memories. But a mouse can’t tell you what it dreamed about. And the sleep stage that’s richest in dreams — REM sleep — typically kicks in about 90 minutes after a person conks out, making it time consuming to gather data on dreams. The noisy fMRI brain scanning machine doesn’t help. To skirt these experimental issues, the researchers recorded brain activity in three adult male volunteers during the early stages of sleep. After the subjects had dozed off, they were repeatedly awakened and asked for detailed reports on what they had seen while sleeping. In an example, one participant stated: “Well, there were persons, about three persons, inside some sort of hall. There was a male, a female and maybe like a child. Ah, it was like a boy, a girl and a mother. I don't think that there was any color.” © Society for Science & the Public 2000 - 2013

Keyword: Sleep; Brain imaging
Link ID: 17995 - Posted: 04.05.2013

by Gisela Telis Insomniacs desperate for some zzzs may one day have a safer way to get them. Scientists have developed a new sleep medication that has induced sleep in rodents and monkeys without apparently impairing cognition, a potentially dangerous side effect of common sleep aids. The discovery, which originated in work explaining narcolepsy, could lead to a new class of drugs that help people who don't respond to other treatments. Between 10% and 15% of Americans chronically struggle with getting to or staying asleep. Many of them turn to sleeping pills for relief, and most are prescribed drugs, such as zolpidem (Ambien) and eszopiclone (Lunesta), that slow down the brain by binding to receptors for GABA, a neurotransmitter that's involved in mood, cognition, and muscle tone. But because the drugs target GABA indiscriminately, they can also impair cognition, causing amnesia, confusion, and other problems with learning and memory, along with a number of strange sleepwalking behaviors, including wandering, eating, and driving while asleep. This has led many researchers to seek out alternative mechanisms for inducing sleep. Neuroscientist Jason Uslaner of Merck Research Laboratories in West Point, Pennsylvania, and colleagues decided to tap into the brain's orexin system. Orexin (also known as hypocretin) is a protein that controls wakefulness and is missing in people with narcolepsy. Past studies successfully induced sleep by inhibiting orexin, but had not looked into its effects on cognition. The researchers developed a new orexin-inhibiting compound called DORA-22 and confirmed that it could induce sleep in rats and rhesus monkeys as effectively as the GABA-modulating drugs. © 2010 American Association for the Advancement of Science.

Keyword: Sleep
Link ID: 17994 - Posted: 04.05.2013

By Nathan Seppa Tiny components of amyloid plaques, the notorious protein clumps found littering the brains of people with Alzheimer’s disease, might fight inflammation. Researchers report that several of these sticky protein fragments, or peptides, glom onto inflammatory compounds and reverse paralysis in mice that have a condition similar to multiple sclerosis. A fragment of tau protein, which shows up in other brain deposits in Alzheimer’s patients, has a similar effect. When tested on blood taken from three MS patients, the tau peptide weeded out some inflammatory culprits there, too, researchers report in the April 3 Science Translational Medicine. “This is a seriously good study. It opens up more questions than it answers,” says Jian-Guo Geng, a cell biologist at the University of Michigan in Ann Arbor who wasn’t part of the research team. “But I don’t think we’re anywhere close to using these peptides for treatments.” Amyloid is a broad term for clusters of protein in the brain, including those arising with the aid of misfolded versions of tau or another protein implicated in brain disease called a prion. Viewing amyloid-forming peptides as good guys runs against the scientific thinking, since amyloid plaques are a hallmark of Alzheimer’s disease. But study coauthor Lawrence Steinman, a neurologist at Stanford University, points out that the actual role of amyloid plaques in the disease is unclear. He suggests the tiny peptides holding the plaques together might have an alternative, useful role in the body. © Society for Science & the Public 2000 - 2013

Keyword: Alzheimers
Link ID: 17993 - Posted: 04.05.2013

Genetic markers that could help highlight who is at risk of developing Alzheimer's disease have been identified by US scientists. The research in Neuron identifies mutations that affect the build-up of certain proteins in the brain. High levels of these tau proteins increase the chance of having the disease. UK experts said the study could help understand the changes that occur in the brains of Alzheimer's patients. Tangles of a kind of tau called phosphorylated tau (ptau) are a hallmark of the disease. One of the new gene variants identified by the Washington University School of Medicine team was also shown to be linked to a small increased risk of developing Alzheimer's and a greater risk of cognitive decline. The team used genetic information from more than 1,200 people, significantly larger than previous studies in this area. Dr Alison Goate, who led the study, said: "We anticipate that knowledge about the role of these genes in Alzheimer's disease may lead to the identification of new targets from therapies or new animal or cellular models of the disease. Lifestyle 'plays a role' UK experts said the study adds to the number of genetic markers that have been linked to the development of Alzheimer's disease. BBC © 2013

Keyword: Alzheimers; Genes & Behavior
Link ID: 17992 - Posted: 04.05.2013

By Puneet Kollipara Rats that will go to great lengths to get a cocaine fix might blame a group of sluggish neurons. Controlling the problem may come down to a flick of a light switch: Stimulating those brain cells with lasers reduces the addicted rats’ cocaine use, researchers report in the April 4 Nature. “It's an outstanding piece of work,” says neuroscientist A.J. Robison of Michigan State University, who wasn’t involved in the study. The findings could help researchers better understand the role of neural circuitry in drug addiction in humans, he says. Scientists know that when certain neurons fire less frequently in the prelimbic cortex, a brain region that handles impulse control and reward-driven behavior, a person’s self-control can decrease. But researchers didn’t know whether using cocaine chronically could make the neurons drowsy to begin with, and whether that sluggishness could also promote drug use in spite of ill consequences. Billy Chen, then of the National Institutes of Health, and colleagues trained rats to take cocaine. The rats learned to press levers to receive a dose of drug through an IV. After about two months, researchers started giving the rats shocks roughly one-third of the time when the animals pressed the levers. Most of the rats stopped taking cocaine, but about 30 percent continued. These were compulsive cocaine users, says coauthor Antonello Bonci, a neuroscientist at the NIH’s National Institute on Drug Abuse. © Society for Science & the Public 2000 - 2013

Keyword: Drug Abuse
Link ID: 17991 - Posted: 04.05.2013

by Emily Underwood For neuroscientist Rafael Yuste, sitting in an ornate White House chamber yesterday listening to President Barack Obama heap praise—and some $100 million—on a brain-mapping initiative that he helped hatch was a "luminous" experience. "It felt like history," says the researcher, who works at Columbia University. "There is this enormous mystery waiting to be unlocked," Obama told the East Room crowd packed with leaders of American neuroscience during a 12-minute paean to brain research (likely the most expansive yet delivered by an American president). By "giving scientists the tools they need to get a dynamic picture of the brain in action," he said, the new initiative will help scientists find a cure for complex brain processes such as traumatic brain injury and Parkinson's, and create jobs that "we haven't even dreamt up yet." For all the lofty rhetoric, however, the White House didn't provide many details about how the BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative will accomplish its mission. And the lack of detail is worrying not only BRAIN skeptics—who argue that it targets the wrong goal and could detract from other research efforts—but also even some staunch advocates such as Yuste. The way that the White House has packaged and plans to fund and coordinate the initiative, they say, is creating some unease. "As the proposal stands, it's still awfully vague, so it's hard not to have some reservations," says biophysicist Jeremy Berg of the University of Pittsburgh in Pennsylvania, who is a former director of the National Institute of General Medical Sciences at the National Institutes of Health (NIH). © 2010 American Association for the Advancement of Science

Keyword: Brain imaging
Link ID: 17990 - Posted: 04.05.2013

Dana Smith In January, the European Commission pledged 500 million euros to work towards creating a functional model of the human brain. Then, yesterday, Barack Obama officially announced an initiative to advance neuroscience, funding a large-scale research project aimed at unlocking the secrets of the brain that involves over $100 million in federal spending in the first year alone, as well as investments from private organizations. Both projects are geared towards creating a working model of the brain, mapping its 100 billion neurons. The first, the Human Brain Project, is being spearheaded by Professor Henry Markram of École Polytechnique Fédérale de Lausanne. Together with collaborators from 86 other European institutions, they aim to simulate the workings of the human brain using a giant super computer. This would mean compiling information about the activity of individual neurons and neuronal circuits throughout the brain in a massive database. They then hope to integrate the biological actions of these neurons to create theoretical maps of different subsystems, and eventually, through the magic of computer simulation, a working model of the entire brain. Neurologic and psychiatric disorders collectively "affect 100 million Americans and cost us $500 billion each year in terms of health-care costs." Similarly, the United States' recently renamed Brain Research Through Advancing Innovative Neurotechnologies, or BRAIN (previously the Brain Activity Map Project, or BAM), is an initiative that will be organized through the National Institutes of Health, National Science Foundation, and Defense Advanced Research Projects Agency, and carried out in a number of universities and research institutes throughout the U.S. © 2013 by The Atlantic Monthly Group.

Keyword: Brain imaging
Link ID: 17989 - Posted: 04.05.2013