By Felicity Muth This move from my old site to the Scientific American network has also coincided with my own physical move from the UK to the USA to start some new research. Given this is the closing of a chapter of my life (or rather, my PhD thesis, which will now no doubt sit on a dusty shelf somewhere until a grad student picks it up in 10 years time to use as a door stop), I felt now might be an appropriate time to write a little bit about what I have been doing for the past three years. In the past I have only written about other people’s research, but given that I am now a few months beyond the shock (I will resist using the word ‘trauma’ here) of it ‘all being over’, I feel like it might be time now to share a bit of what I did over my PhD. In one of my first meetings with my PhD supervisor, she said to me, ‘The way that I see it, you can either spend three months reading the limited amount of literature in your subject area, or you can go to Africa and get some data for yourself.’ This may have been the point where I realised I had chosen a good topic to study. Not only did not having much ‘literature’ to read due to the dearth of previous work done on this topic mean that I could kid myself that I was an ‘expert’ in the field after a few weeks, it was also liberating to know that most experiments that I carried out would be finding out new things. So, even before moving my books into my new PhD office, I was on a plane to Botswana to collect data on the nest building behaviour of the Southern masked weaverbird. When I tell people that the aim of my research is to work out how birds learn how to build nests, I usually get one of two responses. The first is, ‘they don’t learn anything of course, nest building in birds is innate.’ The other response is ‘surely that’s been done already?’ But actually, both of these (perfectly reasonable) assumptions are incorrect. © 2013 Scientific American,

Keyword: Learning & Memory
Link ID: 17939 - Posted: 03.23.2013

By Gary Stix A little shuteye refreshes. Right, but what does that really mean? Not talking here about leaping out of bed ready for a five-mile run upon awakening, but rather about what’s happening at the level of individual brain cells deep inside your head. A new study by R. Douglas Fields, a pioneer in researching out-of-the-mainstream brain areas and neural activity, holds one promising suggestion. Fields’s team at the National Institutes of Child Health and Development in Bethesda, Maryland, built on an earlier observation that during sleep (or even when just chilling out), neural signals travel the “wrong way” in cells of a critical region of the hippocampus, the brain structure involved with forming some types of new memories. The new study by Fields demonstrates, in a lab dish, that this reverse trafficking functions as a form of “editing,” a physical paring back of inessential parts of a brain cell to ensure that you don’t forget what you learned the previous day. Specifically, electrical signals in the CA1 area of the hippocampus reverse direction like the opposite flow of cars during the evening rush hour. The spiking electrical pulses move up instead of down the long extensions of nerve cells known as axons. The train of spikes pass through the cell body where the nucleus resides before reaching the ends of thousands of tiny branching tendrils called dendrites. © 2013 Scientific American

Keyword: Sleep
Link ID: 17938 - Posted: 03.23.2013

Arran Frood Two studies have decoded the structure of two of the brain's serotonin receptors. Here shown is a receptor known as 1B with the migraine drug ergotamine (pink) locked into one of its binding pockets. Researchers have deciphered the molecular structures of two of the brain's crucial lock-and-key mechanisms. The two molecules are receptors for the natural neurotransmitter serotonin — which regulates activities such as sleep, appetite and mood — and could provide targets for future drugs to combat depression, migraines or obesity. “This is huge,” says Bryan Roth, a neuropharmacologist at the University of North Carolina Chapel Hill Medical School, and a co-author of the two studies published in Science today1, 2. “Before this there was no crystal structure for any serotonin receptor. A lot of what was theoretical is now known with a great degree of certainty,” he says. Scientists have been trying to decipher serotonin receptors for years. Armed with information on the atomic level, they might now be able to make breakthroughs in drug discovery and in understanding how the physical structures of the brain produce consciousness, says Roth. Christoph Anacker, a neuropharmacologist at King's College London, agrees that the findings are important for drug discovery. “These receptors are involved in so many conditions, especially depression, and knowing the molecular structures will help to develop more specific drugs and avoid the expression of undesired side effects.” © 2013 Nature Publishing Group,

Keyword: Depression
Link ID: 17937 - Posted: 03.23.2013

Joshua P. Johansen Anxiety does not arise from a single neural circuit. An interplay between neighbouring, yet opposing, circuits produces anxiety, and outputs from these circuits regulate specific anxiety responses. We all know anxiety. We might have experienced it while waiting to hear about a promotion at work, or on our way to see the doctor because she wants to talk about test results in person. A diffuse uneasiness, sometimes accompanied by perspiration and subtle changes in breathing, anxiety ebbs and flows depending on life's circumstances, and can even occur for no apparent reason. The condition can be healthy and adaptive, but research in the United States1 shows that, for roughly one-third of people, anxiety is a debilitating disorder at some point in their lives. Nevertheless, answers to important questions — such as how different neuronal populations represent anxiety, and how the various components of the anxious state are constructed and represented in neural circuits — remain elusive. In two papers published on Nature's website today, Jennings et al.2 and Kim et al.3 address these questions using optogenetics to manipulate distinct neuronal subpopulations in mice and so dissect out the contribution of intermixed but functionally distinct cell groups. Both teams analysed a large, diffuse brain region called the bed nucleus of the stria terminalis (BNST). Previous studies4, 5, 6, 7 have found that lesions of the BNST reduce anxiety and fear of specific environments. Other work has discovered8, 9 distinct subregions and subpopulations of BNST neurons, and has found that the region has connections with several other brain areas that are involved in motivated behaviour and stress responses. However, the functions of the various BNST subpopulations and subregions, as well as the significance of these connections, have remained unclear. © 2013 Nature Publishing Group,

Keyword: Emotions; OCD - Obsessive Compulsive Disorder
Link ID: 17936 - Posted: 03.23.2013

by Emily Underwood Hallucinations and paranoia aren't the only symptoms that make life difficult for people with schizophrenia. Problems with memory and other cognitive functions also interfere with daily tasks, such as remembering the way to the office or balancing a checkbook. Now, by dampening the activity of a small group of neurons deep within the mouse brain, researchers have produced cognitive deficits similar to those found in those with schizophrenia, a discovery that they say could potentially lead to new treatments for the disorder, which affects roughly 24 million people worldwide. There's an ongoing debate over how much mice can mirror human psychiatric diseases, ranging from autism to depression. Still, neuroscientists often turn to rodents to study specific features of these human conditions. One abnormality that researchers have observed in functional magnetic resonance imaging scans of the brains of people with schizophrenia is an unusually low level of activity from a specific group of neurons near the brain stem. Called the mediodorsal thalamus (MD), the region appears to work with the prefrontal cortex—an area associated with planning and decision-making—to carry out tasks that require us to remember and process multiple pieces of information at once. (Going to the kitchen to fetch something, while remembering what it was you needed, for example.) In the past, scientists have studied the effects of low brain activity in the MD by cutting it out in mice—an extreme measure that didn't accurately mimic the "mild" reduction in activity seen in schizophrenia, says Columbia University psychiatrist Joshua Gordon. To create a more realistic mouse model of low MD activity, the team devised a new method that uses a virus to embed into the surface of MD neurons receptors that block cellular activity in the presence of a compound called clozapine-N-oxide. The beauty of this approach is its "exquisite specificity," Gordon says—it targets only neurons in the MD, and you can control how many neurons get shut down. © 2010 American Association for the Advancement of Science

Keyword: Schizophrenia
Link ID: 17935 - Posted: 03.23.2013

By Tina Hesman Saey Like many women with parents of the Mad Men generation, Susan Murphy grew up in a household full of cigarette smoke. Both dad and mom smoked heavily, even while Murphy was still in her mother’s womb. “That explains a lot,” Murphy quips, poking fun at herself. But Murphy isn’t worried about her own health. She’s fine. Her children aren’t, though. One boy died of cancer as a toddler. Another has autism. And her daughter has attention deficit disorder. Murphy knows the scientific evidence isn’t in yet, but she still can’t help wondering whether their fates might have been affected by her exposure to tobacco smoke before she was born. Murphy, a researcher at Duke University, studies links between a mother’s diet and chemical exposures during pregnancy with the child’s later health. She and others have established that the womb is the antithesis of Las Vegas; what happens there not only doesn’t stay there, it can influence a child’s health for life. Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring. Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down. © Society for Science & the Public 2000 - 2013

Keyword: Epigenetics; Genes & Behavior
Link ID: 17934 - Posted: 03.23.2013

By Smitha Mundasad Health reporter, BBC News The risk of developing autism may be passed on through - and not just to - future generations, researchers say. The international study suggests older fathers are more likely to have grandchildren with autism than their younger counterparts. The mechanism is unclear but it is thought they may transmit "silent mutations" to their grandchildren. But experts have urged caution, stressing autism is the result of many different factors. The study, looking at almost 6,000 people with the condition, is published in the journal Jama Psychiatry. According to the National Autistic Society, more than one in every 100 people in the UK have the condition. Previous studies suggested older fathers may be at greater risk of having children with autism than younger dads. But the team of UK, Swedish and Australian researchers say this is one of the first pieces of evidence to show the risk can be passed on through - rather than just straight to - future generations. The "silent mutations" - changes in genetic material - are likely to have no obvious impact on older fathers' own children, but they may build up through subsequent generations, or interact with other genes and environmental factors, to increase the chance of their grandchildren developing the condition, the researchers say. BBC © 2013

Keyword: Autism; Epigenetics
Link ID: 17933 - Posted: 03.23.2013

by Peter Aldhous Women abused in childhood are more likely to have children with autism, a new epidemiological study suggests. The finding adds a disturbing new dimension to the heated debate over the condition's underlying causes. Andrea Roberts of the Harvard School of Public Health suspected that there might be a link between childhood abuse and having an autistic child: women abused early in life are more likely to smoke, suffer from gestational diabetes and have premature babies – all factors that may affect fetal brain development. To investigate, Roberts and her colleagues turned to the Nurses' Health Study II, which includes almost 55,000 women who had indicated if they had a child with autism spectrum disorder and also answered a questionnaire about their experience of abuse as a child. This allowed the researchers to develop a scale rating all the women for the intensity of abuse in their childhood. There was a clear link between the "dose" of abuse received and the risk of having an autistic child. "The associations get stronger as the level of abuse increases," Roberts says. After accounting for demographic factors such as age and socioeconomic status, the 2 per cent of women who reported the most serious childhood abuse – who were frequently hit and also sexually abused – were about 3.5 times as likely to have a child with autism as those who reported no abuse at all. "I think it's a really interesting, innovative and well-conducted study," says Hannah Gardener at the University of Miami in Florida. "There aren't a lot of risk factors with that magnitude." © Copyright Reed Business Information Ltd.

Keyword: Autism; Epigenetics
Link ID: 17932 - Posted: 03.23.2013

At 7 months of age, children who are later diagnosed with autism take a split second longer to shift their gaze during a task measuring eye movements and visual attention than do typically developing infants of the same age, according to researchers supported by the National Institutes of Health. The difference between the groups’ test results was 25 to 50 milliseconds on average, the researchers found, too brief to be detected in social interactions with an infant. However, they showed that this measurable delay could be accounted for by differences in the structure and organization of actively developing neurological circuits of a child’s brain. Image of brain structure known as the splenium of the corpus callosum When they were infants, children who were later diagnosed with autism took longer to shift their gaze during a measure of eye movements than did infants who were not diagnosed with autism. The researchers believe that brain circuits involved with a brain structure known as the splenium of the corpus callosum (shown in this scan) may account for the differences in gaze shifting between the two groups. Image courtesy of Jason Wolff, Ph.D., University of North Carolina at Chapel Hill. Efficiently shifting attention early in infancy is thought to be important for later social and cognitive development. Split-second delays, the researchers suggested, could be a precursor to such well known symptoms of autism as difficulty making eye contact or following a parent’s pointing finger, problems that generally emerge after a child turns 1. Typically, autism spectrum disorder (ASD) is not diagnosed until after 3 or 4 years of age. The study appears in the American Journal of Psychiatry.

Keyword: Autism; Vision
Link ID: 17931 - Posted: 03.23.2013

By Bruce Bower Malnutrition in the first year life, even when followed by a good diet and restored physical health, predisposes people to a troubled personality at age 40, new research suggests. The study of 77 formerly malnourished people represents the first evidence linking malnutrition shortly after birth to adult personality traits. The traits in some cases may foretell psychiatric problems, says a team led by psychiatrist Janina Galler of Harvard Medical School in Boston and psychologist Paul Costa of Duke University Medical Center in Durham. Compared with peers who were well-fed throughout their lives, formerly malnourished men and women reported markedly more anxiety, vulnerability to stress, hostility, mistrust of others, anger and depression, Galler’s team reports March 12 in the Journal of Child Psychology and Psychiatry. Survivors of early malnutrition also cited relatively little intellectual curiosity, social warmth, cooperativeness and willingness to try new experiences and to work hard at achieving goals. Previous studies of people exposed prenatally to famine have reported increased rates of certain personality disorders and schizophrenia. Another investigation found that malnutrition at age 3 predisposed youngsters on the Indian Ocean island of Mauritius to delinquent and aggressive behavior at ages 8, 11 and 17. As is true in the new study, distrust of others, anxiety and depression often accompany high levels of anger, says psychologist Adrian Raine of the University of Pennsylvania in Philadelphia, who directed the Mauritius research. “Poor nutrition early in life seems to predispose individuals to a suspicious personality, which may then fuel a hostile attitude toward others,” Raine proposes. © Society for Science & the Public 2000 - 2013

Keyword: Development of the Brain; Emotions
Link ID: 17930 - Posted: 03.23.2013

By Meghan Rosen Shushing neural chitchat in mouse brains can spark schizophrenia-like symptoms, a new study suggests. The findings are the first to demonstrate — at least in mice — that curbing communication among neurons in certain parts of the brain can cause some of the cognitive problems associated with schizophrenia. By muzzling neurons in the mediodorsal thalamus, or MD — a cell cluster that sends signals to the brain’s outer layer — researchers hindered mouse memory and learning in much the same way that schizophrenia seems to do in humans, scientists report March 20 in Neuron. Cognitive problems in schizophrenia have long been a mystery to scientists and a troubling symptom for people with the condition. The findings suggest that the problems stem from the thalamus, says neuropsychologist Neil Woodward of Vanderbilt University in Nashville, who was not involved with the new work. People with schizophrenia suffer from a range of debilitating symptoms: hallucinations, delusions and social disorders, says study coauthor Christoph Kellendonk of Columbia University. Patients also have problems with short-term memory and learning. Unlike other symptoms, these cognitive problems have been nearly impossible to treat. Brain imaging of people with schizophrenia had previously linked cognitive defects to changes in the MD — part of a walnut-sized chunk of gray matter snuggled above the brain stem. Normally, the MD relays information to and from the prefrontal cortex, the brain region behind the forehead that controls complex thought. In people with schizophrenia, the imaging showed, the MD is unusually quiet. © Society for Science & the Public 2000 - 2013

Keyword: Schizophrenia; Brain imaging
Link ID: 17929 - Posted: 03.23.2013

by Sara Reardon When she returned from serving in the Gulf conflict in 1991, US Air Force nurse Denise Nichols experienced sudden aches, fatigue and cognitive problems, but had no idea 'what was causing them. They grew worse: even helping her daughter with multiplication tables became difficult, she says, and eventually she had to quit her job. Nichols wasn't alone. About a third of Gulf war veterans – possibly as many as 250,000 – returned with a similar set of symptoms. Now an imaging study has found that these veterans have what appear to be unique structural changes in the wiring of their brains. This fits with the scientific consensus that Gulf War syndrome (GWS) is a physical condition rather than a psychosomatic one, and should be treated with painkilling drugs instead of counselling. The military in various countries has in the past consistently denied that there is a physical basis to GWS. Although the US Department of Veterans Affairs (VA) now officially accepts that the disorder is physical, the issue has been mired in controversy. Earlier this month, Steven Coughlin, a former senior epidemiologist at the VA, testified to a Congressional panel that the VA had suppressed and manipulated research data so as to suggest that the disorder was psychosomatic. © Copyright Reed Business Information Ltd.

Keyword: Stress; Brain imaging
Link ID: 17928 - Posted: 03.23.2013

A staggering 1 in 3 seniors dies with Alzheimer's disease or other types of dementia, says a new U.S. report that highlights the impact the mind-destroying disease is having on the rapidly aging population. Dying with Alzheimer's is not the same as dying from it. But even when dementia isn't the direct cause of death, it can be the final blow — speeding someone's decline by interfering with their care for heart disease, cancer or other serious illnesses. That's the assessment of the report released Tuesday by the Alzheimer's Association, which advocates for more research and support for families afflicted by it. "Exacerbated aging," is how Dr. Maria Carrillo, an association vice president, terms the Alzheimer's effect. "It changes any health care situation for a family." In fact, only 30 per cent of 70-year-olds who don't have Alzheimer's are expected to die before their 80th birthday. But if they do have dementia, 61 per cent are expected to die, the report found. Already, 5.2 million Americans have Alzheimer's or some other form of dementia. Those numbers will jump to 13.8 million by 2050, Tuesday's report predicts. That's slightly lower than some previous estimates. Count just the deaths directly attributed to dementia, and they're growing fast. Nearly 85,000 people died from Alzheimer's in 2011, the U.S. Centers for Disease Control and Prevention estimated in a separate report Tuesday. Those are people who had Alzheimer's listed as an underlying cause on a death certificate, perhaps because the dementia led to respiratory failure. Those numbers make Alzheimer's the sixth leading cause of death. © CBC 2013

Keyword: Alzheimers
Link ID: 17927 - Posted: 03.20.2013

Nursing home residents who take a class of sleep medications that includes Lunesta and Ambien may be at higher risk for hip fractures compared with those who do not take these nonbenzodiazepine hypnotic drugs, according to a Harvard Medical School study. The study involved more than 15,000 nursing home residents who were on average 81 years old and were documented by Medicare to have had a hip fracture between July 2007 and December 2008. Nearly 11 percent of the residents with hip fractures took these drugs. Residents who took the prescription sleep medications were 66 percent more likely to sustain a hip fracture than those who did not. The risk was greater among new users of the medications and those suffering mild to moderate mental and physical decline. Those who took the medication for less than two months were more than twice as likely to fracture their hip, the study found. Nonbenzodiazepenes have been known to alter memory, attention, and balance, which may be why there is a greater risk of physical injury when taking the medication, the researchers wrote. Based on the findings, nursing home staff should try to treat sleep problems using nondrug strategies first, such as increased daytime activity and discouraging daytime napping, according to the researchers. © 2012 NY Times Co

Keyword: Sleep; Drug Abuse
Link ID: 17926 - Posted: 03.20.2013

By ANAHAD O'CONNOR Slurred and incoherent speech is one of the classic signs of a stroke. But new research finds that another symptom may be garbled and disjointed text messages, which could provide early clues to the onset of a stroke. In Detroit, doctors encountered a 40-year-old patient who had no trouble reading, writing or understanding language. His only consistent problem was that he had lost the ability to type coherent text messages on his phone. An imaging scan showed that he had suffered a mild ischemic stroke, caused by a clot or blockage in his brain. The case represents at least the second instance of what doctors are calling “dystextia.” In December, a report in The Archives of Neurology described a 25-year-old pregnant woman whose husband grew concerned after she sent him a series of incoherent text messages. Doctors found that the woman had also been experiencing weakness in her right arm and leg, and that she had earlier had difficulty filling out an intake form at her obstetrician’s office. The case in Detroit was particularly unusual because garbled texting appeared to be the only conspicuous problem, at least initially, said Dr. Omran Kaskar, a senior neurology resident at Henry Ford Hospital who treated the patient in late 2011. “Stroke patients usually present with multiple neurologic deficits,” he said. The findings suggest that text messaging may be a unique form of language controlled by a distinct part of the brain. And because texts are time-stamped, they may potentially be useful as a way of helping doctors determine precisely when a patient’s stroke symptoms began. The patient was a businessman who had traveled to southeast Michigan one evening for a work trip. Shortly after midnight, the man sent text messages to his wife that were disjointed and nonsensical – and not because he was using shorthand. Copyright 2013 The New York Times Company

Keyword: Stroke; Language
Link ID: 17925 - Posted: 03.20.2013

By BARRY MEIER A group of 18 doctors, researchers and public health experts jointly urged the Food and Drug Administration on Tuesday to take action on energy drinks to protect adolescents and children from the possible risks of consuming high amounts of caffeine. “There is evidence in the published scientific literature that the caffeine levels in energy drinks pose serious potential health risks,” the doctors and researchers wrote.In their letter to Dr. Margaret A. Hamburg, the F.D.A. commissioner, the group argued that energy drink makers had failed to meet the regulatory burden placed on them to show that the ingredients used in their beverages were safe, specifically where children, adolescents and young adults are concerned. As a result, the group urged the F.D.A. to restrict caffeine content in the products and to require manufacturers to include caffeine content on product labels. A similar letter was sent to the agency by the San Francisco city attorney, Dennis J. Herrera, who is one of several public officials conducting investigations of the energy-drink industry. Energy drink makers have insisted their products are safe and that their levels of caffeine, a stimulant, are on a par with other widely consumed drinks, like coffee. The F.D.A. has said that it is safe for adults to consume about 400 milligrams of caffeine daily, though many experts say that most adults can consume 600 milligrams or more of caffeine without ill effect. A 16-ounce cup of Starbucks coffee has about 330 milligrams of caffeine, an amount about twice that of some similarly sized energy drinks. © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 17924 - Posted: 03.20.2013

A compact, self-contained sensor recorded and transmitted brain activity data wirelessly for more than a year in early stage animal tests, according to a study funded by the National Institutes of Health. In addition to allowing for more natural studies of brain activity in moving subjects, this implantable device represents a potential major step toward cord-free control of advanced prosthetics that move with the power of thought. The report is in the April 2013 issue of the Journal of Neural Engineering. “For people who have sustained paralysis or limb amputation, rehabilitation can be slow and frustrating because they have to learn a new way of doing things that the rest of us do without actively thinking about it,” said Grace Peng, Ph.D., who oversees the Rehabilitation Engineering Program of the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of NIH. “Brain-computer interfaces harness existing brain circuitry, which may offer a more intuitive rehab experience, and ultimately, a better quality of life for people who have already faced serious challenges.” Recent advances in brain-computer interfaces (BCI) have shown that it is possible for a person to control a robotic arm through implanted brain sensors linked to powerful external computers. However, such devices have relied on wired connections, which pose infection risks and restrict movement, or were wireless but had very limited computing power. Building on this line of research, David Borton, Ph.D., and Ming Yin, Ph.D., of Brown University, Providence, R.I., and colleagues surmounted several major barriers in developing their sensor. To be fully implantable within the brain, the device needed to be very small and completely sealed off to protect the delicate machinery inside the device and the even more delicate tissue surrounding it. At the same time, it had to be powerful enough to convert the brain’s subtle electrical activity into digital signals that could be used by a computer, and then boost those signals to a level that could be detected by a wireless receiver located some distance outside the body. Like all cordless machines, the device had to be rechargeable, but in the case of an implanted brain sensor, recharging must also be done wirelessly.

Keyword: Robotics
Link ID: 17923 - Posted: 03.20.2013

Monya Baker At first glance, it looks like an oddly shaped campfire: smoky grey shapes light up with red sparks and flashes. But the video actually represents a different sort of crackle — the activity of individual neurons across a larval fish brain. It is the first time that researchers have been able to image an entire vertebrate brain at the level of single cells. “We see the big picture without losing resolution,” says Phillipp Keller, a microscopist at the Howard Hughes Medical Institute's Janelia Farm Research Campus in Ashburn, Virginia, who developed the system with Janelia neurobiologist Misha Ahrens. The researchers are able to record activity across the whole fish brain almost every second, detecting 80% of its 100,000 neurons. (The rest lie in hard-to-access areas, such as between the eyes; their activity is visible but cannot be pinned down to single cells.) The work is published today in Nature Methods1. “It’s phenomenal,” says Rafael Yuste, a neuroscientist at Columbia University in New York. “It is a bright star now in the literature, suggesting that it is not crazy to map every neuron in the brain of an animal.” Yuste has been leading the call for a big biology project2 that would do just that in the human brain, which contains about 85,000 times more neurons than the zebrafish brain. The resolution offered by the zebrafish study will enable researchers to understand how different regions of the brain work together, says Ahrens. With conventional techniques, imaging even 2,000 neurons at once is difficult, so researchers must pick and choose which to look at, and extrapolate. Now, he says, “you don't need to guess what is happening — you can see it”. © 2013 Nature Publishing Group

Keyword: Brain imaging
Link ID: 17922 - Posted: 03.19.2013

By TIM REQUARTH For months, Henry Markram and his team had been feeding data into a supercomputer, four vending-machine-size black boxes whirring quietly in the basement of the Swiss Federal Institute of Technology in Lausanne. The Blue Brain computer has 10,000 virtual neurons. The colors represent the neurons' electric voltage at a specific moment. The boxes housed thousands of microchips, each programmed to act like a brain cell. Cables carried signals from microchip to microchip, just as cells do in a real brain. In 2006, Dr. Markram flipped the switch. Blue Brain, a tangled web of nearly 10,000 virtual neurons, crackled to life. As millions of signals raced along the cables, electrical activity resembling real brain waves emerged. “That was an incredible moment,” he said, comparing the simulation to what goes on in real brain tissue. “It didn’t match perfectly, but it was pretty good. As a biologist, I was amazed.” Deciding then that simulating the entire brain on a supercomputer would be possible within his lifetime, Dr. Markram, now 50, set out to prove it. That is no small feat. The brain contains nearly 100 billion neurons organized into networks with 100 trillion total connections, all firing split-second spikes of voltage in a broth of complex biological molecules in constant flux. In 2009, Dr. Markram conceived of the Human Brain Project, a sprawling and controversial initiative of more than 150 institutions around the world that he hopes will bring scientists together to realize his dream. © 2013 The New York Times Company

Keyword: Brain imaging; Robotics
Link ID: 17921 - Posted: 03.19.2013

By Ben Thomas In 1956, a legion of famed scientific minds descended on Dartmouth College to debate one of mankind’s most persistent questions: Is it possible to build a machine that thinks? The researchers had plenty to talk about – biologists and mathematicians had suggested since the 1940s that nerve cells probably served as binary logic gates, much like transistors in computer mainframes. Meanwhile, computer theorists like Alan Turing and Claude Shannon had been arguing for years that intelligence and learning could – at least in theory – be programmed into a machine of sufficient complexity. Within the next few decades, many researchers predicted, we’d be building machines capable of conscious thought. Fifty-odd years after that first Dartmouth Conference, our sharpest supercomputers still struggle to hold basic conversations. We’ve created software that can drive our cars and predict our purchases, but the dreams of a true artificial brain – and of a working neuron-by-neuron model of the human brain itself – look even more distant than they did in the 1950s. The more we learn about how the brain works, the more interwoven and inextricable we realize its components and processes are – and the less like a computer it seems. Take synapses, for example – the points where neurons link up and exchange information. Neuroscientists estimate that a human brain may contain about 150 trillion of them, and no two are quite identical – either to one another, or to any synapse in anyone else’s brain. On top of this complexity, every neuron in a brain is constantly learning, adapting, fine-tuning its sensitivity, tinkering with its synaptic connections – rarely wired the same way from one day to the next. In light of all this, it’s not hard to see why many scientists seriously doubt that we’ll map an entire human brain any time this century – much less engineer a digital version from scratch. © 2013 Scientific American

Keyword: Brain imaging
Link ID: 17920 - Posted: 03.19.2013