By DIANE ACKERMAN A RELATIVELY new field, called interpersonal neurobiology, draws its vigor from one of the great discoveries of our era: that the brain is constantly rewiring itself based on daily life. In the end, what we pay the most attention to defines us. How you choose to spend the irreplaceable hours of your life literally transforms you. All relationships change the brain — but most important are the intimate bonds that foster or fail us, altering the delicate circuits that shape memories, emotions and that ultimate souvenir, the self. Every great love affair begins with a scream. At birth, the brain starts blazing new neural pathways based on its odyssey in an alien world. An infant is steeped in bright, buzzing, bristling sensations, raw emotions and the curious feelings they unleash, weird objects, a flux of faces, shadowy images and dreams — but most of all a powerfully magnetic primary caregiver whose wizardry astounds. Brain scans show synchrony between the brains of mother and child; but what they can’t show is the internal bond that belongs to neither alone, a fusion in which the self feels so permeable it doesn’t matter whose body is whose. Wordlessly, relying on the heart’s semaphores, the mother says all an infant needs to hear, communicating through eyes, face and voice. Thanks to advances in neuroimaging, we now have evidence that a baby’s first attachments imprint its brain. The patterns of a lifetime’s behaviors, thoughts, self-regard and choice of sweethearts all begin in this crucible. © 2012 The New York Times Company

Keyword: Emotions; Drug Abuse
Link ID: 16571 - Posted: 03.26.2012

Criteria for a broadened syndrome of acute onset obsessive compulsive disorder (OCD) have been proposed by a National Institutes of Health scientist and her colleagues. The syndrome, Pediatric Acute-onset Neuropsychiatric Syndrome (PANS), includes children and teens that suddenly develop on-again/off-again OCD symptoms or abnormal eating behaviors, along with other psychiatric symptoms — without any known cause. PANS expands on Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus (PANDAS), which is limited to a subset of cases traceable to an autoimmune process triggered by a strep infection. A clinical trial testing an immune-based treatment for PANDAS is currently underway at NIH and Yale University (see below). "Parents will describe children with PANS as overcome by a 'ferocious' onset of obsessive thoughts, compulsive rituals and overwhelming fears," said Susan Swedo, M.D., of the NIH’s National Institute of Mental Health (NIMH), who first characterized PANDAS two decades ago. “Clinicians should consider PANS when children or adolescents present with such acute-onset of OCD or eating restrictions in the absence of a clear link to strep.” The PANS criteria grew out of a PANDAS workshop convened at NIH in July 2010, by the NIMH Pediatric and Developmental Neuroscience Branch, which Swedo heads. It brought together a broad range of researchers, clinicians and advocates. The participants considered all cases of acute-onset OCD, regardless of potential cause.

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 16570 - Posted: 03.24.2012

A personality profile marked by overly gregarious yet anxious behavior is rooted in abnormal development of a circuit hub buried deep in the front center of the brain, say scientists at the National Institutes of Health. They used three different types of brain imaging to pinpoint the suspect brain area in people with Williams syndrome, a rare genetic disorder characterized by these behaviors. Matching the scans to scores on a personality rating scale revealed that the more an individual with Williams syndrome showed these personality/temperament traits, the more abnormalities there were in the brain structure, called the insula. "Scans of the brain's tissue composition, wiring, and activity produced converging evidence of genetically-caused abnormalities in the structure and function of the front part of the insula and in its connectivity to other brain areas in the circuit," explained Karen Berman, M.D., of the NIH's National Institute of Mental Health (NIMH). Berman, Drs. Mbemda Jabbi, Shane Kippenhan, and colleagues, report on their imaging study in Williams syndrome online in the journal Proceedings of the National Academy of Sciences. Williams syndrome is caused by the deletion of some 28 genes, many involved in brain development and behavior, in a particular section of chromosome 7. Among deficits characteristic of the syndrome are a lack of visual-spatial ability – such as is required to assemble a puzzle — and a tendency to be overly-friendly with people, while overly anxious about non-social matters, such as spiders or heights. Many people with the disorder are also mentally challenged and learning disabled, but some have normal IQs.

Keyword: Language; Genes & Behavior
Link ID: 16569 - Posted: 03.24.2012

By Rebecca Cheung Some larval sponges search for a shady place to settle down, but they don’t have optic nerves or the genes that are important for vision in most animals. Now biologists have new insight into how sponges might see light. Larvae of the sponge Amphimedon queenslandica have unique eyes made up of cells that contain pigment, a chemical that absorbs certain wavelengths of light, and cilia, which look like tiny hairs. Right next to these pigmented cells are cells with high levels of activated cry2, a gene that makes light-sensitive proteins, Todd Oakley of the University of California, Santa Barbara and others report in the April 15 Journal of Experimental Biology. These light-sensitive proteins could be involved in directing movement in cilia and steering these sponges.The finding could provide clues in how vision developed in these simple animals, Oakley says. © Society for Science & the Public 2000 - 2012

Keyword: Vision; Evolution
Link ID: 16568 - Posted: 03.24.2012

By Laura Sanders In the movie Eternal Sunshine of the Spotless Mind, scientists erase troubling memories from Jim Carrey’s head. In real life, scientists have done the opposite. By reactivating certain nerve cells, researchers make artificial memories pop into mice’s heads. The results, published in the March 23 Science and online March 22 in Nature, offer a deeper understanding of how the brain creates and uses memories. Much of what scientists know about how the brain remembers comes from studies that look for signs of natural memories in the brain or that disrupt memories. In the new work, memories are actually created, says neuroscientist Richard Morris of the University of Edinburgh in Scotland. “To my mind, this is an extremely important step forward,” he says. Though the two teams used different approaches, they both created a false memory of a fearful situation in mice. In the work reported in Science, neuroscientist Mark Mayford and colleagues relied on a molecule that, upon binding a particular drug, could activate nerve cells. The team genetically engineered the mice so that only the nerve cells active during the formation of a particular memory would make the molecule. In a sense, this molecule acts as a trail of bread crumbs in a forest, marking cells in the brain that make a memory and allowing scientists to reactivate those cells later. The marked memory was of a square room with opaque white walls and floor, and no particular odors. The mice played in this room, had their memory tagged and later went into a different room — this time, a wintergreen-scented room with a black-and-white checkered wall and a gridded floor. Here, the animals were subjected to shocks. After a while, the animals learned to freeze in response to being in the room. © Society for Science & the Public 2000 - 2012

Keyword: Learning & Memory
Link ID: 16567 - Posted: 03.24.2012

Sandrine Ceurstemont, editor, New Scientist TV Your eyes and ears can sometimes join forces to trick you. A new illusion, created by Wataru Teramoto from Tohoku University in Japan and colleagues, shows for the first time how the direction of a sound can affect how you perceive motion. The animation above should be viewed up close, while fixing your eyes on the red dot. A white square moves up and down in the periphery as a sound pans back and forth between your left and right ears. How does the square appear to move? The team found that the motion of the square either appeared to be consistent with the changing direction of the sound, in this case horizontally, or it seemed to move diagonally, lying in between the real motion and the motion of the sound. According to Teramoto, this occurs because we use auditory spatial information to help us make sense of what we see. "Sound is especially useful when the reliability of visual information is low, for example in your peripheral vision," he says. Previous studies probing whether sound can modulate motion didn't find an effect but they always considered stimuli central to a scene. Our visual system can clearly interpret detail in this region but it's much less effective when considering information even slightly off centre. In another recent study, Teramoto and his team have shown another example of how our brain links visual and audio information. After being exposed to a sound accompanied by moving visuals for three minutes, the same audio made a static object appear to move. "This indicates that even a very short observation period is enough to associate sound sequences with visual motion in the adult brain," says Teramoto. © Copyright Reed Business Information Ltd.

Keyword: Vision; Hearing
Link ID: 16566 - Posted: 03.24.2012

By Larry Greenemeier Loud, concussive explosions on the battlefield may last only a few seconds, but many soldiers returning from combat in the Middle East are experiencing lingering symptoms that cause them to perceive sounds even when it is quiet. Doctors can do little to treat the problem—typically described as a ringing in the ears—because they lack an effective way of delivering medication to the inner ear. That could change in a few years, in the form of an implantable polymer-based microscale drug-release system that delivers medicine to the inner ear. Called tinnitus, the condition afflicts at least one in every 10 American adults and is the most common disability among Afghanistan and Iraq war veterans, according to the U.S. Department of Veterans Affairs (VA). Up to 40 percent of all veterans may be suffering from tinnitus, and the VA spends about $1 billion annually on disability payments for tinnitus, according to a study published last year in Nature. (Scientific American is part of Nature Publishing Group.) To address the problem, the U.S. Department of Defense has commissioned Draper Laboratory in Cambridge, Mass., to spend the next year fleshing out a concept for a small delivery device inserted near the membrane-covered window—no more than three millimeters in diameter—separating the middle ear from the inner ear. Once at the membrane the device (essentially a polymer capsule, although Draper is not developing any of medicines that might be placed inside) would release a drug into the cochlea, the tubular organ residing in the inner ear that enables us to hear. The plan is to embed wireless communications into the capsule so that a patient or doctor can control the dosage. After the capsule finishes delivering its supply of drugs, it would dissolve. © 2012 Scientific American

Keyword: Hearing
Link ID: 16565 - Posted: 03.24.2012

By KATIE THOMAS Four months before a best-selling Alzheimer’s drug was set to lose its patent protection, its makers received approval for a higher dosage that extended their exclusive right to sell the drug. But the higher dosage caused potentially dangerous side effects and worked only slightly better than the existing drugs, according to an article published Thursday in the British Medical Journal. The drug, Aricept 23, was approved in July 2010 against the advice of reviewers at the Food and Drug Administration. They noted that the clinical trial had failed to show that the higher dosage — 23 milligrams versus the previous dosages of 5 and 10 milligrams — met its goals of improving both cognitive and overall functioning in people with moderate to severe Alzheimer’s disease. The single clinical trial of 1,400 patients also found that the larger dosage led to substantially more nausea and vomiting, potentially dangerous side effects for elderly patients struggling with advanced Alzheimer’s disease. The drug was developed by the Japanese pharmaceutical company Eisai but is marketed in the United States in a partnership with Pfizer. “It doesn’t really have much benefit, but does substantially more harm,” said Dr. Steven Woloshin, one of the co-authors of the journal article and a professor of medicine at the Dartmouth Institute for Health Policy and Clinical Practice. Aricept generated more than $2 billion in annual sales since its first approval in 1996, according to the journal article, but it was set to lose its patent protection in November 2010, opening the door to cheaper generic versions of the drug. © 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 16564 - Posted: 03.24.2012

By MATT SEDENSKY LEESBURG, Fla. — Doreen Watson-Beard cared for more people with dementia than she could count. The nurse was so moved by her patients that she led Alzheimer's support groups. She knew the warning signs and understood there was no cure. But the 49-year-old never thought the disease would affect someone her age. The first clues surfaced around five years ago, when she was 44. She'd forget to pick up her grandchildren at school or plans she made with her husband. She wrote down the wrong medication dosage for a patient. "I have no idea what's going on," she remembered telling her doctor. About 200,000 Americans under 65 are among the 5.4 million Americans suffering from Alzheimer's disease, according to the Alzheimer's Association. Experts' estimates suggest there's a similar number of younger people with other types of dementia, meaning about a half-million Americans, some as young as their 30s, suffer from early-onset or younger-onset dementia. The number of people suffering from all types of dementia is rapidly increasing because of the aging of the baby boom generation — the 78 million Americans born between 1946 and 1964 — though there's no sign the percentage of younger people with dementia is going up. Pat Summit, the 59-year-old Hall of Fame college women's basketball coach, is among the most famous to suffer publicly with it. Watson-Beard is one of a tiny minority, a fascinating, sorrowful subset to a disease trademarked by its slow, cruel overtaking of the mind. Copyright 2012 The Associated Press

Keyword: Alzheimers
Link ID: 16563 - Posted: 03.24.2012

By Scicurious “That’s not FAIR!” This is the line that rings through most houses with at least one kid. We all know when something’s not fair. That car that drove up the shoulder while you waited in traffic (rrrrr)? That’s a cheater, and that’s not fair. The person who cut in line at the grocery store instead of waiting? That’s not fair either. We get a sense of what is fair or unfair at a pretty young age, and we also understand that we are allowed, and indeed encouraged in some cases, to punish unfair behavior. But we don’t all punish unfair behavior the same way, especially when punishment may be detrimental to us. What is responsible for this difference? What mediates our reactions to what is unfair? The authors of this study think it might be serotonin, and that it may have as much to do with honesty as it does with a sense of what is fair. The basis for this paper was a game used in psychology testing, a very common game called the “Ultimatum game”. In this game, you play against one other player (or, often, against a computer). That other player has found some money, say $10. They want to divide the money with you, and you can choose whether you accept their offer, or reject the offer of splitting the money. For example, if they offer to split 50-50, you may take that offer and the $5, while if they offer to split 90-10, you may be insulted and reject it. © 2012 Scientific American,

Keyword: Emotions; Genes & Behavior
Link ID: 16562 - Posted: 03.22.2012

Graham Lawton, deputy magazine editor FOR such a big topic this is an awfully short book. But don't blame neuroscientist Sam Harris for being brief. He had no choice. In a brisk 66 pages Harris explains why we don't have free will, points out why that doesn't matter as much as it might appear to - and then simply stops in order to hammer home his point. Free will touches everything we value - law, politics, relationships, morality and more. And yet it is an illusion. We either live in a deterministic universe where the future is set, or an indeterminate one where thoughts and actions happen at random. Neither is compatible with free will. Having laid this out, Harris tries to salvage something from the wreckage. In the process he ends up rowing back to a position not unlike the "compatibilists" who argue that free will can be reconciled with the laws of physics, a notion he has earlier attacked. Harris starts his rescue mission by pointing out that, even in the absence of free will, there is still a distinction between voluntary action and mere accidents. Imagine, he says, that while he is writing his book somebody outside fires up a leaf blower. He ignores the sound by attending to his work. The decision feels like the exercise of free will, but isn't. © Copyright Reed Business Information Ltd.

Keyword: Attention; Consciousness
Link ID: 16561 - Posted: 03.22.2012

By Brian Vastag So-called atypical antipsychotic drugs have been blockbusters for the drug industry, pulling in $16 billion in 2010. Developed to treat schizophrenia and related disorders, physicians also prescribe these drugs “off label” for bipolar disorder, insomnia, and other problems the drugs are not approved to treat, as Sandra Boodman wrote in the Post on March 12. But a new report finds that psychiatrists have not been given a full picture of these drugs, which include big sellers like Abilify (aripiprazole), Zyprexa (olanzapine), Risperdal (risperidone), and Seroquel (quetiapine). When seeking approval for eight atypical antipsychotic drugs, drug companies performed 24 studies, according to a Food and Drug Administration database. But four of the studies were never published in professional journals — and all four were unflattering for the drug in question. Three of the unpublished studies showed that the new drug did not perform better than a sugar pill. The fourth study showed that while the antipsychotic drug helped patients more than a placebo, older, less expensive drugs helped patients even more. “That’s bad if you’re marketing the drug,” said Erick Turner, the psychiatrist at Oregon Health & Science University who conducted the new analysis, which was published Tuesday in the journal PLoS Medicine . © 1996-2012 The Washington Post

Keyword: Schizophrenia
Link ID: 16560 - Posted: 03.22.2012

By Alan Boyle Software billionaire Paul Allen is pledging $300 million to establish a series of "brain observatories" at the Seattle research facility named after him, with the aim of mapping and manipulating the mouse brain. The project's leaders say the insights gained could be applied as well to higher forms of life, including humans. "We believe that this project has the potential to revolutionize our understanding of the mammalian brain," Christoph Koch, chief scientific officer for the Allen Institute for Brain Science, and Harvard neuroscientist R. Clay Reid said in the journal Nature. Details about the brain observatory project were laid out today at the Allen Institute in Seattle. In an advance interview, Koch cast the effort in terms usually reserved for the multibillion-dollar Hubble Space Telescope project or the $10 billion Large Hadron Collider. "We're focusing a huge amount of resources on trying to understand this piece of highly, highly complex math and science. The most organized piece of matter in the known universe is the cerebral cortex, the one that makes you and me think and smell and hear and talk. That's what we're trying to understand," Koch told me. "Just as people spend a huge amount of time and effort to build these different observatories to look at the origin of space and time, we're going to build these observatories, these very sophisticated instruments, all of them using common standards, all peering at the brain — primarily animal brains, but also the human brain." © 2012 msnbc.com

Keyword: Brain imaging
Link ID: 16559 - Posted: 03.22.2012

Scientists are now one step closer to developing anti-addiction medications, thanks to new research that provides a better understanding of the properties of the only member of the opioid receptor family whose activation counteracts the rewarding effects of addictive drugs. The study was supported by the National Institute on Drug Abuse (NIDA), the National Institute of General Medical Sciences and the National Institute of Mental Health, all components of the National Institutes of Health. Unlike the other opioid receptor subtypes, the kappa opioid receptor (KOR) is not associated with the development of physical dependence or the abuse potential of opiate drugs (e.g., heroin, morphine). Therefore, medications that act at the KOR could have broad therapeutic potential for addressing addiction, pain, as well as other mental disorders. The leading compound in this context is JDTic because its specific binding to the KOR has been shown to reduce relapse to cocaine seeking in animal models. JDTic is currently in clinical trials to assess its safety and tolerability in humans. In this new study, scientists produced a high resolution three-dimensional image of JDTic bound to the human KOR. By mapping all the points of contact between JDTic and the human KOR, researchers were able to see how the two fit together. The emerging picture reveals critical new information that helps explain why JDTic binds so tightly and specifically to this particular opioid receptor. This advance opens the door to the development of compounds targeting the KOR with improved therapeutic profiles, including that of non-addictive pain medications. The study by Wu et al., can be found at: www.nature.com. For information on prescription drug abuse, go to: www.drugabuse.gov/drugs-abuse/prescription-medications.

Keyword: Drug Abuse; Pain & Touch
Link ID: 16558 - Posted: 03.22.2012

By Devin Powell Proteins turned on by opium and similar substances in the body have now been caught in action. Two new snapshots show how cellular proteins lasso molecules in the opium family, revealing the 3-D structure of such pairings for the first time. The work represents a major step toward designing more specific analgesics and other drugs that lack opioids’ nasty side effects, two teams of researchers report online March 21 in Nature. “Both are landmark studies,” says Gavril Pasternak, a neuroscientist who designs opioids at the Sloan-Kettering Institute in New York City, and who wasn’t involved in either study. “These structures will quickly be utilized with goal of developing nonaddicting painkillers and new ways to combat drug abuse.” Proteins that respond to opium and opiumlike molecules protrude from the surfaces of cells throughout the brain, spinal cord and gut. The body’s own hormones and brain chemicals such as endorphins can bind to these proteins to turn the molecular switches on and off to control pain, regulate breathing and change mood. Many of today’s most powerful painkillers work by switching on one of these proteins, called the mu opioid receptor. But the relief this provides comes at a price. Derivatives of opium, such as morphine and codeine, are addictive and can cause breathing problems and constipation. © Society for Science & the Public 2000 - 2012

Keyword: Pain & Touch; Drug Abuse
Link ID: 16557 - Posted: 03.22.2012

Being overweight in later life puts you at higher risk of brain decline, Korean research suggests. A study of 250 people aged between 60 and 70 found those with a high body mass index (BMI) and big waists scored more poorly in cognitive tests. The Alzheimer's Society said the research, in the journal Age and Ageing, added to evidence that excess body fat can affect brain function. Lifestyle changes can help make a difference, it said. The study looked at the relationship between fat levels and cognitive performance in adults aged 60 or over. The participants underwent BMI - a calculation based on a ratio of weight to height - and waist circumference measurements, a scan of fat stored in the abdomen and a mental test. Both a high BMI and high levels of abdominal fat were linked with poor cognitive performance in adults aged between 60 and 70. In individuals aged 70 and older, high BMI, waist circumference and abdominal body fat were not associated with low cognitive performance. The lead author of the study, Dae Hyun Yoon, said: "Our findings have important public health implications. The prevention of obesity, particularly central obesity, might be important for the prevention of cognitive decline or dementia." BBC © 2012

Keyword: Obesity; Alzheimers
Link ID: 16556 - Posted: 03.22.2012

By Deborah Kotz, Globe Staff Another disappointing clinical trial found that over-the-counter dietary supplements work no better than placebos at halting the detrimental effects of Alzheimer’s disease. This time, the supplements tested were antioxidants -- vitamin E, vitamin C, the omega-3 fatty acid ALA, and coenzyme Q. The same research group determined in a study published 18 months ago that fish oil supplements didn’t stop the progresson of Alzheimer’s either. The current study, published Monday in the Archives of Neurology, was small but well designed, randomly assigning two different combinations of daily antioxidants or placebos to some 60 patients with mild to moderate Alzheimer’s disease for nearly four months. At the end of the study, samples of spinal fluid collected from the patients at the beginning and end of the study showed no change in levels of markers associated with Alzheimer’s, including amyloid proteins that form telltale plaques in the brain. What’s troubling, though, is that the group that received a combination of vitamins E, C, and the fatty acid ALA had a greater amount of cognitive decline compared with the group given placebos or the one given coenzyme Q. “That was a really surprising finding,” said Dr. Gad Marshall, associate medical director of clinical trials at Brigham and Women’s Hospital’s Center for Alzheimer Research & Treatment, who wasn’t involved in the study. “I would have expected these supplements to have had a neutral effect on symptoms.” © 2012 NY Times Co.

Keyword: Alzheimers
Link ID: 16555 - Posted: 03.22.2012

By Lenny Bernstein, Kris Brott was more amazed than alarmed when her tongue suddenly seemed to turn upside down in her mouth. She was in the office at Quince Orchard High School in Gaithersburg, dropping off a check for her son’s baseball team, when she suddenly found herself quite literally tongue-tied. Her puzzlement gave way to panic when she reached her car and looked in the mirror. The left side of her face had collapsed. By the time she reached home, her left arm had gone numb. Soon she was dragging her left leg. It was March 15, 2010, the day before her 45th birthday. This couldn’t be happening, she thought. She was too young and much too fit. “I still kept thinking, ‘I’m not having a stroke,’ ” she recalled. She was wrong. At the hospital, emergency room physicians cleared the clot from her brain, but the damage had been done. When Brott was left with little strength on her left side despite physical therapy, she faced a long, difficult future in a body compromised by a disease of the elderly — until she decided to take control of her own recovery by returning to the gym. Researchers are learning that exercise can help younger stroke victims such as Brott regain function, even years after they are stricken. A widely cited 2011 study provides support for therapeutic approaches like the one Brott stumbled upon when she returned to the gym. © 1996-2012 The Washington Post

Keyword: Stroke
Link ID: 16554 - Posted: 03.22.2012

Christof Koch & R. Clay Reid Neuroscience is a splintered field. Some 10,000 laboratories worldwide are pursuing distinct questions about the brain across a panoply of spatio-temporal scales and in a dizzying variety of animal species, behaviours and developmental time-points. At any large neuroscience meeting, one is struck by the pace of discovery, with 50,000 or more practitioners heading away from each other in all directions, in a sort of scientific Big Bang. Although this independence is necessary, it has prevented neuroscience from entering a more mature phase, which would involve developing common standards and collaborative projects. Neurophysiologists are more likely to use each other's toothbrushes than each other's data and software; physiological results are hoarded and rarely made accessible online; molecular compounds and transgenic animals are shared only after publication. All of this has made comparisons across laboratories difficult and has slowed progress. At the Allen Institute for Brain Science in Seattle, Washington, we and our colleagues are initiating an experiment in the sociology of neuroscience — a huge endeavour that will involve several hundred scientists, engineers and technicians at the institute. Philanthropist Paul G. Allen, who founded the institute in 2003, has pledged US$300 million for the first four years of an ambitious ten-year plan that will accelerate progress in neuroscience, bringing his total commitment so far to $500 million. Our goal is to attract the best young scientists and build a series of 'brain observatories', with the aim of identifying, recording and intervening in the mouse cerebral cortex, the outermost layer of the brain. Unlike the telescopes that peer at remote events in space and time, our instruments will track the flow of information in complex, interbraided neural circuits within a layer of tissue one millimetre thick. © 2012 Nature Publishing Group,

Keyword: Brain imaging
Link ID: 16553 - Posted: 03.22.2012

by Carl Zimmer If I didn’t know Sebastian Seung was a neuroscientist, I would have pegged him as a computer game designer. His onyx-black hair seems frozen in a windstorm. He wears black sneakers, jeans, and a frayed bomber jacket over an untucked shirt covered in fluorescent blobs. If someone had blindfolded me on Vassar Street in Cambridge, Massachusetts, led me into Building 46 on the campus of MIT, past the sign that says Department of Brain and Cognitive Science, taken me up in the elevator to the fifth floor and whisked off the blindfold in Seung’s lab, I still wouldn’t have guessed he had anything to do with brains. There are no specimens floating in jars on the shelves. There are no electrodes plugged into the heads of sea slugs. Instead, I see a dozen young men gazing at monitors, some pushing their computer mice, others drawing tethered pens across digital tablets to manipulate 3-D images, each packed with more megabytes than a feature film on a Blu-ray Disc. And there is Seung himself, gazing over the shoulder of postdoc Daniel Berger, whose monitor looks like a science fiction forest, with branches and trunks colored turquoise and cherry, floating unrooted in space. I almost find myself wondering when Seung’s next game will hit the stores. But appearances to the contrary, Seung is an expert on the web of neurons that make up the brain. And the images he’s creating are part of an ambitious attempt to understand how the connections between those brain cells give rise to the mind. “How do you put together dumb cells and get something smart?” he asks. © 2012, Kalmbach Publishing Co.

Keyword: Brain imaging
Link ID: 16552 - Posted: 03.22.2012