By Sandra G. Boodman, For the first decade of his life, every doctor who saw Jack DeWitt inevitably zeroed in on the harrowing circumstances of his premature birth. Delivered by emergency Caesarean section in December 1999, doctors universally ascribed his developmental problems to his being born six weeks early, said his mother, Ruth DeWitt. “It always came back to that.” When Jack’s walking became odd at age 5, doctors chalked it up to a mild form of cerebral palsy that can occur in children born too soon. “We were okay with it,” his mother said, because mild cerebral palsy would not “affect the length of his life or his enjoyment of it.” Jack’s parents were also reassured by his ability to catch up; with help, he mastered various skills: jumping, walking and writing in cursive. But by age 10, when his ability to walk badly deteriorated, a reevaluation by his doctors resulted in a very different diagnosis and prognosis. “We had all those years of feeling that he was a normal, healthy kid with some challenges,” his mother recalled. Discovering what was really wrong has been a heavy blow, magnified by Jack’s perceptive awareness of its implications. Ruth DeWitt, who lives with her family in Howell, Mich., outside Ann Arbor, was in the hospital undergoing a test for preeclampsia, or pregnancy-induced hypertension, when she began hemorrhaging, a sign of placental abruption. The life-threatening condition occurs when the placenta prematurely detaches from a woman’s uterus. Rushed into surgery, Jack was born weighing 3 pounds, 9 ounces, and was transferred to the neonatal intensive care unit at the University of Michigan Medical Center. Small but strong, he needed oxygen but no ventilator, and he came home 15 days later. © 1996-2012 The Washington Post

Keyword: Movement Disorders; Genes & Behavior
Link ID: 17615 - Posted: 12.18.2012

By CLAUDIA DREIFUS In a world of proliferating professions, S. Matthew Liao has a singular title: neuroethicist. Dr. Liao, 40, the director of the bioethics program at New York University, deploys the tools of philosophy, history, psychology, religion and ethics to understand the impact of neuroscientific breakthroughs. You’re a philosopher by training. How did philosophy lead to neuroethics? Mine’s the typical immigrant’s story. My family moved to Cincinnati from Taiwan in the early 1980s. Once here, my siblings gravitated towards the sciences. I was the black sheep. I was in love with the humanities. So I didn’t go to M.I.T. — I went to Princeton, where I got a degree in philosophy. This, of course, worried my parents. They’d never met a philosopher with a job. Do you have any insight on why scientific careers are so attractive to new Americans? You don’t need to speak perfect English to do science. And there are job opportunities. Define neuroethics. It’s a kind of subspecialty of bioethics. Until very recently, the human mind was a black box. But here we are in the 21st century, and now we have all these new technologies with opportunities to look inside that black box — a little. With functional magnetic imaging, f.M.R.I., you can get pictures of what the brain is doing during cognition. You see which parts light up during brain activity. Scientists are trying to match those lights with specific behaviors. At the same time this is moving forward, there are all kinds of drugs being developed and tested to modify behavior and the mind. So the question is: Are these new technologies ethical? © 2012 The New York Times Company

Keyword: Miscellaneous
Link ID: 17614 - Posted: 12.18.2012

By Scicurious Depression is a disease with a difficult set of symptoms. Not only are the symptoms difficult to describe (how do you really describe anhedonia, before you know the word for it?), symptoms of depression manifest in different ways for different people. One person will eat more, sleep all the time, move slowly. Another will eat almost nothing, never sleep, and be irritable and nervous. They are both depressed. The only universal symptom is the feeling of…depression, and the need for successful treatment. Treatments which often take several weeks to work, are often ineffective, and which come with a host of side effects. So I was particularly intrigued when Nature published two papers this week looking at the role of dopamine in depressive-like behavior. What I particularly like is that these two papers have somewhat opposite results, due to different behavioral methods, something which I think highlights some of the problems associated with studying depression. Ed Yong covered both of the studies together fabulously over at Not Exactly Rocket Science, but I’d like to look at them both separately, to take a deeper look at each one, see what they’ve achieved, and what other questions they raise. So I will start with one today, and post the other tomorrow, looking at both sides. While you often hear about serotonin in studies of depression (serotonin is, after all, a target of many current antidepressants), there are many other neurotransmitters and systems that are also under investigation, and many of them are bearing some fruitful results. Ketamine, for example. And of course there is the role of dopamine. © 2012 Scientific American

Keyword: Depression
Link ID: 17613 - Posted: 12.18.2012

By ANAHAD O'CONNOR Chronic sleep loss has many downsides, among them weight gain, depression and irritability. But now scientists have found a new one: It also weakens your tolerance for pain. In recent studies, researchers have shown that losing sleep may disrupt the body’s pain signaling system, heightening sensitivity to painful stimuli. Though it is not clear why, one theory is that sleep loss increases inflammation throughout the body. Catching up on sleep if you are behind may reduce inflammation. Scientists believe this could have implications for people with chronic pain. It could also have an impact on the effects of painkillers, which appear to be blunted after chronic sleep loss. In one study published in the journal Sleep, scientists at the sleep disorders and research center at Henry Ford Hospital in Detroit recruited 18 healthy adults and split them into two groups. One was allowed to sleep for an average of nine hours, while the other averaged two fewer hours of sleep each night. To assess pain thresholds, the researchers measured how long the subjects were able to hold a finger to a source of radiant heat. After four nights, the group that was allowed to sleep the longest was able to withstand the painful stimuli much longer, by about 25 percent on average. Several studies in the past have had similar findings, including one in 2006 that showed that one night of cutting sleep in half could significantly reduce a person’s threshold for physical pain. Copyright 2012 The New York Times Company

Keyword: Sleep; Pain & Touch
Link ID: 17612 - Posted: 12.18.2012

By James Gallagher Health and science reporter, BBC News Unrivalled control of a robotic arm has been achieved using a paralysed woman's thoughts, a US study says. Jan Scheuermann, who is 53 and paralysed from the neck down, was able to deftly grasp and move a variety of objects just like a normal arm. Brain implants were used to control the robotic arm, in the study reported in the Lancet medical journal. Experts in the field said it was an "unprecedented performance" and a "remarkable achievement". Jan was diagnosed with spinocerebellar degeneration 13 years ago and progressively lost control of her body. She is now unable to move her arms or legs. She was implanted with two sensors - each four millimetres by four millimetres - in the motor cortex of her brain. A hundred tiny needles on each sensor pick up the electrical activity from about 200 individual brain cells. "The way that neurons communicate with each other is by how fast they fire pulses, it's a little bit akin to listening to a Geiger counter click, and it's that property that we lock onto," said Professor Andrew Schwartz from the University of Pittsburgh. The pulses of electricity in the brain are then translated into commands to move the arm, which bends at the elbow, wrist and could grab an object. BBC © 2012

Keyword: Robotics
Link ID: 17611 - Posted: 12.17.2012

By DOUGLAS MARTIN Dr. William F. House, a medical researcher who braved skepticism to invent the cochlear implant, an electronic device considered to be the first to restore a human sense, died on Dec. 7 at his home in Aurora, Ore. He was 89. The cause was metastatic melanoma, his daughter, Karen House, said. Dr. House pushed against conventional thinking throughout his career. Over the objections of some, he introduced the surgical microscope to ear surgery. Tackling a form of vertigo that doctors had believed was psychosomatic, he developed a surgical procedure that enabled the first American in space to travel to the moon. Peering at the bones of the inner ear, he found enrapturing beauty. Even after his ear-implant device had largely been supplanted by more sophisticated, and more expensive, devices, Dr. House remained convinced of his own version’s utility and advocated that it be used to help the world’s poor. Today, more than 200,000 people in the world have inner-ear implants, a third of them in the United States. A majority of young deaf children receive them, and most people with the implants learn to understand speech with no visual help. Hearing aids amplify sound to help the hearing-impaired. But many deaf people cannot hear at all because sound cannot be transmitted to their brains, however much it is amplified. This is because the delicate hair cells that line the cochlea, the liquid-filled spiral cavity of the inner ear, are damaged. When healthy, these hairs — more than 15,000 altogether — translate mechanical vibrations produced by sound into electrical signals and deliver them to the auditory nerve. Dr. House’s cochlear implant electronically translated sound into mechanical vibrations. His initial device, implanted in 1961, was eventually rejected by the body. But after refining its materials, he created a long-lasting version and implanted it in 1969. © 2012 The New York Times Company

Keyword: Hearing; Robotics
Link ID: 17610 - Posted: 12.17.2012

By Kate Clancy I tend to go to bed freezing, especially so in the winter, so I pile our flannel sheet, blanket, and down comforter over me when I settle in to sleep. A few times each menstrual cycle, clustered together in the luteal phase between ovulation and menses, I wake up from sleep completely soaked in my own sweat – not a delightful sight or experience. Usually I get up, change pajamas, and try to find a dry spot on the bed to go back to sleep (I promise the sheets eventually get washed, but I’m not about to wake my husband – and sometimes daughter – to change the bed at 3am). These night sweats started when I was still intensively breastfeeding my daughter and was marathon training, when she was under a year old. At first, I thought it was because we were co-sleeping and we slept next to each other. But I never experienced them next to my husband before that point, and he is a six foot four heat generating machine. When the marathon was over and I returned to less strenuous activity, breastfeeding frequency was also starting to decline. I didn’t get any night sweats again for quite some time. Then there was roller derby. At first, roller derby was a pastime, a recreational activity where I got to learn something totally new and hang out with women I respected. But of course, being the competitive person I am, it became an obsession, and in addition to roller derby practices I was working out quite a lot on my own time. Over the last year I’ve made additional nutritional adjustments to further improve my performance, and I’ve increased the intensity of my off-skates workouts. I work out a minimum of five hours a week, but in the middle of the season it is usually a minimum of nine hours per week. © 2012 Scientific American

Keyword: Hormones & Behavior
Link ID: 17609 - Posted: 12.17.2012

By Mark Changizi The human fascination with color never ceases to amaze me. Our perceptual experience is filled with shapes and pitches and textures and timbres and depths and on and on, yet color seems to get the lion share of our excitement and philosophical attention. Color seems somehow more artistic than our other perceptual dimensions; it’s simply wonderful to behold, as evinced by the double rainbow guy; and we can’t resist wondering what it would be like to see dimensions of color beyond our own. In fact, RadioLab recently put out a great show on color that nicely conveys the romance we all have toward it. Question is: Why do we find color so enthralling? One of the reasons may be that the world can seem arbitrarily labeled in color, as if a painter dabbed over everything in order to make it beautiful… and that naturally makes us wonder what a different artist might do. What sort of splendor is a bird—who has an extra dimension of color beyond ours—treated to, for example? While I, too, feel the wonder of color, I don’t share this above intuition about color and its arbitrariness. It’s an unfortunate intuition, one that seeps its way not only into the minds of laymen, but into our “enhancement” products and even the hallowed halls of philosophy. In trying to explain what’s wrong with the intuition, let me begin with a thought experiment concerning a product that gives the wearer “shape enhancement” vision. “With our sunglasses’ shape-enhancement filter, you’ll see the world with more vibrant and interesting shapes. Round things will be rounder, regular polygons more muted…”

Keyword: Vision
Link ID: 17608 - Posted: 12.17.2012

By Jason G. Goldman While second nature to many of us, driving a car is actually a fairly complex process. At its most stripped down version, first you sit in the driver’s seat, then you start the engine, then you shift into gear, and then you must simultaneously steer while keeping your foot on the gas pedal. That doesn’t include things like adjusting your mirrors, verifying that you won’t drive into another person or car, and so on. In one sense, it is incredibly impressive that three dogs in New Zealand have learned – in a fairly rudimentary way – to drive a car. They sit in the driver’s seat, shift into gear, operate the steering wheel, and step on the accelerator. Those deserving the true accolades however are not the dogs, but the human trainers for their impressive patience and determination. The training that led man’s best friend to operate a car is no different from the kind of training behind the bird shows found at zoos all over the world, or the dolphin, killer whale, seal, or sea lion displays you might see at Sea World. It’s the same kind of training that scientists use to probe the emotional and cognitive lives of rats, mice, and the other critters that populate their laboratories. At the end of the day, it all comes down to a form of learning first described by Edward L. Thorndike at the beginning of the 1900s, which was later expanded and popularized by B.F. Skinner and taught to every student of Introductory Psychology: operant conditioning. While classical conditioning is a form of learning that binds external stimuli to reflexive, involuntary responses, operant conditioning involves voluntary behaviors, and is maintained over time by the consequences that follow those behaviors. In one experiment, Skinner placed pigeons individually into experimental chambers (sometimes referred to as “Skinner boxes”) that were designed to deliver food rewards at systematic intervals. He found that by rewarding a bird after it displayed a desired behavior, he could motivate the bird to increase the frequency of that particular behavior. © 2012 Scientific American

Keyword: Learning & Memory
Link ID: 17607 - Posted: 12.14.2012

by Kai Kupferschmidt Human beings tend to avoid places that smell of urine. But to mice, there is something positively addictive about the scent; they like to go back to a spot where they found the excretions again and again. Now, researchers have discovered that this behavior is triggered by a single protein in the urine of male mice. Mice use scent to mark their territory, advertise their social dominance, and convey information about their health and reproductive status. But these are usually volatile pheromones that disperse quickly, and it has remained unclear what exactly stimulates a female to be attracted to a specific male. Previous research had shown that female laboratory mice often return to a place where they have come across cage bedding soiled by males. Now, researchers at the University of Liverpool in the United Kingdom have confirmed this. Female mice spent five times as much time in a place where they had encountered a dish with male urine than at a place where they encountered water. Just 10 minutes of exposure to the urine was enough for the mice to show this place preference even after 14 days. However, if the mice were prevented from by a mesh screen touching the urine with their nose, the place seemed to lose its attractiveness. "That suggested that the story was not as simple as everybody assumed and volatile pheromones were not responsible," says behavioral ecologist Jane Hurst, one of the authors of the study. By separating the urine into different fractions, the scientists showed that a protein called darcin that they had identified in 2005—and which mice can only detect if their noses touch the urine—is responsible for the frequent visits. Pure darcin, produced in cell culture in the lab, elicited the same reaction, the authors report online today in Science. © 2010 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 17606 - Posted: 12.14.2012

By JAMES DAO Reviving a 20-year debate over illnesses of veterans of the 1991 Persian Gulf war, a new scientific paper presents evidence that nerve agents released by the bombing of Iraqi chemical weapons depots just before the ground war began could have carried downwind and fallen on American troops staged in Saudi Arabia. The paper, published in the journal Neuroepidemiology, tries to rebut the longstanding Pentagon position, supported by many scientists, that neurotoxins, particularly sarin gas, could not have carried far enough to sicken American forces. The authors are James J. Tuite and Dr. Robert Haley, who has written several papers asserting links between chemical exposures and gulf war illnesses. They assembled data from meteorological and intelligence reports to support their thesis that American bombs were powerful enough to propel sarin from depots in Muthanna and Falluja high into the atmosphere, where winds whisked it hundreds of miles south to the Saudi border. Once over the American encampments, the toxic plume could have stalled and fallen back to the surface because of weather conditions, the paper says. Though troops would have been exposed to low levels of the agent, the authors assert that the exposures may have continued for several days, increasing their impact. Though chemical weapons detectors sounded alarms in those encampments in the days after the January 1991 bombing raids, they were viewed as false by many troops, the authors report. © 2012 The New York Times Company

Keyword: Stress; Neurotoxins
Link ID: 17605 - Posted: 12.14.2012

A specific pattern of neuronal firing in a brain reward circuit instantly rendered mice vulnerable to depression-like behavior induced by acute severe stress, a study supported by the National Institutes of Health has found. When researchers used a high-tech method to mimic the pattern, previously resilient mice instantly succumbed to a depression-like syndrome of social withdrawal and reduced pleasure-seeking — they avoided other animals and lost their sweet tooth. When the firing pattern was inhibited in vulnerable mice, they instantly became resilient. "For the first time, we have shown that split-second control of specific brain circuitry can switch depression-related behavior on and off with flashes of an LED light," explained Ming-Hu Han, Ph.D. External Web Site Policy, of the Mount Sinai School of Medicine, New York City, a grantee of NIH’s National Institute of Mental Health (NIMH). "These results add to mounting clues about the mechanism of fast-acting antidepressant responses." Han, Eric Nestler, M.D., Ph.D. External Web Site Policy,of Mount Sinai, and colleagues, report on their study in the journal Nature. In a companion article, NIMH grantees Kay Tye, Ph.D. External Web Site Policy, of the Massachusetts Institute of Technology, Cambridge, Mass., and Karl Deisseroth, M.D., Ph.D. External Web Site Policy, of Stanford University, Stanford, Calif., used the same cutting-edge technique to control mouse brain activity in real time. Their study reveals that the same reward circuit neuronal activity pattern had the opposite effect when the depression-like behavior was induced by daily presentations of chronic, unpredictable mild physical stressors, instead of by shorter-term exposure to severe social stress.

Keyword: Stress; Depression
Link ID: 17604 - Posted: 12.14.2012

Gary Taubes. “It is better to know nothing,” wrote French physiologist Claude Bernard in An Introduction to the Study of Experimental Medicine (1865), “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek.” Embracing a fixed idea is one of the main dangers in the evolution of any scientific discipline. Ideally, errors will be uncovered in the trial-by-fire of rigorous testing and the science will right itself. In rare cases, however, an entire discipline can be based on a fundamental flaw. As a science journalist turned science historian, I have written at length about how and why this may have happened in obesity research. I have suggested that the discipline may be a house of cards — as, by extension, may much research into the chronic diseases associated with obesity, such as diabetes. Before the Second World War, European investigators believed that obesity was a hormonal or regulatory disorder. Gustav von Bergmann, a German authority on internal medicine, proposed this hypothesis in the early 1900s. The theory evaporated with the war. After the lingua franca of science switched from German to English, the German-language literature on obesity was rarely cited. (Imagine the world today if physicists had chosen to ignore the thinking that emerged from Germany and Austria before the war.) Instead, physicians embraced the ideas of the University of Michigan physician Louis Newburgh, who argued that obese individuals had a “perverted appetite” that failed to match the calories that they consumed with their bodies' metabolic needs. “All obese persons are alike in one fundamental respect,” Newburgh insisted, “they literally overeat.” This paradigm of energy balance/overeating/gluttony/sloth became the conventional, unquestioned explanation for why we get fat. It is, as Bernard would say, the fixed idea. © 2012 Nature Publishing Group

Keyword: Obesity
Link ID: 17603 - Posted: 12.13.2012

by Peter Aldhous IT HAS been more than a decade in the works, but finally we know the main changes that will be introduced next May, when the American Psychiatric Association publishes the next edition of its Diagnostic and Statistical Manual of Mental Disorders, known as DSM-5. Those changes, which could influence the way millions are treated, include new definitions of autism and related conditions, and a shift in the criteria for depression to include some people grieving after bereavement. Debate over DSM-5 seems likely to rumble on. But now there is a deeper problem to ponder: while discoveries about the genes and brain circuits that underlie human behaviour are accumulating rapidly, they haven't led to major clinical advances. That's largely because these findings don't map well on to the constellation of conditions described in the DSM. When the last major revision was completed in 1994, its authors hoped that neurobiologists would soon home in on specific disruptions to brain circuitry involved in the main psychiatric disorders. "I was naive enough to think that it was just a matter of time," says Michael First of Columbia University in New York City. It hasn't worked out that way. Take schizophrenia: what was once considered to be a distinct psychotic disorder actually seems to cover a variety of disruptions to normal brain functioning. This suggests that many of psychiatry's diagnostic labels do not describe coherent conditions with common underlying causes. No wonder, then, that many conditions are so hard to treat. © Copyright Reed Business Information Ltd.

Keyword: Schizophrenia; Depression
Link ID: 17602 - Posted: 12.13.2012

By Laura Sanders Signs of depression can be turned on and off in mice with the flip of a switch. Activating or silencing the behavior of certain brain cells with laser light causes the animals to change their depressive behavior, two new studies find. Although the experiments were done in rodents, the results have direct relevance to human depression, says neurologist Helen Mayberg of the Emory University School of Medicine in Atlanta. The new work may point out places in the human brain that doctors can similarly stimulate to treat depression. The results, published online December 13 in Nature, took advantage of a technique called optogenetics, which allows scientists to control nerve cell behavior with a tiny fiber-optic light. In the studies, mice were genetically engineered to harbor nerve cell proteins that respond to light. The researchers could make certain nerve cells fire off messages by shining blue light, and quiet them by shining yellow light. These cells, which produce the chemical messenger dopamine, nestle in a brain region called the ventral tegmental area, a spot known for handling rewards. This system may be skewed in people with depression, since the disorder often keeps people from responding normally to things that used to be enjoyable. One tiny fiber-optic flash had an instant and profound effect on the mice’s behavior, says psychiatrist and neuroscientist Karl Deisseroth of Stanford University, who coauthored both papers. “That was pretty amazing for us.” © Society for Science & the Public 2000 - 2012

Keyword: Depression
Link ID: 17601 - Posted: 12.13.2012

By Ed Yong In a lab at Stanford University, a mouse is showing signs of depression. For around 10 weeks, it has experienced a series of irritations, from bouts without food or water, to erratic sleep patterns. Now, its motivation is low—when picked up by the tail, it makes few attempts to escape, and it doesn’t try to explore new spaces. It’s also less willing to sip from a sugary liquid– a sign that it gets less pleasure from normally pleasurable activities. It is never easy to assess the mental health of an animal, but this mouse is clearly showing some of the classic symptoms of depression. But not for long. Earlier, Kay Tye and Julie Mirzabekov altered the mouse so that a flash of light can activate a small part of its brain—the ventral tegmental area (VTA), near the bottom of the brain and close to the midline. A burst of light, and the mouse’s behaviour changes almost instantly. It struggles when held aloft, it explores open areas, and it regains its sweet tooth. A burst of light, and its symptoms disappear. But on the other side of the country, at the Mount Sinai School of Medicine, Dipesh Chaudhury and Jessica Walsh are doing the same thing to completely different effect. Their mice have been altered in a similar way, so that light can also switch on their VTA neurons. But these rodents have endured a shorter but more intense form of stress—10 days of being placed in cages with dominant, aggressive rivals. Because of the resulting attacks, some of them have developed depressive symptoms. Others are more resilient. But when Chaudhury and Walsh flashed the VTAs of these mice, resilient individuals transformed into susceptible ones.

Keyword: Depression
Link ID: 17600 - Posted: 12.13.2012

by Elizabeth Norton From a strictly Darwinian viewpoint, homosexuality shouldn't still be around. It isn't the best way to pass along one's genes, and to complicate the picture further, no "gay genes" have even been identified. According to a newly released hypothesis, the explanation may not lie in DNA itself. Instead, as an embryo develops, sex-related genes are turned on and off in response to fluctuating levels of hormones in the womb, produced by both mother and child. This tug of war benefits the unborn child, keeping male or female development on a steady course even amid spikes in hormones. But if these so-called epigenetic changes persist once the child is born and has children of its own, some of those offspring may be homosexual, the study proposes. Evolutionary geneticist William Rice of the University of California, Santa Barbara, felt there had to be a reason why homosexuality didn't just fade away down the generations. Research estimates that about 8% of the population is gay, and homosexuality is known to run in families. If one of a set of identical twins is gay, there's a 20% probability that the other will be, too. Furthermore, Rice notes, "homosexuality isn't just a human thing." Among California gulls, which he watches from his office window, about 14% of pairs are female-female. In Australian black swans, some 6% of pairs are male-male, and 8% of male sheep are attracted exclusively to male partners. But many genetic screens have failed to turn up genes that are responsible for sexual orientation. So to find out what makes homosexuality persist, Rice and colleagues began a comprehensive survey of the literature. © 2010 American Association for the Advancement of Science

Keyword: Sexual Behavior; Epigenetics
Link ID: 17599 - Posted: 12.13.2012

By KATIE THOMAS The drug maker Eli Lilly & Company said on Wednesday that it planned an additional study of an experimental Alzheimer’s drug that failed to improve the condition of people with the disease, saying that it remained hopeful about the drug’s prospects. The newest study is expected to get under way in the third quarter of 2013 and will focus on patients with mild Alzheimer’s disease. Lilly released results of two clinical trials in August that showed the drug, called solanezumab, did not significantly improve either the cognition or the daily functioning of people with mild and moderate forms of the disease. But despite that failure, the results also gave some reason for hope: when patients with mild Alzheimer’s were separated out, the drug was shown to significantly slow their decline in cognition. In a statement on Wednesday, the company said it decided not to pursue approval of the drug based on existing study results after it met with officials from the Food and Drug Administration. A Lilly executive said, however, that the company was still optimistic. “We remain encouraged and excited by the solanezumab data,” David Ricks, a senior vice president at Lilly and president of Lilly Bio-Medicines, said in the statement. “We are committed to working with the F.D.A. and other regulatory authorities to bring solanezumab to the millions of patients and caregivers suffering from this devastating disease who urgently need this potential treatment.” The Lilly drug is the second Alzheimer’s treatment to fail in clinical trials this year. Pfizer and Johnson & Johnson stopped development of a similar treatment, bapineuzumab, after it, too, was not shown to work. Both drugs target beta amyloid, a protein in the brain that is found in people with Alzheimer’s disease. © 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 17598 - Posted: 12.13.2012

Posted by Heidi Ledford Just in time for the holidays, a team of MIT and Max Planck researchers has released EyeWire: an online game that allows users to trace neural connections through the retina. In the proud tradition of Foldit and other ‘citizen science’ endeavours, EyeWire aims to harness the power of the people to map the projections of retinal cells called JAM-B cells. JAM-B cells respond specifically to upward motion (which appears downward to the retina, because it receives inverted images), and were the first retinal ganglion cells distinguished on the basis of a molecular marker — a protein called ‘Junctional Adhesion Molecule B’ (JAM-B). Does the downward trajectory of the JAM-B cell projections relate to their function? The scientists behind EyeWire hope to find out. EyeWire, launched 10 December, is spearheaded by MIT’s Sebastian Seung, best known for taking the concept of mapping neural connections and turning it into the surprisingly digestible and well-read popular science book Connectomics: How the Brain’s Wiring Makes Us Who We Are. Seung and his colleagues chart the retinal connectome by taking serial electron micrographs of thin slices of tissue. They then trace individual neural projections through each slice and stitch it all together again into a three dimensional image. Seung’s team could use all the help it can get: in a review of Seung’s book, Caltech neuroscientist Christoph Koch estimated that to map a cubic millimetre of brain would require a billion images and a million working-years of analysis time for a trained technician. © 2012 Nature Publishing Group

Keyword: Brain imaging
Link ID: 17597 - Posted: 12.11.2012

Analysis by Emily Sohn Older people who remembered going hungry as children were slower to lose their mental sharpness as they reached old age. The new finding was only true for African-Americans, suggesting that the study hit on a particularly resilient group of people who thrived despite extreme childhood adversity. Even so, the study offers insight into how the experiences we have at very young ages can affect our health much later in life. "We know that the social experiences of African-Americans and Caucasians in this country have been very different, at least for people over age 65," said Lisa Barnes, a cognitive neuropsychologist at Rush University Medical Center in Chicago. "We wanted to measure that and see if it had any effect at all." In an effort to add to a growing interest in the long-term health influence of childhood adversity, Barnes and colleagues started by interviewing about 6,100 people who lived in Chicago and were enrolled in a study of Alzheimer's. All participants were at least 65 years old when the study began. The average starting age was 75. In the first interview, seniors answered questions about their childhoods, including details about health, the financial situations of their families and how often someone read books to them. They also took a cognitive exam that included tests of memory. © 2012 Discovery Communications, LLC.

Keyword: Alzheimers; Obesity
Link ID: 17596 - Posted: 12.11.2012