Helen Thomson, biomedical news editor, San Diego When told I was being sent to the world's biggest neuroscience conference, I knew I would meet a lot of interesting people, but a five-time Oscar nominee wasn't what I was expecting. Yet here I am in San Diego at the Society for Neuroscience annual meeting listening to Glenn Close - famous for her roles as scheming aristocrat in Dangerous Liaisons and psychotic stalker in Fatal Attraction - call for science and society to work together to change the stigmas attached to mental illness. Close is well-known for having had a successful acting career. "I'm still pissed off that I had to chuck Robert Redford out of my apartment," she tells us. Yet today she defines herself not as an actress but as a series of numbers. It is her genome sequence that takes pride of place on the big screen this morning - a picture she says clearly shows she is "fabulous, sexy, and divinely complex". The real reason Close is opening this year's conference is down to her family ties to mental disease. Her sister and nephew suffer from biopolar and schizoaffective disorder respectively, which encouraged Close to launch BringChange2Mind, a not-for-profit organisation which helps to provide information about mental illness. A highlight of her speech was an interlude by nephew Calen Pick who spoke of trying to "get into the real world" while struggling with his disorder. "At my lowest point I knew I was Jesus and the psychological examinations I was taking were just a test to see if I was God or the devil," he says. © Copyright Reed Business Information Ltd.

Keyword: Schizophrenia
Link ID: 14664 - Posted: 11.15.2010

By Laura Sanders PEEK-A-BOOA new retinal prosthetic creates an image (middle) that more accurately reconstructs a baby's face (left) than the standard approach (right).S. Nirenberg SAN DIEGO — A new type of prosthetic eye may someday allow blind people to seamlessly see the broad sweep of an ocean or the dimples in a baby’s face. The approach, presented November 13 at the Society for Neuroscience’s annual meeting, may benefit the estimated 25 million people worldwide who have lost sight due to retinal diseases. “This is a spectacular example of what we all hoped to be able to do,” said Jonathan Victor, a computational systems neuroscientist who was not involved in the new work. “It’s a solution to an abstract problem” that could be useful in many kinds of systems. Sheila Nirenberg and Chethan Pandarinath, both of Weill Medical College of Cornell University in New York City, tested their new retinal prosthetic in blind mice and found that it allowed the mice to see a baby’s face. Current prosthetics are limited to reproducing simple features, such as bright spots or edges, but miss much of a scene. Many scientists are intent on boosting the retinal prosthetics’ power, so that the message from the artificial eye to the brain is stronger. But Nirenberg’s work suggests that a second, underappreciated area is also important: the pattern of cell activity in the retina, something she called “a big problem lurking in the background.” © Society for Science & the Public 2000 - 2010

Keyword: Vision; Robotics
Link ID: 14663 - Posted: 11.15.2010

Melissa Dahl Terrible jokes? Or a sign of a brain disorder? Actually, sometimes it's hard to tell. Witzelsucht (the Germans just have the best words for everything, don't they?) is a brain dysfunction that causes all sorts of compulsive silliness: bad jokes, corny puns, wacky behavior. It's also sometimes called the "joking disease," and as Taiwanese researchers phrased it in a 2005 report, it's a "tendency to tell inappropriate and poor jokes." We've covered all sorts of strange disorders of the mind in earlier Body Odd posts: one disorder makes you believe your loved ones are strangers, another convinces you that your hand has taken on a life of its own. Now, we give you a brain disorder that actually causes a poor sense of humor. It's a symptom of an injury to the right frontal lobe, which could be caused by brain trauma or a stroke, tumor, infection or a degenerative disease. "Patients who have disease of the left frontal lobe often are sad, anxious and depressed," explains Dr. Kenneth Heilman, a neurologist at the University of Florida College of Medicine in Gainesville, Fla. "In contrast ... patients with right-hemisphere disease often (appear) indifferent or euphoric and have inappropriate jocularity." Heilman says he sees several cases of Witzelsucht each year. "One of the most dramatic cases (that I've seen) appeared to be attracted to my reflex hammer," Heilman says. "After I checked his deep tendon reflexes and put my hammer down, he picked up the hammer and started to check my reflexes, while giggling." © 2010 msnbc.com

Keyword: Emotions; Stroke
Link ID: 14662 - Posted: 11.13.2010

By Katherine Harmon Misapprehension of statistics and scientific process has been even more apparent in the misunderstandings surrounding vaccines and the onset of autism. Given the age at which children receive immunizations and that at which many cases of regressional autism manifest themselves (in which a seemingly normally developing child suddenly loses much of the ability to communicate as well as other acquired functions), "by chance alone" there will be a lot of children who regress at some point after getting their scheduled vaccines, Daniel Salmon, a vaccine safety specialist at the U.S. Department of Health and Human Services (HHS), said here on Tuesday. As he pointed out, however, "temporality is insufficient to show causality." But underlying—and perhaps highlighted by—this "logical fallacy," he explained, is a frequent hang-up of science communication: the devil is in the details, and the details can be complicated (and not too catchy) to explain. When former Jenny McCarthy, an advocate of the vaccine-autism link, goes on CNN's Larry King Live and says, "'Vaccines cause autism,' that's a very clear, simple message," Salmon noted. Most respected scientific bodies, however, are not prone to such blanket statements. In a 2004 report essentially dismissing the assertion that vaccines cause autism, the Institute of Medicine (IOM) was notably more measured than McCarthy, concluding that "based on this body of evidence, the committee concludes that the evidence favors a rejection of a causal relationship between thimerosal-containing vaccines and autism…" © 2010 Scientific American

Keyword: Autism
Link ID: 14661 - Posted: 11.13.2010

By Bruce Bower A wandering mind often stumbles downhill emotionally. People spend nearly half their waking lives thinking about stuff other than what they’re actually doing, and these imaginary rambles frequently feel bad, according to a new study that surveyed volunteers at random times via their iPhones. People’s minds wander at least 30 percent of the time during all activities except sex, say graduate student Matthew Killingsworth and psychologist Daniel Gilbert, both of Harvard University. Individuals feel considerably worse when their minds wander to unpleasant or neutral topics, as opposed to focusing on current pursuits, Killingsworth and Gilbert report in the Nov. 12 Science. These new findings jibe with philosophical and religious teachings that assert happiness is found by living in the moment and learning to resist mind wandering, Killingsworth says. Mind wandering serves useful purposes, he acknowledges, such as providing a way to reflect on past actions, plan for the future and imagine possible consequences of important decisions. “We may tend to reflect on things that went poorly or are a cause for worry,” Killingsworth proposes. “That’s not a recipe for happiness, even if it’s necessary.” In his new study, people’s minds actually wandered more often to pleasant topics than to unpleasant or neutral topics. But those reveries offered no measurable mood boost over thinking about tasks at hand, the researchers found. © Society for Science & the Public 2000 - 2010

Keyword: Attention; Emotions
Link ID: 14660 - Posted: 11.13.2010

by Greg Miller Written language poses a puzzle for neuroscientists. Unlocking the meaning in a string of symbols requires complex neural circuitry. Yet humans have been reading and writing for only about 5000 years—too short for major evolutionary changes. Instead, reading likely depends on circuits that originally evolved for other purposes. But which ones? To investigate, cognitive neuroscientist Stanislas Dehaene of the Institut National de la Santé et de la Recherche Médicale in Gif-sur-Yvette, France, teamed up with colleagues in France, Belgium, Portugal, and Brazil to scan the brains of 63 volunteers, including 31 who learned to read in childhood, 22 who learned as adults, and 10 who were illiterate. Those who could read, regardless of when they learned, exhibited more vigorous responses to written words in several areas of the brain that process what we see, the group reports online today in Science. Based on previous work, Dehaene has argued that one of these areas, at the junction of the left occipital and temporal lobes of the brain, is especially important for reading. In literate, but not illiterate, people, written words also triggered brain activity in parts of the left temporal lobe that respond to spoken language. That suggests that reading utilizes brain circuits that evolved to support spoken language, a much older innovation in human communication, Dehaene says. It makes sense that reading would rely on brain regions that originally evolved to process vision and spoken language, says Dehaene. But this repurposing may have involved a tradeoff. The researchers found that in people who learned to read early in life, a smaller region of the left occipital-temporal cortex responded to images of faces than in the illiterate volunteers. © 2010 American Association for the Advancement of Science.

Keyword: Language
Link ID: 14659 - Posted: 11.13.2010

by Jocelyn Kaiser Many of us are zombies without 8 hours of sleep, while envied others seem to get by just fine on much less. Now geneticists have homed in on the first gene in the general population that seems to influence how much sleep we need. Sleep interests biologists in part because it varies with other factors, such as weight, that make people more prone to diabetes or heart disease. (The larger a person's body mass index, the less they generally sleep.) In search of sleep genes, a group of European researchers studied populations in seven countries, from Estonia to Italy, for a total of 4260 subjects. Each one filled out a simple questionnaire asking about his or her sleep habits and donated a DNA sample. The researchers then scanned the participants' DNA for thousands of genetic markers, looking for ones that were more common in people who slept more than those who slept less. Sleep duration correlated strongly with a single genetic marker in a gene called ABCC9. When allowed to sleep as long as they want, those who have two copies of one version of this marker sleep on average 6% less than those carrying two copies of the other version, or about 7.5 hours versus 8 hours, says postdoc Karla Allebrandt, who is leading the study at the Centre for Chronobiology headed by Till Roenneberg at the University of Munich in Germany. Allebrandt presented the work last week at the annual meeting of the American Society of Human Genetics in Washington, D.C. The ABCC9 gene codes for a protein called SUR2 that is part of a potassium channel, a structure that funnels potassium ions into and out of cells. When the researchers knocked down the corresponding gene in two species of fruit flies, the flies slept significantly less at night compared with controls, Allebrandt reported. © 2010 American Association for the Advancement of Science.

Keyword: Sleep; Genes & Behavior
Link ID: 14658 - Posted: 11.11.2010

by Andy Coghlan Elderly people who did 10 sessions of brain training had half as many crashes on the road as untrained counterparts – even though the training didn't directly relate to driving itself. "There are no other cognitive training programs, or 'brain games', that have been demonstrated by published, peer-reviewed studies to enhance driving performance," says Jerri Edwards of the University of South Florida in Tampa, a co-leader of the study. The results contradict a study of 11,000 people earlier this year, carried out by Adrian Owen at the University of Cambridge and colleagues, which found that brain training didn't help improve cognitive skills outside the game itself. "Overall, people need to know that not all brain training is equal," says Edwards. "Some programs work and some don't." With an average age of 73, the 908 participants in the latest study were assigned to one of three different computer training programs or to no training at all. One program focused on improving reaction speed, another on reasoning skills and the third on memory. Each course lasted for 10 sessions, and then the participants were tracked for six years to see how many times they had road crashes for which they were personally responsible. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory; Alzheimers
Link ID: 14657 - Posted: 11.11.2010

by Jennifer Carpenter As surprising at it may seem, wasps, bees, and even ants have relatively large and complex brains. That allows these "social insects" to keep track of the intricate relationships between the thousands of individuals in their colony—or so researchers thought. A new study indicates that these insects didn't grow big brains to cope with social living; they evolved them millions of years earlier when they were solitary parasites. The link between brain size and social living was first noted in 1850, when scientists identified mushroom bodies in the insect brain. Aptly named because they're shaped like mushrooms, the structures contain thousands of neurons responsible for processing and remembering smells and sights. Social insects tend to have larger mushroom bodies than solitary ones, leading researchers to believe that the transition from solitary to social living increased the size of these brain regions. But Sarah Farris has found a different explanation. Instead of comparing social insects with solitary ones, Farris, a neurobiologist at West Virginia University in Morgantown, looked into the past. To get a sense of how the wasp brain evolved over time, she and taxonomist Susanne Schulmeister of the American Museum of Natural History in New York City compared the mushroom bodies of parasitic wasps with those of nonparasitic wasps, which represent the very oldest form of wasp. The parasitic wasps had consistently larger and more elaborate mushroom bodies than the nonparasites, the duo reports online today in the Proceedings of the Royal Society B. In particular, the caps, called calyces, of the parasitic mushroom bodies were twice the size of nonparasites. © 2010 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 14656 - Posted: 11.11.2010

By Larry Greenemeier Party beverages that go by "blackout in a can" and other monikers may soon be banned from store shelves in some U.S. states, thanks to a number of incidents that have left drinkers unconscious and with dangerously high blood alcohol levels. The Michigan Liquor Control Commission (MLCC) last week effectively prohibited the sale of all alcoholic energy drinks after considering several studies regarding such beverages as well as concerns voiced by substance abuse prevention and parental groups, the general public, and an ongoing U.S. Food and Drug Administration (FDA) investigation. The Commission called the packaging of these products "misleading," and an attempt to appeal to younger customers "encouraging excessive consumption while mixing alcohol with various other chemical and herbal stimulants." The ban takes effect in early December. The MLCC pointed out that a typical alcoholic energy drink is 24 ounces (0.7 liters) and has a 12 percent alcohol content—compared with a 12-ounce (0.35-liter) can of beer, which normally has 4 to 5 percent—plus the caffeine equivalent of five cups of coffee. Some of the beverage lines singled out for their 12 percent alcohol content were Associated Brewing's Axis, United Brands's Max and Phusion Projects's Four Loko offerings. The commission concluded that a person need only consume one can of such a beverage to become intoxicated—and that because these drinks typically cost $2 to $5 per can they are "easily accessible and affordable." Such beverages were in the news last month when nine Central Washington University students were hospitalized following a party. © 2010 Scientific American,

Keyword: Drug Abuse
Link ID: 14655 - Posted: 11.11.2010

By Dave Lee BBC World Service Young offenders are more likely to have suffered a brain injury compared with the rest of society, a study suggests. A survey of 197 young male offenders found about half reported having had a childhood brain injury - three times higher than in non-offenders. Multiple head injuries were linked with carrying out more violent crimes, says the University of Exeter team. Better assessment of injuries could help prevent re-offending, they add. The researchers asked 197 offenders aged 11 to 19 years about their past medical history, convicted crimes, mental health and drug use. They considered the effects of traumatic brain injury alongside other factors such as deprivation and lack of life opportunities to determine if a childhood brain injury contributed to future acts of criminal behaviour. The study, published in the journal Neuropsychological Rehabilitation, found that while a brain injury alone is unlikely to increase a child's chances of criminal activity, it could play a factor in those already susceptible to crime, and may increase the chance of repeat offences. "The associations between brain injuries and crime are very problematic," explained Huw Williams, associate professor of clinical neuropsychology at the University of Exeter, on Radio 4's All in the Mind. "It may not be causal in the sense of increasing the chances of crime, but it may well be a factor in terms of re-offending." BBC © MMX

Keyword: Aggression; Brain Injury/Concussion
Link ID: 14654 - Posted: 11.11.2010

by Andy Coghlan Women who take mild painkillers such as aspirin and paracetamol during pregnancy are slightly more likely to have boys with undescended testicles, a study from Denmark has reported. The risk of having a son with the condition remains low, with or without painkillers, but the finding may explain why it has become more common in recent decades. However, a similar investigation in Finland found no links at all. The risk rose significantly for women in the Danish group who took more painkillers, particularly between 8 and 14 weeks: it increased 21-fold if women took more than one type of painkiller daily for more than a fortnight during this period. "The most important message is that if you take the occasional paracetamol, it's not going to do your baby any harm," says Richard Sharpe of the University of Edinburgh, UK, who was not involved in the study but who investigates the causes and origins of fetal sexual development in boys. "It's prolonged usage that might be a problem." In the study itself, Henrik Leffers of the University Hospital of Copenhagen led a team that followed women through their pregnancies, 834 of which resulted in boys. The researchers identified which women took paracetamol, aspirin or ibuprofen for pain relief during pregnancy, and investigated whether this raised the likelihood that their sons would have undescended testicles at birth, a condition called cryptorchidism. © Copyright Reed Business Information Ltd.

Keyword: Sexual Behavior; Pain & Touch
Link ID: 14653 - Posted: 11.11.2010

by Catherine de Lange Calcium activity in the brain plays an important role in the onset of Parkinson's disease, according to a study in mice. The finding helps explain why common calcium-blocking drugs, such as those used to control blood pressure, appear to protect against the disease. Damage to dopamine-releasing cells in a brain area called the substantia nigra (SN) is known to be involved in the onset of Parkinson's disease. "Pacemaking" cells in this area release pulses of dopamine, a hormone crucial for movement and balance. So damage to these cells leads to the symptoms of Parkinson's – such as tremors and stiffness. A key question is why cells of the SN are so much more susceptible to damage than those in surrounding areas. Now it seems that calcium, which enters these cells to regulate their activity, is the culprit. Jaime Guzman from Northwestern University in Chicago and colleagues compared the effect of calcium activity in two brain areas in mice – the pacemaking SN and a neighbouring area where there was no pacemaking activity. They found that the calcium influx in the SN caused much higher levels of oxidative stress – pressure on cells to counteract the effects of molecules such as free radicals, that can damage proteins and DNA. Oxidative stress is thought to be the source of the cell damage that leads to Parkinson's disease. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons; Apoptosis
Link ID: 14652 - Posted: 11.11.2010

by Douglas Fox Steven and David Elmore were born identical twins, but their first days in this world could not have been more different. David came home from the hospital after a week. Steven, born four minutes later, stayed behind in the ICU. For a month he hovered near death in an incubator, wracked with fever from what doctors called a dangerous viral infection. Even after Steven recovered, he lagged behind his twin. He lay awake but rarely cried. When his mother smiled at him, he stared back with blank eyes rather than mirroring her smiles as David did. And for several years after the boys began walking, it was Steven who often lost his balance, falling against tables or smashing his lip. Those early differences might have faded into distant memory, but they gained new significance in light of the twins’ subsequent lives. By the time Steven entered grade school, it appeared that he had hit his stride. The twins seemed to have equalized into the genetic carbon copies that they were: They wore the same shoulder-length, sandy-blond hair. They were both B+ students. They played basketball with the same friends. Steven Elmore had seemingly overcome his rough start. But then, at the age of 17, he began hearing voices. The voices called from passing cars as Steven drove to work. They ridiculed his failure to find a girlfriend. Rolling up the car windows and blasting the radio did nothing to silence them. Other voices pursued Steven at home. Three voices called through the windows of his house: two angry men and one woman who begged the men to stop arguing. Another voice thrummed out of the stereo speakers, giving a running commentary on the songs of Steely Dan or Led Zeppelin, which Steven played at night after work. His nerves frayed and he broke down. Within weeks his outbursts landed him in a psychiatric hospital, where doctors determined he had schizophrenia. © 2010, Kalmbach Publishing Co.

Keyword: Schizophrenia
Link ID: 14651 - Posted: 11.11.2010

Some people hear voices that are the products only of processes in their brains. These hallucinations can lead to persistent delusions that someone is plotting against them or urging them to harm others. When a person acts on those delusions, headline-grabbing tragedy can ensue, usually involving someone close to the protagonist. Violence is not a symptom of schizophrenia — only a tiny proportion of sufferers with the condition are homicidal. Yet these incidents dominate the media coverage of the disease. The reality of schizophrenia is much more complex. Hallucinations are one of several symptoms, others of which — cognitive dysfunction, loss of motivation and of social engagement — are much less amenable to medication, and are often more damaging to the ability of those with schizophrenia to function. In recent years it has been increasingly appreciated that this collection of symptoms, which typically first fully manifest in early adulthood, represents a late stage of the illness, and that the illness itself may perhaps turn out to be a collection of syndromes, rather than a single condition. Motivated by the undue stigma and by the recent advances reported in our own pages and elsewhere, Nature this week examines the state of our understanding of schizophrenia, and how researchers can hope to make progress in an entangled landscape of innate and environmental influences. The image on this issue's cover and in the logo that links the associated content is a piece of art by a schizophrenia sufferers. It is one of many compiled by NARSAD, a US charity based in New York that spends significant public donations on psychiatric health research. The image reflects a world of confusion and distorted reality — but not a 'split personality', which is a mythical symptom of the condition, and leads to a misleading metaphorical use of the word 'schizophrenic' that those involved with the condition perpetually seek to eradicate. © 2010 Nature Publishing Group

Keyword: Schizophrenia
Link ID: 14650 - Posted: 11.11.2010

Kerri Smith Halfway through a satellite meeting at the Federation of European Neurosciences conference in Amsterdam in July, researcher Ken McCarthy takes the stage to give his presentation. He sports a black shirt and jeans, and his strong cheekbones, shock of white hair and tanned skin give him the look of a film star. But he doesn't have the confidence to match. I find this a little bit daunting, he says, as he organizes his slides. McCarthy, a geneticist at the University of North Carolina School of Medicine in Chapel Hill, is about to fan the flames of a debate about whether glia, the largest contingent of non-neuronal cells in the brain, are important in transmitting electrical messages. For many years, neurons were thought to be alone in executing this task, and glia were consigned to a supporting role regulating a neuron's environment, helping it to grow, and even providing physical scaffolding (glia is Greek for 'glue'). In the past couple of decades, however, this picture has been changing. Some glia, known as astrocytes, have thousands of bushy tendrils that nestle close to the active junctions between neurons the synapses (see 'Neural threesome'). Here they seem to listen in on neuronal activity and, in turn, to influence it. Studies show that chemical transmitters released by neurons cause an increase in the levels of calcium inside astrocytes, spurring them to release transmitters of their own. These can enhance or mute the signalling between neurons, or influence the strength of their connections over time. Moreover, astrocytes activated at one synapse might communicate with other synapses and astrocytes with which they make contact. © 2010 Nature Publishing Group,

Keyword: Glia; Brain imaging
Link ID: 14649 - Posted: 11.11.2010

by Ann Gibbons With brains as big as ours, Neandertals were no dumb brutes. But their brains may have developed in a manner much different from the way ours do, according to anew study. The differences suggest that Neandertals did not see the world the same way we do and may not have been as adept at language or forming complex social networks. Paleoanthropologists Jean—Jacques Hublin, Philipp Gunz, and Simon Neubauer of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, made the find by first comparing CT scans of the brains of 58 humans and 60 chimps, varying in age from birth to adulthood. The researchers used three—dimensional imaging and several hundred landmarks on the braincases to match the brains accurately despite differences in size. As the team reports this month in the Journal of Human Evolution, humans—but not chimps—preferentially expand their parietal lobes and cerebellums and widen their temporal lobes in the first year of life. This results in the characteristic rounded dome of our skulls. In another study published online today in Current Biology, the researchers and a colleague used the same imaging methods to study nine fossil Neandertals, including a newborn, a year—old baby, and three children. Because the brain does not fossilize, they studied endocasts, imprints of the brain left in the skull. They found that at birth, both Neandertal and modern human infants had elongated braincases that were similar in shape, although Neandertal faces were already larger. But by age 1 or so, modern humans had grown globular brains, whereas Neandertal babies had not; like chimpanzees, they did not show the preferential bulging in the parietal and cerebellar regions, even though the brain grew overall. © 2010 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 14648 - Posted: 11.09.2010

By PAM BELLUCK Much of the research on Alzheimer’s next year will be about going back in time, trying to determine when and how the brain begins to deteriorate. Scientists now know Alzheimer’s attacks the brain long before people exhibit memory loss or cognitive decline. But the specifics are crucial because so far, drug after drug has failed to effectively treat Alzheimer’s in people who already show symptoms. Many scientists now think the problem may be that the drugs were given too late, when, as Dr. John C. Morris, an Alzheimer’s expert at Washington University in St. Louis, puts it, “there’s a heck of a lot of brain cell damage and we’re trying to treat a very damaged brain.” If drugs could be given sooner, tailored to specific biological changes, or biomarkers, in the brain, treatment, or even prevention, might be more successful. “We’re trying to go earlier and earlier in the course of the disease,” said Neil Buckholtz, chief of the Dementias of Aging branch at the National Institute on Aging. “The idea is to locate how people move through these stages and what indications there are of each stage.” Several research projects are expecting to make strides next year. One involves the world’s largest family to experience Alzheimer’s disease, an extended clan of about 5,000 people in Colombia, many of whom have inherited a genetic mutation that guarantees they will develop dementia, usually in their 40s. Except for its clear genetic cause and that it strikes people so young, the Colombian condition is virtually identical in its disease process to more common Alzheimer’s, which has unknown causes and afflicts millions of elderly people. Copyright 2010 The New York Times Company

Keyword: Alzheimers
Link ID: 14647 - Posted: 11.09.2010

By DENISE GRADY It was a desperate measure, for a desperate disease. Fourteen months ago, Dennis Sugrue let doctors thread a fine tube through his blood vessels and up into his head, so they could spray the drug Avastin directly into the part of his brain where a tumor had been cut out. It was an experiment, devised mainly to find out whether the procedure was safe, and to gauge how much Avastin the brain could tolerate. But Mr. Sugrue, then 50, was hoping the experiment would also free him of cancer. He had glioblastoma, a brain tumor that fights off every known therapy. The same disease killed Senator Edward M. Kennedy last year. Mr. Sugrue’s cancer was diagnosed in April 2009 and bombarded with the usual weapons: surgery, radiation and chemotherapy. Within months, the tumor was growing back. That was when he signed up for the Avastin study. About 10,000 Americans a year develop glioblastoma. Nearly all find that the standard treatments seem to work — for a while. And then the clock starts to run down. With treatment, the median survival is about 15 months. Only 25 percent of patients make it to two years. The disease is the focus of much research, and will almost certainly be for years to come. Hundreds of studies are being conducted in glioblastoma and other brain cancers. Among other things, they involve vaccines, drug combinations and special drug-delivery techniques. Progress is measured in small steps — a few more months of survival, more patients managing to survive two years. On paper the gains may seem minute, but for patients the added time may translate into a graduation or wedding that might otherwise have been missed. Copyright 2010 The New York Times Company

Keyword: Miscellaneous
Link ID: 14646 - Posted: 11.09.2010

Jessica Marshall A man lies in a brain scanner, with his foot in one end of a long, narrow box, which is divided into six compartments of equal size. On a screen he watches a tarantula crawling in one of the compartments. A hand reaches in and moves the spider into another compartment, first one further away from the man's foot, then one closer. Although the subject was led to believe he was viewing the scene unfold in real-time, the man was actually watching a previously recorded video of the tarantula creeping through the boxes, nowhere near the subject. His fear, however, was real. The scanner -- a functional magnetic resonance imager (fMRI) -- allowed researchers to capture that fear by recording the activity in his brain as he watched the spider, illuminating the hallmarks of the human fear response in the man's brain. In a study of 20 individuals who watched the same video, researchers report today that our brains evaluate fear in a nuanced way, drawing on several different regions depending on the proximity, trajectory and our expectations of the feared object -- in this case a Brazilian salmon pink tarantula. By better understanding which of these brain regions fail to function normally when confronted with fear, the authors hope their findings could one day help treat people with phobias. © 2010 Discovery Communications, LLC.

Keyword: Emotions; Brain imaging
Link ID: 14645 - Posted: 11.09.2010