Allie Bidwell, Chronicle Staff Writer For most of his adult life, Michael Berg has suffered from sinus problems that led to strange reactions to the way he smelled and tasted things. Drinking a glass of wine or smoking a cigar, for example, would drastically reduce his sense of smell. He knew that alcohol and smoking could dull the senses, so he thought nothing of it. Then one day in 2005, his sense of smell completely vanished. "Literally one day we were having dinner, and I remember I couldn't smell or taste anything," Berg, 55, said. Experts estimate that about 2 percent of the U.S. population suffers from Berg's condition, a lack of smell known as anosmia. And research by neuroscientists at UC Berkeley provides hope of new therapies for those who have lost their sense of smell, whether due to aging, trauma or a viral infection. In the study published this month in the journal Neuron, the researchers - led by campus neurobiology Professor John Ngai - found a genetic trigger responsible for renewing smell sensors in the nose. That gene, known as p63, tells olfactory stem cells whether to replace themselves or to change into different types of cells. Under normal circumstances, Ngai said, there is a balance between the two outcomes. © 2011 Hearst Communications Inc.

Keyword: Chemical Senses (Smell & Taste); Neurogenesis
Link ID: 16189 - Posted: 12.27.2011

By KAREN BARROW Imagine being unable to recognize your children or your closest friend. You can see their faces perfectly fine, but if you passed them on the street you wouldn’t be able to place their unique eyes, nose and ears. James Cooke, 66, and Dori Frame, 51, live with a condition called prosopagnosia, or face blindness. They both suffered separate events that affected their brains and caused them to suddenly lose the ability to recognize the faces of even their closest family members. However, there are others born with this condition. While it is unclear how many people suffer from face blindness, researchers are beginning to make progress in understanding how the prosopagnosia works by clarifying how the brain processes the both the face and the voice to help them recognize someone. One of the keys to understanding face recognition, it seems, is understanding how the brain comes to recognize voices. Some scientists had believed that faces and voices, the two main ways people recognize one another, were processed separately by the brain. Indeed, a condition parallel to prosopagnosia, called phonagnosia, similarly leaves a person unable to distinguish a familiar voice from an unfamiliar one. © 2011 The New York Times Company

Keyword: Attention
Link ID: 16188 - Posted: 12.27.2011

By KAREN BARROW Close your eyes. Picture your closest friend. Maybe you see her blue eyes, long nose, brown hair. Perhaps even her smile. If you saw her walking down the street it would match your imagined vision. But what if you saw nothing at all? James Cooke, 66, of Islip, N.Y., can’t recognize other people. When he meets someone on the street, he offers a generic “hello” because he can’t be sure if he’s ever met that person before. “I see eyes, nose, cheekbones, but no face,” he said. “I’ve even passed by my son and daughter without recognizing them.” He is not the only one. Those with prosopagnosia, also known as face blindness, can see perfectly well, but their brains are unable to piece together the information needed to understand that a collection of features represents an individual’s face. The condition is a neurological mystery, but new research has shed light on this strange malady. One of the keys to understanding face recognition, it seems, is understanding how the brain comes to recognize voices. Some scientists had believed that faces and voices, the two main ways people recognize one another, were processed separately by the brain. Indeed, a condition parallel to prosopagnosia, called phonagnosia, similarly leaves a person unable to distinguish a familiar voice from an unfamiliar one. © 2011 The New York Times Company

Keyword: Attention
Link ID: 16187 - Posted: 12.27.2011

Drug companies are working to develop a pure, more powerful version of a highly abused medicine, which has addiction experts worried that it could spur a new wave of abuse. The new pills contain the highly addictive painkiller hydrocodone, packing up to 10 times the amount of the drug as existing medications such as Vicodin. Four companies have begun patient testing, and one of them — Zogenix of San Diego — plans to apply early next year to begin marketing its product, Zohydro. If approved, it would mark the first time patients could legally buy pure hydrocodone. Existing products combine the drug with nonaddictive painkillers such as acetaminophen. Critics say they are especially worried about Zohydro, a timed-release drug meant for managing moderate to severe pain, because abusers could crush it to release an intense, immediate high. 'The next Oxycontin' "I have a big concern that this could be the next OxyContin," said April Rovero, president of the National Coalition Against Prescription Drug Abuse. "We just don't need this on the market." OxyContin, introduced in 1995 by Purdue Pharma of Stamford, Conn., was designed to manage pain with a formula that dribbled one dose of oxycodone over many hours. Abusers quickly discovered they could defeat the timed-release feature by crushing the pills. © CBC 2011

Keyword: Pain & Touch; Drug Abuse
Link ID: 16186 - Posted: 12.27.2011

By Laura Sanders Sea snails learn more effectively on an oddly timed series of training sessions rather than regularly spaced lessons, a new study finds. If the results extend to humans, they might suggest ways of improving students’ study habits. The work, published online December 25 in Nature Neuroscience, shows how a deep knowledge of biology and powerful computer models can lead to insights about the brain, says neuroscientist Eric Kandel of Columbia University, who won a Nobel prize in 2000 for his work on sea snail memory. When the rat-sized Aplysia californica receives an unpleasant shock, it retracts its gill and an appendage called a siphon. After numerous shocks, it will become sensitized, learning to retract the siphon and keep it in for a while. Scientists normally expose sea snails to the signal at regular intervals over several hours to sensitize the animals. But Jack Byrne of the University of Texas Medical School at Houston and colleagues wondered whether there was a better way. “There’s no real logic for why people use one protocol over another, other than it works,” he says. Kandel and others have worked out a lot of the biochemical details of how sea snails learn and form memories. When the creatures start to learn something, two major molecular cascades kick off in nerve cells. Genes jump into action, churning out proteins that then spur other genes into action. One of these cascades happens quickly, and the other one is sluggish, but both need to deliver their products at the same time for a memory to stick. Y. Zhang et al. Computational design of enhanced learning protocols. Nature Neuroscience. Published online December 25, 2011. doi: 10.1038/nn.2990. © Society for Science & the Public 2000 - 2011

Keyword: Learning & Memory; Evolution
Link ID: 16185 - Posted: 12.27.2011

By NATALIE ANGIER VIEWED superficially, the part of youth that the psychologist Jean Piaget called middle childhood looks tame and uneventful, a quiet patch of road on the otherwise hairpin highway to adulthood. Said to begin around 5 or 6, when toddlerhood has ended and even the most protractedly breast-fed children have been weaned, and to end when the teen years commence, middle childhood certainly lacks the physical flamboyance of the epochs fore and aft: no gotcha cuteness of babydom, no secondary sexual billboards of pubescence. Yet as new findings from neuroscience, evolutionary biology, paleontology and anthropology make clear, middle childhood is anything but a bland placeholder. To the contrary, it is a time of great cognitive creativity and ambition, when the brain has pretty much reached its adult size and can focus on threading together its private intranet service — on forging, organizing, amplifying and annotating the tens of billions of synaptic connections that allow brain cells and brain domains to communicate. Subsidizing the deft frenzy of brain maturation is a distinctive endocrinological event called adrenarche (a-DREN-ar-kee), when the adrenal glands that sit like tricornered hats atop the kidneys begin pumping out powerful hormones known to affect the brain, most notably the androgen dihydroepiandrosterone, or DHEA. Researchers have only begun to understand adrenarche in any detail, but they see it as a signature feature of middle childhood every bit as important as the more familiar gonadal reveille that follows a few years later. © 2011 The New York Times Company

Keyword: Development of the Brain; Hormones & Behavior
Link ID: 16184 - Posted: 12.27.2011

by Richard Knox Debra Meyerson was hiking near Lake Tahoe 15 months ago when a stroke destroyed part of the left side of her brain, leaving her literally speechless. It happens to more than 150,000 Americans a year. But now Meyerson is learning to talk again through an approach that trains the undamaged right side of her brain to "speak." Specifically, it's a region that controls singing. For more than 100 years, it's been known that people who can't speak after injury to the speech centers on the left side of the brain can sing. In the 1970s, Boston researchers started to use a sort of "singing therapy" to help stroke survivors speak again. However, it never caught on much – perhaps because a lot of therapists, not to mention patients, weren't comfortable singing what they wanted to say. And back then, the science wasn't advanced enough to show the actual changes in the brain that result from the therapy. That's changing fast. Congresswoman Gabrielle Giffords, who has had a version of "singing therapy," astounded everyone by her ability to speak again – albeit so far in single words and short phrases. Nearly a year ago, a would-be assassin's bullet tore through the speech center in Giffords' left brain. Copyright 2011 NPR

Keyword: Stroke; Language
Link ID: 16183 - Posted: 12.27.2011

By Kay Lazar, Globe Staff Boston researchers say they have found a new method for detecting subtle brain changes in people who have no memory problems but who may already be in the earliest stages of Alzheimer’s disease. The findings, published online today in the medical journal Neurology, may help speed clinical trials for potential Alzheimer’s treatments, according to Dr. Bradford Dickerson, an associate professor of neurology at Harvard Medical School and lead author of the study. “We need efficient, cost-effective ways to screen people for research,” said Dickerson, who also is a brain specialist at Massachusetts General Hospital. “This will potentially give us a tool that will help identify people in a more efficient manner.” Dickerson said his screening method is not ready for use in physicians’ offices. Researchers and the medical community still must pinpoint reliable markers for the disease, that could be used much the same way doctors now measure early signs of heart disease by monitoring patients’ cholesterol levels. Dickerson’s team used brain scans to measure the thickness in nine specific areas of the brain in 159 people who did not show signs of dementia or other cognitive problems. © 2011 NY Times Co.

Keyword: Alzheimers
Link ID: 16182 - Posted: 12.23.2011

By Ferris Jabr Once adult lab mice learn to associate a particular stimulus—a sound, a flash of light—with the pain of an electric shock, they don't easily forget it, even when researchers stop the shocks. But a new study in the December 23 issue of Science shows that the antidepressant Prozac (fluoxetine) gives mice the youthful brain plasticity they need to learn that a once-threatening stimulus is now benign. The research may help explain why a combination of therapy and antidepressants is more effective at treating depression, anxiety and post-traumatic stress disorder (PTSD) than either drugs or therapy alone. Antidepressants may prime the adult brain to rewire faulty circuits during therapy. Nina Karpova, Eero Castrén and their colleagues at the University of Helsinki's Neuroscience Center created and extinguished fearful behaviors in mice. First, Castrén placed mice in a cage and repeatedly played a tone just before electrically shocking their feet. Soon the animals froze in fear whenever they heard the tone, at which point Castrén put them through "extinction training." He moved the mice to a different cage and played the same tone again. This time there was no electric shock. Researchers have previously shown that young mice less than three weeks old quickly learn that the tone is no longer a herald of danger and stop freezing in fear. But adult mice are harder to put at ease. Even if the adults become less fearful during extinction training, their relaxation is not permanent—a week later the tone turns them into statues again. © 2011 Scientific American,

Keyword: Depression; Neurogenesis
Link ID: 16181 - Posted: 12.23.2011

The reindeer of Christmas myth must meet high expectations this time of year -- not just hauling heavy loads of gifts over long distances -- but also helping navigate from the tundra to the rest of the world. And even though most real reindeer never pull sleighs through snowy nights, new research suggests that their eyes would be far better suited to the task than Santa's are. Unlike people, the study found, reindeer can see ultraviolet light -- which probably allows them to detect food and predators in a mostly white environment. The study makes reindeer the first large mammal known to have UV vision. And it raises questions about how animals that are highly specialized to their environments will adapt as their environments change. "Reindeer are mammals and what we find may be related to humans," said Karl-Arne Stokkan, an Arctic biologist at the University of Tromsø in Norway. "In the view of potential climate change, we have also realized that reindeer may be an important 'signal-animal' because of their strong adaptation to an environment believed to suffer the biggest changes." Many animals are able to see or respond to ultraviolet light, including some birds, rodents, fish, bees and bats. But UV light is invisible to the human eye and with enough exposure, can even cause damage. Most dangerous are bright, snowy and icy conditions at high elevations or high latitudes, where lots of UV intensity and reflectivity can cause snow blindness in human eyes. © 2011 Discovery Communications, LLC.

Keyword: Vision; Evolution
Link ID: 16180 - Posted: 12.23.2011

By Tina Hesman Saey By kick-starting a gene that is naturally inactivated, chemotherapy drugs could help reverse a genetic brain disorder that is sometimes mistaken for autism or cerebral palsy. The unexpected finding may also spark a new avenue of research on a type of gene regulation known as imprinting. The genetic disorder, Angelman syndrome, occurs in about one in 15,000 live births. It is caused when the copy of a gene called UBE3A inherited from the mother goes missing or is damaged by a mutation. That’s a problem because the copy of the gene inherited from the father is already turned off in brain cells, leaving no way to make UBE3A protein. Genes such as UBE3A that turn off one parent’s copy are called imprinted genes. Until now, researchers knew of no way short of gene therapy to override the imprinting and restore gene activity. Now, researchers from the University of North Carolina at Chapel Hill have discovered that a type of chemotherapy drug called topoisomerase inhibitors can turn on the father’s inactive copy of the gene in brain cells of mice with a version of Angelman syndrome. The team reports the achievement online December 21 in Nature. The prospect that a drug could correct the underlying defect responsible for Angelman syndrome is exciting, says Stormy Chamberlain, a geneticist at the University of Connecticut Health Center in Farmington. “There’s every reason to have hope that it will help our Angelman syndrome kids,” she says. © Society for Science & the Public 2000 - 2011

Keyword: Genes & Behavior
Link ID: 16179 - Posted: 12.23.2011

By Susan Milius Pigeons, who aren’t even distant uncles to a monkey, have matched primates in a test of learning an abstract numerical concept. Trained on one-two-three, the pigeons then had to put pairs of numbers up to nine in order, says comparative psychologist Damian Scarf of the University of Otago in New Zealand. Pigeons rivaled rhesus monkeys tested earlier at the same task, Scarf and his colleagues report in the Dec. 23 Science. The results “suggest that despite completely different brain organization and hundreds of millions of years of evolutionary divergence, pigeons and monkeys solve this problem in a similar way,” says Elizabeth Brannon of Duke University, a coauthor of the original study of numerical order in monkeys. Humankind may be pretty proud of its numerical prowess, but numbers — four succulent fruits versus eight, one lurking lion versus three — matter very much in animal life, too. Research is uncovering various kinds of number-related abilities in animals as diverse as the honeybee, mosquitofish, grey parrot, Plethodon salamanders and a waterbird called a coot. So pigeons could be compared with other species, Scarf used Brannon’s numerical-order test, which baboons and lemurs as well as some monkeys have passed. For training, pigeons saw computer screens displaying sets of three images, each with one, two or three shapes. The shapes varied so that a bird couldn’t get the number order right just by pecking at increasing surface area. Scarf then rewarded birds for pecking in one-shape, two-shapes, three-shapes order. © Society for Science & the Public 2000 - 2011

Keyword: Evolution
Link ID: 16178 - Posted: 12.23.2011

by Curtis Abraham, Uganda Large areas of northern Uganda are experiencing an outbreak of nodding syndrome, a mysterious disease that causes young children and adolescents to nod violently when they eat food. The disease, which may be an unusual form of epilepsy, could be linked to the parasitic worm responsible for river blindness, a condition that affects some 18 million people, most of them in Africa. The current outbreaks are concentrated in the districts of Kitgum, Pader and Gulu. In Pader alone, 66 children and teenagers have died. More than 1000 cases were diagnosed between August and mid-December. Onchocerca volvulus, a nematode worm that causes river blindness, is known to infest all three affected districts. Nearly all the children with nodding syndrome are thought to live near permanent rivers, another hint of a connection with river blindness. The link is not clear cut, though. "We know that [Onchocerca volvulus] is involved in some way, but it is a little puzzling because [the worm] is fairly common in areas that do not have nodding disease," says Scott Dowell, who researches paediatric infectious diseases and is lead investigator into nodding syndrome with the US Centers for Disease Control and Prevention. There is no known cure for nodding syndrome, so Uganda's Ministry of Health has begun using anticonvulsants such as sodium valproate to treat its signs and symptoms. Meanwhile the disease is continuing to spread, say Janet Oola, Pader's health officer, and Sam William Oyet, the district's medical entomology officer. © Copyright Reed Business Information Ltd.

Keyword: Movement Disorders
Link ID: 16177 - Posted: 12.23.2011

by Sarah C. P. Williams When a rattlesnake shakes its tail, does it hear the rattling? Scientists have long struggled to understand how snakes, which lack external ears, sense sounds. Now, a new study shows that sound waves cause vibrations in a snake's skull that are then "heard" by the inner ear. "There's been this enduring myth that snakes are deaf," says neurobiologist Bruce Young of the University of Massachusetts, Lowell, who was not involved in the new research. "Behavioral studies have suggested that snakes can in fact hear, and now this work has gone one step further and explained how." In humans, sound waves traveling through the air hit the eardrum, causing the movement of tiny bones and vibrations of tiny hair cells in the inner ear. These vibrations are then translated into nerve impulses that travel to the brain. Snakes have fully formed inner ear structures but no eardrum. Instead, their inner ear is connected directly to their jawbone, which rests on the ground as they slither. Previous studies have shown that vibrations traveling through the ground—such as the footsteps of predators or prey—cause vibrations in a snake's jawbone, relaying a signal to the brain via that inner ear. It was still unclear, however, whether snakes could hear sounds traveling through the air. So Biologist Christian Christensen of Aarhus University in Denmark took a closer look at one particular type of snake, the ball python (Python regius). Studying them wasn't easy. "You can't train snakes to respond to sounds with certain behaviors, like you might be able to do with mice," says Christensen. Instead, he and his colleagues used electrodes attached to the reptiles' heads to monitor the activity of neurons connecting the snakes' inner ears to their brains. Each time a sound was played through a speaker suspended above the snake's cage, the researchers measured whether the nerve relayed an electrical pulse (the snakes showed no outward response to the sounds). The nerve pulses were strongest, the researchers found, with frequencies between 80 and 160 hertz—around the frequency for the lowest notes of a cello, though not necessarily sounds that snakes encounter often in the wild. © 2010 American Association for the Advancement of Science

Keyword: Hearing; Evolution
Link ID: 16176 - Posted: 12.23.2011

By Courtney Humphries A video screen shows a man in his late 60s lying awake on an operating table. Just outside the camera's view, a doctor is moving his finger in front of the man's face, instructing him to follow it back and forth with his eyes. Seconds later, after a dose of the powerful anesthetic drug propofol, his eyelids begin to droop. Then his pupils stop moving. Only the steady background beeping of the heart monitor serves as a reminder that the man isn't dead. "He's in a coma," the doctor, Emery Brown, explains. "General anesthesia is a drug-induced reversible coma." As an anesthesiologist at Massachusetts General Hospital (MGH), Brown is constant witness to one of the most profound and mysterious feats of modern medicine. Every day, nearly 60,000 patients in the United States undergo general anesthesia, enabling them to survive even the grisliest operations unaware and free of pain. But though doctors have been putting people under for more than 150 years, what happens in the brain during general anesthesia is a mystery. Scientists don't know much about the extent to which these drugs tap into the same brain circuitry we use when we sleep, or how being anesthetized differs from other ways of losing consciousness, such as slipping into a coma following an injury. Are parts of the brain truly shutting off, or do they simply stop communicating with each other? How is being anesthetized different from a state of hypnosis or deep meditation? And what happens in the brain in the transition between consciousness and unconsciousness? "We know we can get you in and out of this safely," Brown says, "but we still can't quite tell you how it works." © 2011 Technology Review

Keyword: Sleep
Link ID: 16175 - Posted: 12.23.2011

By Eric Niiler A new light bulb in the works could avoid tinkering with your body's sleep patterns. As late-night workers and long-distance travelers already know, shifting time zones or work periods throws the body's natural clock out of whack. Even regular folks often find it nearly impossible to get a restful sleep for several hours after sitting under bright lights after the sun has gone down (some call it the Fenway Park phenomena). Now a Florida inventor is testing a new LED bio-bulb that could regulate the body's circadian rhythm by helping control the production of melatonin, the body's sleep hormone that tells us when it's nighttime. This can be done by eliminating a small segment of the blue wavelength of light (around 465 to 485 nanometers) produced by the lightbulb, according to Fred Maxik, founder and chief technology officer of Lighting Science Group Corp., a Satellite Beach, Fla., firm. "We're looking at a way to filter out that part of the spectrum, and still have a white light," Maxik said. "Our ability to restore the natural position of where we were and natural hormonal secretions is an appealing one." Nearly 20 years ago, medical researchers discovered that the eye has a separate photoreceptor that picks up wavelengths of light, and then sends a signal to the hypothalamus which secretes melatonin. © 2011 Discovery Communications, LLC.

Keyword: Biological Rhythms; Sleep
Link ID: 16174 - Posted: 12.20.2011

By BARRON H. LERNER, M.D. Most of us recall lobotomies as they were depicted in the movie “One Flew over the Cuckoo’s Nest”— horrifying operations inappropriately used to control mentally ill patients. But in the 1950s, surgeons also used them to treat severe pain from cancer and other diseases. Now a Yale researcher has uncovered surprising new evidence of a famous patient who apparently received a lobotomy for cancer pain during that time: Eva Perón, the first lady of Argentina, who was known as Evita. The story is an interesting, sad footnote in the history not only of lobotomy, but of pain control. The nature of Perón’s illness was initially shrouded in silence. Her doctors diagnosed advanced cervical cancer in August 1951, but as was common at the time, the patient was told only that she had a uterine problem. According to the biographers Nicholas Fraser and Marysa Navarro, secrecy was so paramount that an American specialist, Dr. George Pack, performed Perón’s cancer operation without her or the public ever knowing. He entered the operating suite after she was under anesthesia. Despite surgery, radiation and chemotherapy, Perón gradually worsened, dying in late July 1952 at age 33. Only then was it revealed that she had died of cervical cancer, although details of her treatment, including Dr. Pack’s involvement, remained concealed. In a 1972 biography, Erminda Duarte, Perón’s sister, claimed she had suffered intense pain and distress. © 2011 The New York Times Company

Keyword: Schizophrenia
Link ID: 16173 - Posted: 12.20.2011

By NICHOLAS WADE Social behavior among primates — including humans — has a substantial genetic basis, a team of scientists has concluded from a new survey of social structure across the primate family tree. The scientists, at the University of Oxford in England, looked at the evolutionary family tree of 217 primate species whose social organization is known. Their findings, published in the journal Nature, challenge some of the leading theories of social behavior, including: ¶ That social structure is shaped by environment — for instance, a species whose food is widely dispersed may need to live in large groups. ¶ That complex societies evolve step by step from simple ones. ¶ And the so-called social brain hypothesis: that intelligence and brain volume increase with group size because individuals must manage more social relationships. By contrast, the new survey emphasizes the major role of genetics in shaping sociality. Being rooted in genetics, social structure is hard to change, and a species has to operate with whatever social structure it inherits. If social behavior were mostly shaped by ecology, then related species living in different environments should display a variety of social structures. But the Oxford biologists — Susanne Shultz, Christopher Opie and Quentin Atkinson — found the opposite was true: Primate species tended to have the same social structure as their close relatives, regardless of how and where they live. © 2011 The New York Times Company

Keyword: Genes & Behavior; Aggression
Link ID: 16172 - Posted: 12.20.2011

By BENEDICT CAREY SMYRNA, Del. — The taste of cocaine and the slow-motion sensation of breaking the law were all too familiar, but the thrill was long gone. Antonio Lambert was not a young hoodlum anymore but a family man with a career, and here he was last fall, high as any street user, sneaking into his workplace at 9 o’clock at night, looking for — what, exactly? He didn’t really know. He left the building with a few cellphones (which he threw away) and a feeling that he was slipping, falling back down into a hole. He walked in the darkness, walked with no place to go, and then he began to do what he has taught others in similar circumstances to do: turn, face the problem, and stand back up. “I started talking to myself, out loud; that’s one of my coping strategies, and one reason I relapsed is I had forgotten to use those,” said Mr. Lambert, 41, a mental health educator who has a combined diagnosis — mood disorder with drug addiction — that is among the scariest in psychiatry. He texted a friend, someone who knew his history and could help talk him back down. And he checked himself into a hospital. “I know when it’s time to reach out for help.” The mental health care system has long made use of former patients as counselors and the practice has been controversial, in part because doctors and caseworkers have questioned their effectiveness. But recent research suggests that peer support can reduce costs, and in 2007, federal health officials ruled that states could bill for the services under Medicaid — if the state had a system in place to train and certify peer providers. © 2011 The New York Times Company

Keyword: Drug Abuse
Link ID: 16171 - Posted: 12.20.2011

by Nicholas Mackintosh NEUROSCIENTISTS seek to understand how the brain underpins our behaviour, thoughts and feelings. Given that the law is also concerned with human behaviour, albeit for quite different reasons, it is hardly surprising that remarkable advances in our understanding of the brain have led many to believe that neuroscience is becoming increasingly relevant to the law. In the US, a number of universities teach courses on the interface between neuroscience and the law, and the Chicago-based MacArthur Foundation has invested several million dollars to fund research in this area. In the UK, the Royal Society has just published a report on neuroscience and the law. Some argue that neuroscience has already cast doubt on the idea of free will, and therefore raises questions about the legitimacy of punishing people for actions over which they had no control. In the US there is a steady increase in defence attorneys seeking to introduce neuroscientific evidence. So is "my brain made me do it" a legitimate defence in a criminal trial? There will surely be cases where such evidence is relevant. Most countries specify an age of criminal responsibility somewhere between 6 and 16; in England and Wales it is 10. Brain imaging studies have shown that the brain continues to develop throughout adolescence, with the prefrontal cortex, implicated in impulse control and decision-making, not reaching maturity until 20 or so. Such studies have also shown that there are huge individual differences. It is hard to believe that all 10-year-olds should be held fully responsible when they break the law. © Copyright Reed Business Information Ltd.

Keyword: Attention; Aggression
Link ID: 16170 - Posted: 12.20.2011