By CELIA WATSON SEUPEL When I got up, Mom was already awake. I could hear her rummaging in the kitchen. Through the glass doors in the living room, sunlight flared so brightly off the hillocks of snow that I had to shield my eyes. It was my birthday, and I was afraid. What if my husband had neglected to take Mom shopping for a card? Once Mom found out it was my birthday, she would be devastated that she had forgotten and had nothing to give me. Little matter that she has dementia and can’t remember what we did two hours ago. Birthdays are a big deal to Mom. Birthdays are not a big deal to me. I hate growing older. I don’t mind if Mom forgets my birthday as long as she still remembers me. That someday she might not recognize me has been my biggest fear ever since Mom got dementia. I can’t imagine anything more devastating than being forgotten by your own mother. When Mom was diagnosed with vascular dementia seven years ago, I was told she did not have Alzheimer’s disease. I hoped that meant she would never forget her family. But as Mom’s dementia progressed, I realized that I had no idea whether vascular dementia could be as bad as Alzheimer’s. I really didn’t understand the difference. Recently I decided to find out, and the answers were not very reassuring. Although vascular dementia and Alzheimer’s disease are hardly the same, with time the differences start to blur. © 2011 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 15095 - Posted: 03.11.2011

Jessica Hamzelou, reporter This overlapping rainbow of connecting cells represents new insights into how mammalian brains work. The techniques used to create this three-dimensional map of a tiny chunk of mouse brain could help neuroscientists understand the connections that make up our own brains. To create this map - which shows the neurons in a piece of mouse visual cortex just 8 thousandths of a cubic millimetre in volume - Clay Reid and his colleagues at Harvard Medical School in Boston combined two imaging techniques. First, the group measured the activity of neurons in the visual cortex of a living mouse in order to spot the cells that were excited by visual information. They then killed the mouse and cut the visual cortex into 1215 slices, before using an electron microscope to capture more than 3 million images of the slices. Finally they stitched the pictures together to form this 3D image using a computer capable of handling the 30 to 40 terabytes of information. That was the relatively easy part. Next, Reid's team painstakingly traced all of the connections made by 10 of the neurons that were active in the first stage of the study. That involved tracing 240 axons and dendrites through the tangled mess created by other axons and dendrites in the 3D image. The results are already shedding light on the detailed behaviour of the brain. The team found that neurons that inhibit brain activity received input from all the excitatory neurons in the chunk. That finding offers new insight into the debate over whether these neurons receive specific or random inputs, and may inform research into conditions characterised by a lack of brain activity inhibition, such as epilepsy, says Reid. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging
Link ID: 15094 - Posted: 03.10.2011

Brain imaging techniques to find out more about patients in a coma are being developed by University of Aberdeen scientists. The new Aberdeen Coma Science Group - believed to be the first of its kind in Scotland - hopes to provide greater insights into coma patient awareness. This would be used to help guide treatment and provide information for relatives and clinicians. North east of Scotland patients will initially assist the research. The scanning technique is called functional MRI - fMRI. Prof Christian Schwarzbauer is leading the work, which will involve patients being given fMRI scans while exposed to stimuli such as pictures, sounds, smell and touch. He said: "Thanks to advances in medical care our chances of surviving a severe accident are much higher than they used to be. "Doctors can save the lives of many patients who suffer brain injury, but, if the injury is severe, the patient may not regain consciousness and slip into a coma. "Some will regain consciousness but others will remain in a so-called vegetative state. With their eyes open and possibly even wandering, these patients appear to be awake but show no signs of awareness of themselves or their environment." BBC © MMXI

Keyword: Brain imaging; Attention
Link ID: 15093 - Posted: 03.10.2011

By PAM BELLUCK A federal panel will meet on Thursday to evaluate growing concerns about whether anesthesia in young children, used in millions of surgical procedures, can in some cases lead to cognitive problems or learning disabilities. The meeting was prompted by a growing body of research, so far primarily in animals, that suggests a correlation between anesthesia exposure and brain cell death or learning problems, said Dr. Bob Rappaport, the Food and Drug Administration’s director of the division of anesthesia and analgesia products, who wrote about the issue in Wednesday’s New England Journal of Medicine. The F.D.A. advisory panel will evaluate the research, suggest further studies and discuss whether parents whose children are facing surgery should be informed of possible cognitive or behavioral risks. “We don’t know what this means for children at this time,” Dr. Rappaport said, adding, “That’s exactly why it’s so critical that we get all of the necessary information.” In the meantime, he said, “how do we communicate what we do know at this point without causing undue concern in parents and in physicians?” Medical advances are allowing more fragile and premature infants to survive birth, often to require critical surgical procedures. © 2011 The New York Times Company

Keyword: Development of the Brain
Link ID: 15092 - Posted: 03.10.2011

Analysis by Marianne English To every nap lover's delight, it turns out that sleeping may play a larger role in learning than previously thought, according to a new study featured in the journal Current Biology. Researchers at the University of California-Berkeley studied 44 college-aged participants at two different times of day -- once at noon and again at 6 p.m. Half the group was allowed to take a nap from 2 p.m. to 3:40 p.m., while the rest stayed awake throughout the day. At noon and 6 p.m., researchers measured how both groups performed in facial memory tests, finger tapping memory tests and an alertness test. The "Nap" group performed significantly better at learning tasks when tested later in the day in comparison to subjects who did not take a lengthy nap. The team also measured brain activity while subjects napped using an electroencephalogram. They found that success in learning correlated with the amount of stage-2 non rapid eye movement (NREM) sleep, the stage preceding deep rapid eye movement (REM) sleep. The research is unique because it points to a mechanism that may reveal sleep's importance for encoding new information -- sleep spindles, or short bursts of cell activity between areas of the brain during NREM. © 2011 Discovery Communications, LLC

Keyword: Sleep; Learning & Memory
Link ID: 15091 - Posted: 03.10.2011

Analysis by Amy Dusto For people with spinal injuries or other conditions that impair use of the arms or vocal cords -- or for the curious who just think it's cool -- the intendiX spells words based on brain waves. A skullcap along with a computer interface, the system is in development by Austrian company Guger Technologies. It was demonstrated at CeBIT, an annual worldwide digital industry event, held this year in Hanover, Germany, from March 1 to 5. To pick up brain activity, the skullcap is covered in electroencephalographic (EEG) electrodes. Unfortunately, this early model requires that the user put gel between his and her head and the EEG electrodes to function properly (though a dry version is forthcoming). The wearer stares at a computer screen, which flashes highlights over different rows in a matrix of letters and symbols set up like a keyboard on the screen. Simply by paying attention to the desired letter for a few seconds, the program can determine what the user intended to pick. According to Guger Technologies, most people become competent thought-communicators after 10 minutes of training on the system and are able to spell out five to 10 characters a minute. Designed for use by the severely handicapped in the home or with caregivers, intendiX can do more than just write out a text message. The user can also make it read the message out loud in digitized prose, print the text, or send it in email or via another electronic messaging system -- intendiX is Bluetooth-ready. The only ability needed to use the system, besides a few seconds of concentration, is eyesight. © 2011 Discovery Communications, LLC.

Keyword: Robotics
Link ID: 15090 - Posted: 03.10.2011

By Laura Sanders With a flip of a switch, researchers can make a mouse can shed its anxious, shy demeanor. The scientists can dial mouse anxiety up or down by lighting up a very specific connection between two parts of the brain. The results, reported online March 9 in Nature, “gets us that much closer to understanding how the [anxiety] system works or how it doesn’t work in clinical cases,” says neuroscientist and psychiatrist Kerry Ressler, a Howard Hughes Medical Institute investigator at Emory University in Atlanta who was not involved in the study. The results, he says, will help researchers gain a deeper understanding of circuits in the human brain important for psychiatric disorders. The new study focused on the amygdalae, a pair of structures buried deep within the brain, one on each side. These bundles of nerve cells are important for emotions, including fear, but it’s been less clear what role this brain region plays in anxiety, which unlike fear doesn’t require a specific trigger. Researchers led by neuroscientist and psychiatrist Karl Deisseroth, a Howard Hughes Medical Institute investigator at Stanford University, genetically engineered light-sensitive proteins that can turn brain cells on or off in mice, a trick that forms the basis of the growing field of optogenetics (SN: 1/30/10, p. 18). But the researchers added a new twist: Instead of manipulating an entire nerve cell, which would affect all of the cell’s many fingerlike projections that carry information to other cells, the team targeted very specific parts of connections between cells. © Society for Science & the Public 2000 - 2011

Keyword: Emotions
Link ID: 15089 - Posted: 03.10.2011

by Sara Reardon Most male mammals wield a penis covered with spines made of keratin, the same material that forms fingernails, to sweep out competitors' sperm and irritate a female into ovulating. You can add humans' lack of penile spines to the list of ways we are misfits among primates, along with our absence of tails and fur. Even chimpanzees, our closest relatives, have penile spines. A new study suggests that this feature disappeared due to a chunk of DNA that went missing after our evolutionary divergence from chimps. The researchers have identified another DNA deletion that may have contributed to humans' bigger brains. The question of what makes us distinctly human is hardly a new one, of course, but developmental genomicist Gill Bejerano and developmental geneticist David Kingsley, both of Stanford University in Palo Alto, California, decided to look at the issue from another angle. Maybe humans don't have an advantage over chimps genetically, as we often like to think we do—maybe we've actually lost something. Bejerano and Kingsley compared the chimp genome with the human genome, looking for DNA regions that chimps had but humans did not. And rather than looking at genes, as most research in the past has done, they examined DNA regions that don't code for genes but instead regulate how nearby genes are expressed. They found 583 deletions in the human genome, and Bejerano says choosing which to study first was a tough decision. "Each region could be its own adventure," he says. They ended up choosing two: a deleted region near a gene for male hormone response and a region close to a gene involved in brain development. The Neandertal genome also lacks these regions, indicating that these deletions occurred more than half a million years ago. © 2010 American Association for the Advancement of Science.

Keyword: Evolution; Genes & Behavior
Link ID: 15088 - Posted: 03.10.2011

ANNE McILROY University of Lethbridge neuroscientists are investigating whether early brain injuries can permanently alter the way genes work in the brain and predispose people to dementia as they age. Evidence suggests that brain injury early in life, including concussion, may contribute to later dementia, says neuroscientist Robert Sutherland. He and his colleagues at the Canadian Centre for Behavioral Neuroscience want to know why. The experiments, although still in laboratory animals, could help explain why some athletes who suffered repeated concussions, such as former National Hockey League player Reggie Fleming, developed a distinctive type of brain damage and symptoms similar to Alzheimer’s disease. Dr. Sutherland is part of a team that includes Bryan Kolb, Robbin Gibb, Robert McDonald and Olga Kovalchuk. The researchers are looking at how brain injuries influence the chemical switching system that activates and deactivates genes in the brain, or what’s known as the epigenetics of brain injuries. Thousands of genes are active in the brain and each produces one of the proteins that are essential for memory, learning, keeping brain cells alive and working, and for repairing damage. The hypothesis is that brain injuries may trigger permanent changes to the switching system, Dr. Sutherland said. This results in either too much or too little of particular protein getting produced, which over the years can lead to problems or perhaps even changes in the architecture of the brain that might make someone more vulnerable to dementia. © Copyright 2011 The Globe and Mail Inc.

Keyword: Brain Injury/Concussion; Alzheimers
Link ID: 15087 - Posted: 03.10.2011

Scientists have discovered what they say are four different species of "zombie fungus" in the Brazilian rainforest, which take over the brains of their host ants, forcing them to move to a location ideally suited to the fungus before killing them. In a study published March 2 in the journal Plos ONE, researchers from Brazil, the United Kingdom and the United States say they began to investigate after noticing different types of fungus growing out of the bodies of carpenter ants. "This so-called zombie or brain-manipulating fungus alters the behaviour of the ant host, causing it to die in an exposed position, typically clinging onto and biting into the adaxial surface of shrub leaves," the authors write. The fungus then grows — usually out of the ant's head and neck region — and releases its spores. The fungus, Ophiocordyceps, was originally thought to be a single species, but the researchers determined that there were actually four species at work. "It is tempting to speculate that each species of fungus has its own ant species that it is best adapted to attack," study leader David Hughes, an entomologist at Penn State University, told National Geographic. "This potentially means thousands of zombie fungi in tropical forests across the globe await discovery," he told the magazine. "We need to ramp up sampling - especially given the perilous state of the environment." © CBC 2011

Keyword: Evolution
Link ID: 15086 - Posted: 03.08.2011

by Virginia Morell Elephants know when they need a helping hand—or rather, trunk. That's the conclusion of a new study that tested the cooperative skills of Asian elephants (Elephas maximus) in Thailand and showed that the pachyderms understand that they will fail at a task without a partner's assistance. The ability to recognize that you sometimes need a little help from your friends is a sign of higher social cognition, psychologists say, and is rarely found in other species. Elephants now join an elite club of social cooperators: chimpanzees, hyenas, rooks, and humans. To test the elephants' cooperation skills, a team of scientists modified a classic experiment first administered to chimpanzees in the 1930s, which requires two animals work together to earn a treat. If they don't cooperate, neither gets the reward. For the elephants, the researchers used a sliding table with a single rope threaded around it. Two bowls of corn were attached to the table, but the elephants could reach them only by pulling two ends of the rope simultaneously. Working with mahout—Asian elephant trainers—trained elephants at the Thai Elephant Conservation Center in Lampang, the researchers first taught individual animals to pull the rope with their trunks. The 12 elephants were then divided into six pairs, and each pair was released to walk to their waiting ropes. If one animal pulled the rope before the other, the rope would slip out, leaving the table—and treats—in place. "That taught them to pull together," says Joshua Plotnik, a postdoc in experimental psychology at the University of Cambridge in the United Kingdom and the lead author of the study, which appears online this week in the Proceedings of the National Academy of Sciences. © 2010 American Association for the Advancement of Science.

Keyword: Intelligence; Evolution
Link ID: 15085 - Posted: 03.08.2011

By Bill Briggs All these years, I thought it was because I was white. And straight. And old. Sure, I’ll get my freak on if I hear “Disco Inferno,” or when Mary J. is in the spot. (Told you I was old. And let me add: Don’t need no hateration.) But my steps aren’t smooth. Those beats and my body never truly connect -- despite what the cocktails tell me. On the dance floor, I'm the male Elaine from "Seinfeld," all kicks, thumbs and no rhythm. Turns out, it’s all in my head, not my hips or feet. A study, released today by researchers at the University of Oxford in England, claims a tiny messenger in the brain is partly to blame for those among us who struggle to grasp the latest dance moves. This is all about GABA (short for gamma-aminobutyric acid). Again: not Gaga, GABA. A naturally occurring chemical, GABA is a bit like the brain’s traffic cop. Nerve cells in the brain are constantly firing and “talking” to each other. GABA helps keep all that chatter from getting out of control. “Our research suggests that an important first step in learning that new skill is a decrease in GABA levels in the motor cortex,” explained Dr. Charlotte Stagg, a junior research fellow at Oxford and at John Radcliffe Hospital. Her study was published online in the journal Current Biology. © 2011 msnbc.com

Keyword: Miscellaneous
Link ID: 15084 - Posted: 03.08.2011

By Neil Bowdler Science reporter, BBC News Scientists say they have found a mechanism which may explain why a poor diet during pregnancy can increase the risk of offspring developing diabetes in later life. They say rat studies indicate an imbalanced diet in the mother can lead to the "silencing" of a gene linked to insulin production in the child. The Cambridge study is in Proceedings of the National Academy of Sciences. Experts said it showed a healthy diet was important during pregnancy. Silent gene Scientists already suspect that a poor diet during pregnancy can result in health problems such as diabetes for the offspring in later life. What the researchers at the University of Cambridge have come up with is a possible explanation. They believe an imbalanced diet in the expectant mother can compromise the long-term functioning of a gene in the child. The gene, called Hnf4a, is thought to play a role in the development of the pancreas and in insulin production. Because of the difficulties of testing the theory on pregnant women, they fed rats a protein-deficient diet and found higher rates of type 2 diabetes in the offspring, as expected. What they also found in the offspring was that this Hnf4a gene appeared to be "silenced" or "switched off" as the rats aged. The researchers suggest this may both cause diabetes, and can be linked back to the maternal diet. BBC © MMXI

Keyword: Obesity; Development of the Brain
Link ID: 15083 - Posted: 03.08.2011

By ANEMONA HARTOCOLLIS Every morning, Kay Brown engages in a ritual similar to a heroin addict’s, or a diabetic’s: she sticks herself with a syringe. Only hers contains hCG, a pregnancy hormone. Ms. Brown, 35, is not taking hCG to help her bear a child. She believes that by combining the hormone injections with a 500-calorie-a-day diet, she will achieve a kind of weight-loss nirvana: losing fat in all the right places without feeling tired or hungry. “I had a friend who did it before her wedding,” Ms. Brown said. “She looks great.” Women like Ms. Brown are streaming into doctors’ offices and weight-loss clinics all over the country, paying upward of $1,000 a month for a consultation, a supply of the hormone and the syringes needed to deliver it. More than 50 years after a doctor at a Roman clinic began promoting hCG as a dieting aid, it is as popular as ever, even though there is scant evidence that it makes any difference. The regimen combines daily injections with a near-starvation diet, and patients, mostly women, are often enticed by promises that they can lose about a pound a day without feeling hungry. Perhaps even more seductively, they are frequently told that the hCG will prompt their bodies to carry away and metabolize fat that has been stored where they least want it — in their upper arms, bellies and thighs. In response to inquiries stirred up by the diet’s popularity, the Food and Drug Administration warned in January that “homeopathic” forms of hCG, like lozenges and sprays, sold over the Internet and in some health food stores, are fraudulent and illegal if they claim weight-loss powers. © 2011 The New York Times Company

Keyword: Obesity
Link ID: 15082 - Posted: 03.08.2011

By RONI CARYN RABIN A leisurely four-course dinner at a fine restaurant can take two hours to eat, while meals eaten at home are usually over in 30 minutes. Does one leave you more satisfied — and less likely to snack afterward — than the other? Researchers in the Netherlands set out to see whether, all other things being equal — meaning people ate the exact same quantities of the exact same food — the speed of consumption had an effect on diners’ feelings of satiety and hunger and on the chemical signals, or hormones, that are involved in appetite regulation. The researchers also wanted to see how the pace of the meal affected postprandial snacking. Though people said they felt more sated and less hungry after a staggered meal that lasted two hours with breaks between courses and didn’t really want to eat more afterward, the experience didn’t change their snacking behavior, said Sofie G. Lemmens, a postdoctoral fellow at Maastricht University in the Netherlands who was the lead author of the paper, published in the March issue of The Journal of Nutrition. Two and a half hours after the beginning of the meal, when the diners were offered an array of traditional Dutch tea treats like apple cake, chocolate-covered marshmallows, peanuts, chips and waffles, they ate almost as much as they did two and a half hours after a meal that they had consumed in 30 minutes. © 2011 The New York Times Company

Keyword: Obesity
Link ID: 15081 - Posted: 03.08.2011

By Deborah Kotz Dianne Sanborn admits that “it didn’t make any sense’’ to take a sugar pill to relieve the severe constipation, abdominal pain, and bloating — attributed to irritable bowel syndrome — that she’d suffered from since college. But eager to try anything, the 64-year-old entered a clinical trial last spring at Beth Israel Deaconess Medical Center, where she was told to take placebo caplets twice a day for three weeks. “Before I took each pill, I had to tell myself that it was going to make me feel better, but I was very skeptical,’’ says the 64-year-old former nurse practitioner who had to quit her job 13 years ago because of her medical problems. “I certainly knew placebos could work but only if you didn’t know it was a placebo.’’ When her symptoms dissipated three days after she started taking the placebos, however, she became a believer. So did many of the other 36 volunteers who were randomly assigned placebos along with any of their usual treatments in the December study published in the journal PLoS ONE. Nearly 60 percent of them reported an improvement in their irritable bowel symptoms compared to 35 percent of the 43 volunteers who weren’t given placebos but were just told to continue their standard therapy. Other research had already demonstrated that sham treatments could dull pain, alleviate depression, and even quell Parkinson’s tremors. But this study was the first to show that placebos have power even when patients know they’re taking them. And now placebo researchers are gearing up to figure out ways to move side-effect-free sugar pills into mainstream clinical practice — that’s the goal of a placebo-studies program that Harvard Medical School is launching in July with 30 faculty members. “We’d like to eventually see placebo treatments become a full partner in medical care along with active medications, procedures, and surgery,’’ says PLoS ONE study author Dr. Ted Kaptchuk, who will head the program. © 2011 NY Times Co.

Keyword: Pain & Touch; Stress
Link ID: 15080 - Posted: 03.08.2011

By BENEDICT CAREY For years scientists have dreamed of developing a genuine memory booster, a drug that could tune the brain’s biological search engine so that it’s better at retrieving not only recently learned facts, like last night’s dinner menu, but details that seem all but lost in the fog of time, like childhood classmates’ names and antics. Such a substance would have obvious appeal — for people at risk of dementia, to name just one group — but the search has been very slow going. Stimulants like caffeine and nicotine can sharpen the memory, but like other temporary enhancers, they need to be taken when the information is learned or retrieved to make a difference. Now, researchers in Israel and New York report that they have been able to strengthen memories formed well in the past, using a brain substance involved in anchoring and maintaining the memory in the first place. The finding, reported last week in the journal Science, is one of two recent studies in which neuroscientists used molecules active in memory formation to, in effect, goose the system and improve recall. Both studies were conducted in rats, which provide a very rough model for human memory. “The idea that an older memory can be strengthened is a novel and exciting finding,” said Jim McGaugh, a neuroscientist at the University of California, Irvine, who was not involved in the research. “But it also raises the question: How does this work? And, does it apply to all memories?” © 2011 The New York Times Company

Keyword: Learning & Memory
Link ID: 15079 - Posted: 03.08.2011

Using cannabis as a teenager or young adult increases the risk of psychosis, a report suggests. The study published in the British Medical Journal involved tracking 1,900 people over a period of 10 years. Although the link between cannabis and psychosis is well established, it had been unclear whether cannabis triggered the disorder. This research strongly suggests that cannabis use comes first, rather than people taking it for their symptoms. The research was led by Professor Jim van Os from Maastricht University in the Netherlands, and included researchers from the Netherlands, Germany, Switzerland and the UK. They excluded anyone who reported cannabis use or pre-existing psychotic symptoms at the start of the study, which took place in Germany. The participants in the study, aged between 14 and 24, were assessed for cannabis use and psychotic symptoms at three points over a 10-year period. It found that cannabis use "significantly" increased the risk of psychotic symptoms, even when other factors such as socio-economic status, use of different drugs and other psychiatric conditions were taken into account. Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry, said the study added "a further brick to the wall of evidence" showing that use of traditional cannabis is a contributory cause of psychoses like schizophrenia. BBC © MMXI

Keyword: Drug Abuse; Schizophrenia
Link ID: 15078 - Posted: 03.07.2011

By GARDINER HARRIS DOYLESTOWN, Pa. — Alone with his psychiatrist, the patient confided that his newborn had serious health problems, his distraught wife was screaming at him and he had started drinking again. With his life and second marriage falling apart, the man said he needed help. But the psychiatrist, Dr. Donald Levin, stopped him and said: “Hold it. I’m not your therapist. I could adjust your medications, but I don’t think that’s appropriate.” Like many of the nation’s 48,000 psychiatrists, Dr. Levin, in large part because of changes in how much insurance will pay, no longer provides talk therapy, the form of psychiatry popularized by Sigmund Freud that dominated the profession for decades. Instead, he prescribes medication, usually after a brief consultation with each patient. So Dr. Levin sent the man away with a referral to a less costly therapist and a personal crisis unexplored and unresolved. Medicine is rapidly changing in the United States from a cottage industry to one dominated by large hospital groups and corporations, but the new efficiencies can be accompanied by a telling loss of intimacy between doctors and patients. And no specialty has suffered this loss more profoundly than psychiatry. Trained as a traditional psychiatrist at Michael Reese Hospital, a sprawling Chicago medical center that has since closed, Dr. Levin, 68, first established a private practice in 1972, when talk therapy was in its heyday. Then, like many psychiatrists, he treated 50 to 60 patients in once- or twice-weekly talk-therapy sessions of 45 minutes each. Now, like many of his peers, he treats 1,200 people in mostly 15-minute visits for prescription adjustments that are sometimes months apart. © 2011 The New York Times Company

Keyword: Depression
Link ID: 15077 - Posted: 03.07.2011

By PERRI KLASS, M.D. Humans are asymmetric animals. Early in our embryonic development, organs turn to one side or the other — heart to the left, liver to the right and so on. In rare cases, an organ may turn up on the “wrong” side with no untoward effects. (I once examined a child with dextrocardia, or heart on the right.) But there is one form of asymmetry that is common and, until quite recently, stigmatized: handedness. Over the centuries, left-handers have been accused of criminality and dealings with the devil, and children have been subjected to “re-education.” In recent years the stigma has largely vanished; among other things, four of our last five presidents — Reagan, the elder Bush, Clinton, Obama — have been left-handed. (Reagan is sometimes cited as ambidextrous.) But the riddle of why about 10 percent of children are born with this essentially human asymmetry remains. “This is really still mysterious,” said Clyde Francks, the lead author of a 2007 study in which Oxford University researchers identified a genetic variant linked to left-handedness. Hand asymmetry (whether left or right) is related to brain asymmetry. And that, Dr. Francks said, “is not at all understood; we’re really at the very beginning of understanding what makes the brain asymmetrical and what goes wrong — we don’t understand that process in the normal case.” © 2011 The New York Times Company

Keyword: Laterality
Link ID: 15076 - Posted: 03.07.2011