By AMANDA SCHAFFER For years, researchers have investigated how the body loses the ability to produce enough insulin, a hallmark of diabetes. Now an intriguing theory is emerging, and it suggests a potential treatment that few scientists had considered. The hormone insulin helps shuttle glucose, or blood sugar, from the bloodstream into individual cells to be used as energy. But the body can become resistant to insulin, and the beta cells of the pancreas, which produce the hormone, must work harder to compensate. Eventually, the thinking goes, they lose the ability to keep up. “We used to say that the beta cells poop out,” said Alan Saltiel, director of the Life Sciences Institute at the University of Michigan. In reality, he added, this shorthand meant “we have no idea what’s going on.” Some evidence suggested that large numbers of these cells died through a process of programmed cell death called apoptosis. But that was at best a partial explanation. Now, researchers at Columbia University have put forth a surprising alternative. In mice with Type 2 diabetes, the researchers showed that beta cells that had lost function were not dead at all. Most remained alive, but in a changed form. They reverted to an earlier developmental, “progenitor,” state. It’s as if these cells are “stepping back in time to a point where they look like they might have looked during their development,” said Dr. Domenico Accili, director of the Columbia University Diabetes and Endocrinology Research Center, who led the new work. © 2012 The New York Times Company

Keyword: Stress; Obesity
Link ID: 17321 - Posted: 10.02.2012

By Gregory Thomas, During an introductory psychology course at Britain’s University of Essex in 2009, Arnold Wilkins asked his class to participate in a quick experiment. Wilkins projected two images on a wall and asked students to write down whether they found either of them disturbing. One was a photograph of a woody landscape. The other was a close-up of a lotus-flower seedpod — a flat-faced pod pocked with small holes. Most of the students were unmoved, but one, freshman An Le, recalls being both transfixed and revolted by the lotus image. “It felt like I was in shock,” he says. Le is far from alone in his response. Thousands of people claim to suffer trypophobia, a term derived from the Greek “trypo,” which means punching, drilling or boring holes. It refers to an irrational fear of clusters of small holes, such as beehives, ant holes and even bubbles in a pancake on the griddle or air pockets in a chocolate bar. On Web sites and blogs, self-diagnosed trypophobes share tales of vomiting, sleep loss and anxiety attacks at the sight of such objects as honeycombs and rotting wood. They say the fears are haunting and disruptive of their daily lives. But the medical world hasn’t yet embraced the phobia as real. Trypophobia isn’t listed in any major dictionary or in the Diagnostic and Statistical Manual of Mental Disorders. Attempts to add trypophobia to the Oxford English Dictionary and even to establish a Wikipedia page have been rebuffed because there hasn’t been any research published on the subject. A Wikipedia editor who deleted an entry on trypophobia in 2009 noted that trypophobia is “likely hoax and borderline patent nonsense.” © 1996-2012 The Washington Post

Keyword: Emotions; Learning & Memory
Link ID: 17320 - Posted: 10.02.2012

By BENEDICT CAREY Proposed changes to the official diagnosis of autism will not reduce the proportion of children found to have it as steeply as many have feared, scientists reported on Tuesday, in an analysis that contradicts several previous studies. Earlier research had estimated that 45 percent or more of children currently on the “autism spectrum” would not qualify under a new definition now being refined by psychiatric researchers — a finding that generated widespread anxiety among parents who rely on state-financed services for their children. The new report, posted online Tuesday by The American Journal of Psychiatry, concluded that the number who would be excluded is closer to 10 percent. The finding may soothe the anxieties of some parents, but will not likely settle the debate over the effect of the new diagnosis. All sides agree that the proposed criteria are narrower and will likely result in fewer diagnoses of autism, but until doctors begin using the new definition widely, the predictions of its effect are just that: predictions. The debate has simmered over the past year as an expert panel appointed by the American Psychiatric Association has updated its proposals for the association’s Diagnostic and Statistical Manual of Mental Disorders, scheduled to take effect in May 2013. The manual is the field’s standard reference, and several recent studies suggested that the amended autism definition was far narrower than intended. © 2012 The New York Times Company

Keyword: Autism
Link ID: 17319 - Posted: 10.02.2012

By Simon J Makin Humans are born to a longer period of total dependence than any other animal we know of, and we also know that mistreatment or neglect during this time often leads to social, emotional, cognitive and mental health problems in later life. It’s not hard to imagine how a lack of proper stimulation in our earliest years – everything from rich sensory experiences and language exposure to love and care – might adversely affect our development, but scientists have only recently started to pull back the curtain on the genetic, molecular and cellular mechanisms that might explain how these effects arise in the brain. You’ll often hear it said that human beings are “social animals”. What biologists tend to mean by that phrase is behaviour like long-lasting relationships or some kind society, whether that’s the social hierarchy of gorillas or the extreme organisation of bees and ants. But, to an extent, most animals are social. A mother usually bonds with its offspring in any species of bird or mammal you care to mention, and almost all animals indulge in some kind of social behaviour when they mate. But there is another sense in which most animals seem to be fundamentally social. There is an emerging scientific understanding of the way social experience moulds the biochemistry of the brain and it looks like most species don’t just prefer the company of others – they need it to develop properly. Take that staple of genetics research, drosophila – aka the fruit fly. While they are not as social as primates or bees, they are more social than you might think, and there have been studies showing that social isolation can disrupt their mating behaviour or even reduce their lifespan. © 2012 Scientific American,

Keyword: Development of the Brain; Glia
Link ID: 17318 - Posted: 10.02.2012

By NICHOLAS BAKALAR A small study has found that obese children are more likely than others to have a weak sense of taste. German researchers tested tasting ability in 99 obese and 94 normal-weight children, whose average age was 13, by having them try to identify tastes on strips of filter paper and asking them to distinguish among sweet, sour, salty, umami (savory) and bitter. The children also were asked to rate the taste’s intensity on a five-point scale. Girls were better than boys at distinguishing tastes, and older children scored higher than younger; there were no differences by ethnicity. Obese children scored an average of 12.6 out of a possible 20, while the normal-weight children averaged 14.1, a statistically significant difference. On the intensity scale, obese children rated all flavor concentrations lower than did those in the normal-weight group. “We think it’s important, especially for young children, to get different tastes so that they can improve their taste sensitivity,” said the lead author, Dr. Johanna Overberg, a pediatrician at Charité Children’s Hospital in Berlin. “If you taste more and different things at younger ages, you can do this.” The authors, writing online in the Archives of Disease in Childhood, say the reason for the association is unclear, but they suggest that the hormone leptin may affect both body weight and the sensitivity of taste buds. Copyright 2012 The New York Times Company

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 17317 - Posted: 10.02.2012

by Jessica Hamzelou California has become the first US state to ban unfounded therapies that attempt to turn gay teenagers straight. "These practices have no basis in science or medicine and they will now be relegated to the dustbin of quackery," said state governor Jerry Brown in a statement to the San Francisco Chronicle. He signed a bill outlawing the therapies on 29 September. Brown's conclusions are in line with those reached a few years ago by a task force of psychologists who were commissioned by the American Psychological Association to assess all published research on the therapies. The group, led by Judith Glassgold, found no evidence that the treatment was effective. "The scientific evidence does not support such therapies," says Clinton Anderson, director of the APA's Lesbian, Gay, Bisexual and Transgender Concerns office. "They were not helpful and could be harmful," says Glassgold, who is based in Washington DC. "Most people became more depressed and anxious, and could become suicidal." "Usually these talk therapies are based on the assumption that homosexuality is a mental illness caused by poor parenting and confused gender roles," she adds. "They attempt to explain that to the patient, and try to get them to act and behave in a heterosexual manner." © Copyright Reed Business Information Ltd

Keyword: Sexual Behavior
Link ID: 17316 - Posted: 10.02.2012

By Tori Rodriguez A common complaint about wrinkle-masking Botox is that recipients have difficulty displaying emotions on their faces. That side effect might be a good thing, however, for people with treatment-resistant depression. In the first randomized, controlled study on the effect of botulinum toxin—known commercially as Botox—on depression, researchers investigated whether it might aid patients with major depressive disorder who had not responded to antidepressant medications. Participants in the treatment group were given a single dose (consisting of five injections) of botulinum toxin in the area of the face between and just above the eyebrows, whereas the control group was given placebo injections. Depressive symptoms in the treatment group decreased 47 percent after six weeks, an improvement that remained through the 16-week study period. The placebo group had a 9 percent reduction in symptoms. The findings appeared in May in the Journal of Psychiatric Research. Study author M. Axel Wollmer, a psychiatrist at the University of Basel in Switzerland, believes the treatment “interrupts feedback from the facial musculature to the brain, which may be involved in the development and maintenance of negative emotions.” Past studies have shown that Botox impairs people's ability to identify others' feelings, and the new finding adds more evidence: the muscles of the face are instrumental for identifying and experiencing emotions, not just communicating them. © 2012 Scientific American

Keyword: Depression; Emotions
Link ID: 17315 - Posted: 10.02.2012

by Melissa Lee Phillips  Giving a whole new meaning to "pregnancy brain," a new study shows that male DNA—likely left over from pregnancy with a male fetus—can persist in a woman's brain throughout her life. Although the biological impact of this foreign DNA is unclear, the study also found that women with more male DNA in their brains were less likely to have suffered from Alzheimer's disease—hinting that the male DNA could help protect the mothers from the disease, the researchers say. During mammalian pregnancy, the mother and fetus exchange DNA and cells. Previous work has shown that fetal cells can linger in the mother's blood and bone for decades, a condition researchers call fetal microchimerism. The lingering of the fetal DNA, research suggests, may be a mixed blessing for a mom: The cells may benefit the mother's health—by promoting tissue repair and improving the immune system—but may also cause adverse effects, such as autoimmune reactions. One question is how leftover fetal cells affect the brain. Researchers have shown that fetal microchimerism occurs in mouse brains, but they had not shown this in humans. So a team led by autoimmunity researcher and rheumatologist J. Lee Nelson of the Fred Hutchinson Cancer Research Center in Seattle, Washington, took samples from autopsied brains of 59 women who died between the ages of 32 and 101. By testing for a gene specific to the Y chromosome, they found evidence of male DNA in the brains of 63% of the women. (The researchers did not have the history of the women's pregnancies.) The male DNA was scattered across multiple brain regions, the team reports online today in PLoS ONE. Because some studies have suggested that the risk of Alzheimer's disease (AD) increases with an increasing number of pregnancies, the team also examined the brains for signs of the disease, allowing them to determine whether AD correlated with the observed microchimerism. Of the 59 women, 33 had AD—but contrary to the team's expectation, the women with AD had significantly less male DNA in their brains than did the 26 women who did not have AD. © 2010 American Association for the Advancement of Science

Keyword: Sexual Behavior; Stem Cells
Link ID: 17314 - Posted: 09.29.2012

  By Jason G. Goldman In 1976, psychologists John and Sandra Condry of Cornell University had 204 human adults view videotaped footage of an infant boy named David and infant girl named Dana, and asked them to describe the infants’ facial expressions and dispositions. They described their findings in an article in the journal Child Development. In the video, infants were shown responding to various stimuli, which were not visible to the viewer. For example, they’d be shown a teddy bear, so that their reaction could be recorded. They were also videotaped responding to a loud buzzer and to a jack-in-the-box. Participants described David’s response to the jack-in-the-box, for example, as “anger,” while they described Dana’s response to the same toy as “fear.” Participants rated David’s emotional responses to all three stimuli as more “intense” than Dana’s. Here’s the catch: David and Dana were the same infant. Each of the experiment participants were shown the same video of the same infant. Half of them were told the infant was a nine-month-old boy named David, and half were told the infant was a nine-month-old girl named Dana. That they described the “two” infants in such different ways was evidence that the participants’ perceptions were at least based in part upon pre-existing biases and preconceptions about the different ways in which boys and girls experience the world. Now, a group of researchers from Tokyo and Berlin have published a new finding about the relationship between personality and genetics in captive elephants. They collected genetic information from the blood, feces, tissues, cheek swabs, or hair of 196 Asian (Elephas maximus) and African elephants (Loxodonta africana) in Japanese, American, and Canadian zoos, and sanctuaries in Thailand. Personality information was collected for a seventy-five of those elephants by distributing to questionnaires to their keepers. Each elephant was assessed by more than one keeper. An improved understanding of elephant personality would be not only extremely interesting from a basic science perspective, but also extremely useful for more effectively maintaining captive elephant populations in zoos and sanctuaries. The better that zookeepers and curators understand the psychology of the animals in their collections, the better the quality of care can be, which directly impacts animal welfare. © 2012 Scientific American  

Keyword: Genes & Behavior
Link ID: 17313 - Posted: 09.29.2012

  Sandrine Ceurstemont, editor, New Scientist TV Think an object can't be in two places at once? This animation shows how the perceived location of a dot is influenced by what's happening around it. In this video, a flashing dot is surrounded by two diamonds that shift across the screen. When they move horizontally, the dot seems to shift sideways and slightly upwards. In a second version, in which the corners of the diamonds are obscured, the dot appears to move diagonally. In fact, the dot never changes place. The illusion is the work of Peter Kohler from Dartmouth College in Hanover, New Hampshire, and his team. Kohler has been trying to determine if the dot's perceived shift in position is caused by the overall motion of the diamonds or that of its components. For example, although the shapes as a whole are moving sideways, viewing the edges in isolation shows that segments of the diamonds are moving upwards. "Our results show that global motion does influence the shift," he says. "But the fact that even the unoccluded diamond does not yield a purely horizontal shift indicates that local signals are also very important." The team now plans to investigate how quickly our brain perceives the shift. "Integration of local and global motion is known to take about 150 milliseconds," says Kohler. "It would be interesting to see if the effect takes a similar amount of time to kick in." By presenting the illusion for very short amounts of time, the researchers will be able to determine if different versions are initially perceived in the same way. "We also have fMRI work under way to identify brain areas that represent the perceived shifted location rather than the actual location," says Kohler. The illusion was recently presented at the European Conference on Visual Perception in Alghero, Italy. © Copyright Reed Business Information Ltd.  

Keyword: Vision
Link ID: 17312 - Posted: 09.29.2012

By Gary Stix 14 inSharHuntington’ disease, which killed folk singer Woody Guthrie, seems to put into overdrive the main chemical that turns on brain cells, ultimately leading to their death. The normal function of the neurotransmitter glutamate, the chemical overproduced in Huntington’s, is also intimately involved with learning. Researchers from Ruhr University and the University of Dortmund in Germany have been intrigued by the question of whether the neurodegeneration initiated by glutamate in this genetic disorder is all bad. Is it simply  burning out brain circuits? Or might an excess of the chemical also help presymptomatic carriers of the Huntington’s gene or even patients with the disease itself,  learn some things faster or better? “Neurotransmission causes cell death but we know from the vast amount of literature that learning processes very much depend on glutamate neurotransmission; so there may be two effects of one and the same process,” says Christian Beste of Ruhr University. “On the one hand this process may lead to neurodegeneration. But on the other hand, it may augment a cognitive process that depends on glutamate transmission.” Beste is the lead author on a paper published this month in Current Biology that found that those who have the genetic mutation for Huntington’s but who have yet to develop inevitable symptoms of the disease perform better on a learning task than a control group that lacks the mutation. The 29 Huntington’s gene carriers learned to detect twice as fast as the 45 controls a change in brightness of a small bar as its orientation on a computer screen altered. In fact, the Huntington’s carriers with the most pronounced mutations—the number of repetitions of a short DNA segment determines how early disease onset occurs—logged the best performance. © 2012 Scientific American,  

Keyword: Huntingtons
Link ID: 17311 - Posted: 09.29.2012

by Melissa Lee Phillips Giving a whole new meaning to "pregnancy brain," a new study shows that male DNA—likely left over from pregnancy with a male fetus—can persist in a woman's brain throughout her life. Although the biological impact of this foreign DNA is unclear, the study also found that women with more male DNA in their brains were less likely to have suffered from Alzheimer's disease—hinting that the male DNA could help protect the mothers from the disease, the researchers say. During mammalian pregnancy, the mother and fetus exchange DNA and cells. Previous work has shown that fetal cells can linger in the mother's blood and bone for decades, a condition researchers call fetal microchimerism. The lingering of the fetal DNA, research suggests, may be a mixed blessing for a mom: The cells may benefit the mother's health—by promoting tissue repair and improving the immune system—but may also cause adverse effects, such as autoimmune reactions. One question is how leftover fetal cells affect the brain. Researchers have shown that fetal microchimerism occurs in mouse brains, but they had not shown this in humans. So a team led by autoimmunity researcher and rheumatologist J. Lee Nelson of the Fred Hutchinson Cancer Research Center in Seattle, Washington, took samples from autopsied brains of 59 women who died between the ages of 32 and 101. By testing for a gene specific to the Y chromosome, they found evidence of male DNA in the brains of 63% of the women. (The researchers did not have the history of the women's pregnancies.) The male DNA was scattered across multiple brain regions, the team reports online today in PLoS ONE. © 2010 American Association for the Advancement of Science

Keyword: Development of the Brain; Sexual Behavior
Link ID: 17310 - Posted: 09.27.2012

By James Gallagher Health and science reporter, BBC News Too many people may be damaging their health by self-medicating with sleeping pills, according to the Royal Pharmaceutical Society. It said half of people with insomnia diagnosed themselves and took medication without seeking medical advice. However, the society said insomnia was often part of other physical or mental health problems which needed treating. The warning was based on the findings of a survey of 2,077 people. Insomnia is difficulty in getting to sleep, staying asleep or getting enough good quality sleep night after night. One in three people in the UK are thought to have bouts of insomnia. It can be caused by psychiatric problems such as depression, anxiety disorders and schizophrenia. Other illnesses including heart disease, Alzheimer's disease and hormonal problems can also disturb the normal pattern of sleep. In the survey, 30% of people said they had taken sleeping pills for more than a month without getting advice while 14% had gone six months. One pharmacist, Paul Johnson, said: "It's worrying that so many people are overusing sleeping remedies. "They can be effective for short-term treatment of mild insomnia but should not be taken for long periods without advice because they can hide a serious health problem which could get worse if it remains untreated. BBC © 2012

Keyword: Sleep
Link ID: 17309 - Posted: 09.27.2012

FRANK JORDANS, Associated Press BERLIN (AP) — More than half the cases of severe intellectual disability caused by genetic defects are the result of random mutations, not inherited, a European study published Thursday suggests. The findings of the small-scale study give hope to parents of children born with a severe intellectual disabilities who are worried about having another baby with the same condition, said Anita Rauch, a researcher at the Institute of Medical Genetics in Zurich who was one of the study's lead authors. It examined the genetic makeup of 51 children, both of their parents and a control group. The study concluded that in at least 55 percent of cases there was no evidence that parents carried faulty genes responsible for the disability. "The average chances of having another child with the same disability are usually estimated at eight percent, but if we know that it was caused by a random mutation the chances of recurrence drop dramatically," Rauch said. Hans-Hilger Ropers, the director of Berlin's Max Planck Institute for Molecular Genetics, who was not involved in the study, said the basic science appeared sound but noted that it excluded children whose parents were blood relatives and so the results could be biased toward random mutations. Ropers said a larger study that included subjects from parts of the world where marriage between blood relatives is more common could produce different results. © 2012 Hearst Communications Inc.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 17308 - Posted: 09.27.2012

Clint Witchalls James R. Flynn is Professor Emeritus at the University of Otago, New Zealand. Flynn researches intelligence and is best known for the discovery that, over the past century, IQs have been rising at a rate of about 3 points per decade (the Flynn-effect). In advance of his new book on the subject, Clint Witchalls asked him about this and some of Professor Flynn's more recent research findings: Clint Witchalls: How has our way of thinking and of solving problems changed over the past century? James R. Flynn: Today we take it for granted that using logic on the abstract is an ability we want to cultivate and we are interested in the hypothetical. People from 1900 were not scientifically oriented but utilitarian and they used logic, but to use it on the hypothetical or on abstractions was foreign to them. Alexander Luria [a Soviet psychologist] went to talk to headmen in villages in rural Russia and he said to them: "Where there is always snow, bears are white. At the North Pole there is always snow, what colour are the bears there?" And they said: "I've only seen brown bears." And he said: "What do my words convey?" And they said: "Such a thing as not to be settled by words but by testimony." They didn't settle questions of fact by logic, they settled them by experience. Your research found that we have gained 30 points on IQ tests in a century. What is the reason? The ultimate cause of why IQs are rising is the industrial revolution. The proximate cause is how our minds differ from people in 1900 when in the test room. And the intermediate causes, of course, are more cognitively demanding work roles, more cognitively demanding leisure, more formal schooling, and smaller families. © independent.co.uk

Keyword: Intelligence; Learning & Memory
Link ID: 17307 - Posted: 09.27.2012

by Jessica Hamzelou ALZHEIMER'S disease is more prevalent in older people, but we have never known why. Now it seems that about 80 per cent of our brain cells are vulnerable to a process that can turn them toxic. For the first time, cells in the brains of people with Alzheimer's have been shown to "senesce" - a mechanism that stops them dividing and starts them on a path of destruction. With hundreds of experimental treatments for the disease falling by the wayside, we need a new target and it seems as if we have now found one. The discovery of huge numbers of senescent cells in people with Alzheimer's suggests that they play a key role in the condition. Cells that continually replicate in the body, such as those in the skin, lung and kidney, eventually accumulate DNA damage - typically with age. Not all of these damaged cells die though, instead some senesce. When this happens, biological changes within the cell prevent it from dividing or carrying out its normal functions. Research suggests that senescing cells also start producing proteins that trigger inflammation. "It's pretty clear that cell senescence evolved to protect us against cancer," says Judith Campisi of the Buck Institute for Research on Aging in Novato, California. The idea is that once cells accumulate DNA damage, they senesce to avoid incorrect division that can lead to cancer. The benefit of this mechanism over self-destruction is that it sends out a call to the immune system to destroy nearby cells that might also be affected. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 17306 - Posted: 09.27.2012

By Sandra G. Boodman, The 80th birthday party for Josephine van Es marked two milestones, only one of which was apparent at the time. Held in November 2004 at her daughter’s house in Rehoboth Beach, Del., the event was a celebration of her longevity, good health and loving family. It also marked one of the last times van Es can remember feeling well and not beset by the pain that developed soon afterward and has left the inside of her mouth feeling perpetually scalded and with a constant metallic taste. “It’s awful,” said van Es, 87, who says the burning is worse than the taste, which she likens to “sucking on a penny.” Her daughter Karen van Es says that her mother’s problem has taken a toll on both their lives. For nearly eight years, she has taken time from her job at a Northern Virginia veterinary clinic to ferry her mother, who lives independently in a condominium in Lewes, Del., to doctors in Delaware, Philadelphia and Washington. She also has contacted specialists in Florida and Canada hoping one would propose an effective remedy for an ailment that took more than a year to diagnose and has so far eluded treatment. “She tells me, ‘I just feel rotten all the time,’ ” said Karen van Es, 63, an only child who speaks to her mother every day and sees her often. “My mother has lost confidence as a result of this,” Karen van Es said, adding that she often feels helpless and frustrated about not being able to do more. © 1996-2012 The Washington Post

Keyword: Chemical Senses (Smell & Taste); Pain & Touch
Link ID: 17305 - Posted: 09.26.2012

By GRETCHEN REYNOLDS Can you improve your body’s ability to remember by making it move? That rather odd-seeming question stimulated researchers at the University of Copenhagen to undertake a reverberant new examination of just how the body creates specific muscle memories and what role, if any, exercise plays in the process. To do so, they first asked a group of young, healthy right-handed men to master a complicated tracking skill on a computer. Sitting before the screen with their right arm on an armrest and a controller similar to a joystick in their right hand, the men watched a red line squiggle across the screen and had to use the controller to trace the same line with a white cursor. Their aim was to remain as close to the red squiggle as possible, a task that required input from both the muscles and the mind. The men repeated the task multiple times, until the motion necessary to track the red line became ingrained, almost automatic. They were creating a short-term muscle memory. The term “muscle memory” is, of course, something of a misnomer. Muscles don’t make or store memories. They respond to signals from the brain, where the actual memories of any particular movement are formed and filed away. But muscle memory — or “motor memory,” as it is more correctly referred to among scientists — exists and can be quite potent. Learn to ride a bicycle as a youngster, abandon the pastime and, 20 years later, you’ll be able to hop on a bicycle and pedal off. Copyright 2012 The New York Times Company

Keyword: Learning & Memory
Link ID: 17304 - Posted: 09.26.2012

By Gary Stix Market researcher SharpBrains has predicted that the brain fitness industry will range anywhere from $2 billion to $8 billion in revenues by 2015. That’s a wide swath, but the companies that sell brain-tuning software could conceivably hit at least the low end of their sales target by then. The question that persists is whether any of these games and exercises actually enhance the way your brain works, whether it be memory, problem solving or the speed with which you execute a mental task. True, study participants often get better at doing an exercise that is supposedly related to a given facet of cognition. But the ability to master a game or ace a psych test often doesn’t translate into better cognition when specific measures of intelligence are assayed later. One area of research that has shown some promise relates to a method of boosting the mental scratchpad of working memory— keeping in your head a telephone number long enough to dial, for instance. Some studies have demonstrated that a particular technique to energize working memory betters the reasoning and problem-solving abilities known as fluid intelligence. Yet two new studies have now called into question the earlier research on working memory. A recent online publication in the Journal of Experimental Psychology led by a group at the Georgia Institute of Technology showed that 20 sessions on a working memory task did not did not result in a later acing of tests of cognitive ability. Similarly, a group at Case Western Reserve University tried the same “dual n-back test” and published a report in the journal Intellgence that found that better scores did not produce higher tallies for working memory and fluid intelligence. An n-back test requires keeping track of a number, letter or image “n” places back. A dual n-back demands the simultaneous remembering of both a visual and auditory cue perceived a certain number of places back. © 2012 Scientific American

Keyword: Learning & Memory
Link ID: 17303 - Posted: 09.26.2012

The brain that revolutionized physics now can be downloaded as an app for $9.99. But it won't help you win at Angry Birds. While Albert Einstein's genius isn't included, an exclusive iPad application launched Tuesday promises to make detailed images of his brain more accessible to scientists than ever before. Teachers, students and anyone who's curious also can get a look. A medical museum under development in Chicago obtained funding to scan and digitize nearly 350 fragile and priceless slides made from slices of Einstein's brain after his death in 1955. The application will allow researchers and novices to peer into the eccentric Nobel winner's brain as if they were looking through a microscope. "I can't wait to find out what they'll discover," said Steve Landers, a consultant for the National Museum of Health and Medicine Chicago who designed the app. "I'd like to think Einstein would have been excited." After Einstein died, a pathologist named Thomas Harvey performed an autopsy, removing the great man's brain in hopes that future researchers could discover the secrets behind his genius. Harvey gave samples to researchers and collaborated on a 1999 study published in the Lancet. That study showed a region of Einstein's brain - the parietal lobe - was 15 percent wider than normal. The parietal lobe is important to the understanding of math, language and spatial relationships. © 2012 Hearst Communications Inc

Keyword: Miscellaneous
Link ID: 17302 - Posted: 09.26.2012