Chapter 7. Life-Span Development of the Brain and Behavior
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By Charles Q. Choi Scientists have found a kind of brain cell in mice that can instruct stem cells to start making more neurons, according to a new study. In addition, they found that electrical signals could trigger this growth in rodents, raising the intriguing possibility that devices could one day help the human brain repair itself. The study appears in the journal Nature Neuroscience. We knew the brain can generate new neurons, a process known as neurogenesis, via neural stem cells. And neuroscientists knew these stem cells got their instructions from a variety of sources from chemicals in the bloodstream, for instance, and from cells in the structures that hold the cerebrospinal fluid that cushion the brain. Earlier research had suggested brain cells might also be able to command these stem cells to create neurons. Neuroscientist Chay Kuo at the Duke University School of Medicine in Durham, N.C., and his colleagues have now discovered such cells in mice. "It's really cool that the brain can tell stem cells to make more neurons," Kuo says. To begin their experiments, the researchers tested how well a variety of neurotransmitters performed at spurring mouse neural stem cells to produce new neurons; they found that a compound known as acetylcholine performed best. The team then discovered a previously unknown type of neuron that produces an enzyme needed to make acetylcholine. These neurons are found in a part of the adult mouse brain known as the subventricular zone, where neurogenesis occurs. ©2014 Hearst Communication, Inc
Link ID: 19694 - Posted: 06.05.2014
Ian Sample, science correspondent Research on children in Denmark has found that boys with autism were more likely to have been exposed to higher levels of hormones in their mother's wombs than those who developed normally. Boys diagnosed with autism and related disorders had, on average, raised levels of testosterone, cortisol and other hormones in the womb, according to analyses of amniotic fluid that was stored after their mothers had medical tests during pregnancy. The findings add to a growing body of evidence that the biological foundations of autism are laid down well before birth and involve factors that go beyond the child's genetic make-up. The results may help scientists to unravel some of the underlying causes of autism and explain why boys are four to five times more likely to be diagnosed with the condition, which affects around one percent of the population. Amniotic fluid surrounds babies in the womb and contains hormones and other substances that they have passed through their urine. The liquid is collected for testing when some women have an amniocentesis around four months into their pregnancy. Scientists in Cambridge and Copenhagen drew on Danish medical records and biobank material to find amniotic fluid samples from 128 boys who were later diagnosed with autism. Compared to a control group, the boys with autism and related conditions had higher levels of four "sex steroid" hormones that form a biological production line in the body that starts with progesterone and ends with testosterone. "In the womb, boys produce about twice as much testosterone as girls, but compared with typical boys, the autism group has even higher levels. It's a significant difference and may have a large effect on brain development," said Simon Baron-Cohen, director of the Autism Research Centre at Cambridge University. © 2014 Guardian News and Media Limited
Learning a second language can have a positive effect on the brain, even if it is taken up in adulthood, a University of Edinburgh study suggests. Researchers found that reading, verbal fluency and intelligence were improved in a study of 262 people tested either aged 11 or in their seventies. A previous study suggested that being bilingual could delay the onset of dementia by several years. The study is published in Annals of Neurology. The big question in this study was whether learning a new language improved cognitive functions or whether individuals with better cognitive abilities were more likely to become bilingual. Dr Thomas Bak, from the Centre for Cognitive Ageing and Cognitive Epidemiology at the University of Edinburgh, said he believed he had found the answer. Using data from intelligence tests on 262 Edinburgh-born individuals at the age of 11, the study looked at how their cognitive abilities had changed when they were tested again in their seventies. The research was conducted between 2008 and 2010. All participants said they were able to communicate in at least one language other than English. Of that group, 195 learned the second language before the age of 18, and 65 learned it after that time. The findings indicate that those who spoke two or more languages had significantly better cognitive abilities compared to what would have been expected from their baseline test. The strongest effects were seen in general intelligence and reading. The effects were present in those who learned their second language early, as well as later in life. BBC © 2014
Elizabeth Norton It's a sad fact that children born in poverty start out at a disadvantage and continue to fall further behind kids who are more privileged as they grow up. In developing countries, chiefly in Africa and Asia, some 200 million children under age 5 won't reach the same milestones—for physical growth, school performance, and earnings later on—as children who are less deprived. But a new analysis of a long-term study in Jamaica shows that surprisingly simple ways of stimulating children’s mental development can have dramatic benefits later in life. The children were participants in the Jamaican Study, a project geared toward improving cognitive development begun in the mid-1980s by child health specialists Sally Grantham-McGregor of University College London and Susan Walker of the University of the West Indies, Mona, in Jamaica. They focused on children between the ages of 9 and 24 months whose growth was stunted, placing them in the bottom 5% of height for their age and sex (an easy-to-quantify gauge of extreme poverty). Children of normal height in the same neighborhoods were also studied for comparison. For 2 years, community health workers visited the families weekly. One group was given nutritional assistance only (a formula containing 66% of daily recommended calories, along with vitamins and minerals). One group received a mental and social stimulation program only, and one group got stimulation and nutritional assistance. A final group had no intervention and served as a control. The mental stimulation program involved giving parents simple picture books and handmade toys, and encouraging them to read and sing to their children and point out names of objects, shapes, and colors. They were also taught better ways to converse and respond to their toddlers. These everyday interactions aren't always part of the culture in low-income countries, explains Paul Gertler, an economist at the University of California, Berkeley. "Parents might have five or six kids and few toys. They might be working really hard and have a lot of competing demands. They might not have been taught how to talk to their children, or how important and effective it is," he says. Past research attests to the importance of everyday conversation for children’s mental development: A recent study suggests that children of affluent parents do better in life in large part because their parents talk to them more. © 2014 American Association for the Advancement of Science
Pain is a symptom of many disorders; chronic pain can present as a disease in of itself. The economic cost of pain is estimated to be hundreds of billions of dollars annually in lost wages and productivity. “This database will provide the public and the research community with an important tool to learn more about the breadth and details of pain research supported across the federal government. They can search for individual research projects or sets of projects grouped by themes uniquely relevant to pain,” said Linda Porter, Ph.D., Policy Advisor for Pain at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH). “It also can be helpful in identifying potential collaborators by searching for topic areas of interest or for investigators.” Users of the database easily can search over 1,200 research projects in a multi-tiered system. In Tier 1, grants are organized as basic, translational (research that can be applied to diseases), or clinical research projects. In Tier 2, grants are sorted among 29 scientific topic areas related to pain, such as biobehavioral and psychosocial mechanisms, chronic overlapping conditions, and neurobiological mechanisms. The Tier 2 categories are also organized into nine research themes: pain mechanisms, basic to clinical, disparities, training and education, tools and instruments, risk factors and causes, surveillance and human trials, overlapping conditions, and use of services, treatments, and interventions.
By By Tanya Lewis, It's not every day you see a mouse with a mohawk. But that's what researchers saw while studying mice that had a genetic mutation linked to autism. The mohawks that the mice were sporting actually resulted from their "over-grooming" behavior, repeatedly licking each other's hair in the same direction. The behavior resembles the repetitive motions displayed by some people with autism, and the researchers say their experiments reveal a link between the genetic causes of autism and their effects on the brain, suggesting potential avenues for treating the disorder. "Our study tells us that to design better tools for treating a disease like autism, you have to get to the underlying genetic roots of its dysfunctional behaviors, whether it is over-grooming in mice or repetitive motor behaviors in humans," study researcher Gordon Fishell, a neuroscientist at NYU Langone Medical Center, said in a statement. Autism is a spectrum of developmental disorders that involve social impairments and communication deficits. People with autism may also engage in repetitive behaviors, such as rocking or hand flapping. In the study, detailed today (May 25) in the journal Nature, the researchers bred mice that lacked a gene for a protein called Cntnap4, which is found in brain cells called interneurons. Having low levels of this protein leads to the abnormal release of two brain-signaling molecules, known as dopamine and GABA. Dopamine is involved in sensations of pleasure; GABA (which stands for gamma-aminobutyric acid) dampens neural activity and regulates muscle tone. Mice that lacked the gene for this critical brain protein were found to obsessively groom their fellow animals' fur into mohawk-like styles, suggesting a link between genetics, brain function and autistic behaviors.
Claudia M. Gold When Frank was a young boy, and he committed some typical toddler transgression such as having a meltdown when it was time to leave the playground, his father would slap him across the face, hurting and humiliating him in a very public way. When I spoke with Frank over 20 years later, in the context of helping him with his own son Leo's frequent tantrums in my behavioral pediatrics practice, he did not describe this experience as "trauma." Rather, he described it in a very matter-of-fact tone. But when we explored in detail his response to his son's tantrums, we discovered that, flooded by the stress of his own memories, Frank in a sense would shut down. Normally a thoughtful and empathic person, he simply told Leo to "cut it out." As we spoke he recognized how he was emotionally absent during these moments, which were increasing in frequency. It seemed as if Leo was testing Frank, perhaps looking for a more appropriate response that would help him manage this normal behavior. Once this process was brought in to awareness, Frank was able to be present with Leo- to tolerate his tantrums and understand them from his 2-year-old perspective. Soon the frequency and intensity of the tantrums returned to a level typical for Leo's developmental stage. Frank, greatly relieved, once again found himself enjoying his son. The upcoming Boston conference; Psychological Trauma: Neuroscience, Attachment, and Therapeutic Interventions, promises to offer insight in to the developmental neuroscience behind this story. What Frank experienced as a young child might be termed "quotidian" or "everyday" trauma. It was not watching a relative get shot, or having his house washed away in an avalanche. It was a daily mismatch with his father- he was looking for reassurance and containment and instead got a slap across the face. It was what leading researcher Ed Tronick would term "unrepaired mismatch." Frank, in a way that is extremely common- termed "intergenerational transmission of trauma"- was then repeating this cycle with his own child. When this dynamic was brought in to awareness, he was able to "repair the mismatch," setting his relationship with his own son on a healthier path. ©2014 Boston Globe Media Partners, LLC
By Neuroskeptic Nothing that modern neuroscience can detect, anyway. This is the message of a provocative article by Pace University psychologist Terence Hines, just published in Brain and Cognition: Neuromythology of Einstein’s brain As Hines notes, the story of how Einstein’s brain was preserved is well known. When the physicist died in 1955, his wish was to be cremated, but the pathologist who performed the autopsy decided to save his brain for science. Einstein’s son Hans later gave his blessing to this fait accompli. Samples and photos of the brain were then made available to neuroscientists around the world, who hoped to discover the secret of the great man’s genius. Many have claimed to have found it. But Hines isn’t convinced. Some researchers, for instance, have used microscopy to examine Einstein’s brain tissue on a histological (cellular) level. Most famous amongst these studies is Diamond et al, who in 1985 reported that Einstein’s brain had a significantly higher proportion of glial cells than those of matched, normal control brains. However, Hines points out that this ‘finding’ may have been a textbook example of the multiple-comparisons problem: Diamond et al. (1985) reported four different t-tests, each comparing Einstein’s brain to the brains of the controls. Only one of the four tests performed was significant at the .05 level. Although only the results of the neuron to glial cell ratios were reported by Diamond et al. (1985), the paper makes it clear that at least six other dependent measures were examined: (1) number of neurons, (2) total number of glial cells, (3) number of astrocytes, (4) number of oligodendrocytes, (5) neuron to astrocyte ratio and (6) neuron to oligodendrocyte ratio. Thus a total of seven different dependent measures were examined in four different brain areas for a total of 28 comparisons… one p less than 0.05 result out of 28 is not surprising. Other histological studies followed from other researchers, but Hines says that they do not present a coherent picture of clear differences:
By BRUCE WEBER Dr. Gerald M. Edelman at Rockefeller University in 1972, in front of a gamma globulin model. Credit Don Hogan Charles/The New York Times Dr. Gerald M. Edelman, who shared a 1972 Nobel Prize for a breakthrough in immunology and went on to contribute key findings in neuroscience and other fields, becoming a leading if contentious theorist on the workings of the brain, died on Saturday at his home in the La Jolla section of San Diego. He was 84. The precise cause was uncertain, but Dr. Edelman had Parkinson’s disease and prostate cancer, his son David said. Dr. Edelman was known as a problem solver, a man of relentless intellectual energy who asked big questions and attacked big projects. What interested him, he said, were “dark areas” where mystery reigned. “Anybody in science, if there are enough anybodies, can find the answer,” he said in a 1994 interview in The New Yorker. “It’s an Easter egg hunt. That isn’t the idea. The idea is: Can you ask the question in such a way as to facilitate the answer? And I think the great scientists do that.” His Nobel Prize in Physiology or Medicine came in 1972 after more than a decade of work on the process by which antibodies, the foot soldiers of the immune system, mount their defense against infection and disease. He shared the prize with Rodney R. Porter, a British scientist who worked independent of Dr. Edelman. The Nobel committee cited them for their separate approaches in deciphering the chemical structure of antibodies, also known as immunoglobulins. Dr. Edelman discovered that antibodies were not constructed in the shape of one long peptide chain, as thought, but of two different ones — one light, one heavy — that were linked. © 2014 The New York Times Company
By John Horgan Biologist Gerald Edelman–one of the truly great scientific characters I’ve encountered, whose work raised profound questions about the limits of science—has died. I interviewed Edelman in June 1992 at Rockefeller University in New York. Edelman subsequently left Rockefeller to head a center for neuroscience at the Scripps Institute in California. Edelman, 84, died in his home in La Jolla. The following is an edited version of my profile of Edelman in my 1996 book The End of Science. Gerald Edelman, who sought to solve the riddle of consciousness, had "the brain of an empiricist and the heart of a romantic." Gerald Edelman’s career, like that of his rival Francis Crick, has been eclectic, and highly successful. While still a graduate student, Edelman helped to determine the structure of a protein molecule crucial to the body’s immune response. In 1972 he shared a Nobel Prize for that work. Edelman moved on to developmental biology, the study of how a single fertilized cell becomes a full-fledged organism. He found a class of proteins, called cell adhesion molecules, thought to play an important role in embryonic development. All this was merely prelude, however, to Edelman’s grand project of creating a theory of mind. Edelman has set forth his theory in three books: Neural Darwinism, The Remembered Present and Bright Air, Brilliant Fire. The gist of the theory is that just as environmental stresses select the fittest members of a species, so do inputs to the brain select groups of neurons–corresponding to useful memories, for example–by strengthening the connections between them. © 2014 Scientific American
By David Grimm, A shaggy brown terrier approaches a large chocolate Labrador in a city park. When the terrier gets close, he adopts a yogalike pose, crouching on his forepaws and hiking his butt into the air. The Lab gives an excited bark, and soon the two dogs are somersaulting and tugging on each other’s ears. Then the terrier takes off and the Lab gives chase, his tail wagging wildly. When the two meet once more, the whole thing begins again. Watch a couple of dogs play, and you’ll probably see seemingly random gestures, lots of frenetic activity and a whole lot of energy being expended. But decades of research suggest that beneath this apparently frivolous fun lies a hidden language of honesty and deceit, empathy and perhaps even a humanlike morality. Take those two dogs. That yogalike pose is known as a “play bow,” and in the language of play it’s one of the most commonly used words. It’s an instigation and a clarification, a warning and an apology. Dogs often adopt this stance as an invitation to play right before they lunge at another dog; they also bow before they nip (“I’m going to bite you, but I’m just fooling around”) or after some particularly aggressive roughhousing (“Sorry I knocked you over; I didn’t mean it.”). All of this suggests that dogs have a kind of moral code — one long hidden to humans until a cognitive ethologist named Marc Bekoff began to crack it. A wiry 68-year-old with reddish-gray hair tied back in a long ponytail, Bekoff is a professor emeritus at the University of Colorado at Boulder, where he taught for 32 years. He began studying animal behavior in the early 1970s, spending four years videotaping groups of dogs, wolves and coyotes in large enclosures and slowly playing back the tapes, jotting down every nip, yip and lick. “Twenty minutes of film could take a week to analyze,” he says. © 1996-2014 The Washington Post
Sara Reardon The researchers' technique shows neurons throughout the body twinkling with activity. Researchers have for the first time imaged all of the neurons firing in a living organism, the nematode worm Caenorhabditis elegans. The achievement, reported today in Nature Methods1 shows how signals travel through the body in real time. Scientists mapped the connections among all 302 of the nematode's neurons in 19862 — a first that has not been repeated with any other organism. But this wiring diagram, or 'connectome', does not allow researchers to determine the neuronal pathways that lead to a particular action. Nor does it allow researchers to predict what the nematode will do at any point in time, says neuroscientist Alipasha Vaziri of the University of Vienna. By providing a means of displaying signaling activity between neurons in three dimensions and in real-time, the new technique should allow scientists to do both. Vaziri and his colleagues engineered C. elegans so that when a neuron fires and calcium ions pass through its cell membranes, the neuron lights up. To capture those signals, they imaged the whole worm using a technique called light-field deconvolution microscopy, which combines images from a set of tiny lenses and analyses them using an algorithm to give a high-resolution three-dimensional image. The researchers took as many as 50 images per second of the entire worm, enabling them to watch the neurons firing in the brain, ventral cord, and tail (see video). Next, the group applied the technique to the transparent larvae of the zebrafish (Danio rerio), imaging the entire brain as the fish responded to the odours of chemicals pumped into their water. They were able to capture the activity of about 5,000 neurons simultaneously (the zebrafish has about 100,000 total neurons). © 2014 Nature Publishing Group
Keyword: Brain imaging
Link ID: 19631 - Posted: 05.18.2014
By GINIA BELLAFANTE The opening shots of “The Normal Heart,” HBO’s adaptation of Larry Kramer’s 1985 play about the early days of the AIDS crisis in New York, reveal a crew of sinewy and amorous young men disembarking from a ferry on Fire Island on a beautiful July day in 1981. The tableau is meant to suggest the final hour of unburdened desire, the moment before so much youth and beauty would be sacrificed to the cruelest attacks of physiology and cultural indifference. On the way home from the weekend, Ned Weeks, Mr. Kramer’s proxy, a man distanced from the surrounding hedonism, is shown reading a piece in The New York Times headlined, “Rare Cancer Seen in 41 Homosexuals.” The film (which will make its debut on May 25) arrives at a transformative time in the history of AIDS prevention. On May 14, federal health officials, in a move that would have been unimaginable 30 years ago, recommended the use of a prophylactic drug regimen to prevent infection with H.I.V. The drug currently used is known as Truvada, and two years ago, David Duran, a writer and gay-rights campaigner, coined the term “Truvada whore,” controversially, as a judgment against gay men who were abandoning safer sex in favor of taking the antiretroviral. Though he has since characterized this view as “prudish,” there are doctors in the city who continue to harangue patients for what the longtime AIDS activist Peter Staley calls “any break with the condom code.” And yet whatever ideological divisions existed in the period Mr. Kramer’s narrative recalls and whatever have emerged since, the fight against AIDS has been one of the most successful and focused public health movements. In another distinguishing moment, the city health department announced this year that for the first time AIDS had fallen out of the 10 leading causes of death in New York. Replacing it was Alzheimer’s, whose damage is sure to multiply as the number of older New Yorkers increases — by 2030 there will be close to 500,000 more people over age 60 than there were at the beginning of the century. According to a study from Rush University Medical Center in March, the number of deaths attributable to the disease had been vastly undercalculated. The research showed that Alzheimer’s was the underlying cause in 500,000 deaths in the United States in 2010, a figure close to six times the estimate from the Centers for Disease Control. This means that in a single year, Alzheimer’s claimed nearly as many lives as AIDS — responsible for 636,000 deaths in this country — had taken in more than three decades. © 2014 The New York Times Company
Link ID: 19628 - Posted: 05.18.2014
By ALAN SCHWARZ ATLANTA — More than 10,000 American toddlers 2 or 3 years old are being medicated for attention deficit hyperactivity disorder outside established pediatric guidelines, according to data presented on Friday by an official at the Centers for Disease Control and Prevention. The report, which found that toddlers covered by Medicaid are particularly prone to be put on medication such as Ritalin and Adderall, is among the first efforts to gauge the diagnosis of A.D.H.D. in children below age 4. Doctors at the Georgia Mental Health Forum at the Carter Center in Atlanta, where the data was presented, as well as several outside experts strongly criticized the use of medication in so many children that young. The American Academy of Pediatrics standard practice guidelines for A.D.H.D. do not even address the diagnosis in children 3 and younger — let alone the use of such stimulant medications, because their safety and effectiveness have barely been explored in that age group. “It’s absolutely shocking, and it shouldn’t be happening,” said Anita Zervigon-Hakes, a children’s mental health consultant to the Carter Center. “People are just feeling around in the dark. We obviously don’t have our act together for little children.” Dr. Lawrence H. Diller, a behavioral pediatrician in Walnut Creek, Calif., said in a telephone interview: “People prescribing to 2-year-olds are just winging it. It is outside the standard of care, and they should be subject to malpractice if something goes wrong with a kid.” Friday’s report was the latest to raise concerns about A.D.H.D. diagnoses and medications for American children beyond what many experts consider medically justified. Last year, a nationwide C.D.C. survey found that 11 percent of children ages 4 to 17 have received a diagnosis of the disorder, and that about one in five boys will get one during childhood. A vast majority are put on medications such as methylphenidate (commonly known as Ritalin) or amphetamines like Adderall, which often calm a child’s hyperactivity and impulsivity but also carry risks for growth suppression, insomnia and hallucinations. Only Adderall is approved by the Food and Drug Administration for children below age 6. However, because off-label use of methylphenidate in preschool children had produced some encouraging results, the most recent American Academy of Pediatrics guidelines authorized it in 4- and 5-year-olds — but only after formal training for parents and teachers to improve the child’s environment were unsuccessful. © 2014 The New York Times Company
By Pippa Stephens Health reporter, BBC News An anti-depressant drug could be used to slow the onset of Alzheimer's disease, say scientists in the US. Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer's patients. Scientists said they hoped the study could help prevent the disease. Experts said the study was "interesting" and that using an approved drug could be beneficial. Alzheimer's disease is the most common cause of dementia, affecting around 496,000 people in the UK. It affects the brain through protein plaques and tangles which lead to the death of brain cells, and a shortage of chemicals important for transmitting messages. Symptoms include loss of memory, mood changes, and problems with communication and reasoning. Researchers at the University of Pennsylvania and Washington University School of Medicine carried out the study between 2012 and 2014. They bred mice with Alzheimer's disease and looked at the levels of the peptide - or protein component - amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer's. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number. BBC © 2014
Bullying casts a long shadow. Children who are bullied are more prone to depression and suicidal tendencies even when they grow up; they're also more likely to get sick and have headaches and stomach troubles, researchers have discovered. A new study may have found the underlying cause: A specific indicator of illness, called C-reactive protein (CRP), is higher than normal in bullying victims, even when they get older. In contrast, the bullies, by the same gauge, seem to be healthier. The researchers focused on CRP because it's a common, easily tested marker of inflammation, the runaway immune system activity that's a feature of many chronic illnesses including cardiovascular disease, diabetes, chronic pain, and depression, explains lead author William Copeland, a psychologist and epidemiologist at Duke University Medical Center in Durham, North Carolina. To link inflammation to bullying, the researchers asked 1420 youngsters between the ages of 9 and 16 whether, and how often, they had been bullied or had bullied others. Interviewers asked participants whether they felt more teased, bullied, or treated meanly by siblings, friends, and peers than other children—and whether they had upset or hurt other people on purpose, tried to get others in trouble, or forced people to do something by threatening or hurting them. The researchers took finger stick blood tests at each assessment. Interviews took place once a year until the participants turned 16, and again when they were 19 and 21. The children interviewed were participants in the larger Great Smoky Mountains Study, in which some 12,000 children in North Carolina were assessed to track the development of psychiatric conditions. In the short term, the effect of bullying on the victims was immediate. CRP levels increased along with the number of reported bullying instances, and more than doubled in those who said they'd been bullied three times or more in the previous year, compared with kids who had never been bullied. No change was seen in bullies, or in kids who hadn't been involved with bullying one way or the other, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
by Anil Ananthaswamy Children born with split brains – whereby the two hemispheres of their brains are not connected – can develop new brain wiring that helps to connect the two halves, according to brain scans of people with the condition. Such circuitry is not present in normal brains, and explains how some people with split brains can still maintain normal function. It also suggests that the developing brain is even more adaptable than previously thought. Research into people with split brains goes back to the 1960s, when neuroscientists studied people who had undergone brain surgery to treat particularly severe epilepsy. The surgery involved cutting the corpus callosum, the thick bundle of neuronal fibres that connects the brain's two halves. This disconnection prevented epileptic seizures spreading from one brain hemisphere to the other. The recipients of such split-brain surgery showed a form of disconnection syndrome whereby the two halves of their brains could not exchange information. For instance, if a patient touched an object with their left hand without seeing the object, they would be unable to name it. That is because sensory-motor signals from the left hand are processed in the right hemisphere. To put a name to the object, the tactile information from the hand has to reach the brain's left hemisphere, the seat of language. With the central connection between hemispheres severed, the object's naming information cannot be retrieved. Conversely, if that person were to touch an object with their right hand without seeing it, the sensory-motor signals from that hand would go to the left hemisphere, which hosts the brain's language centres, making naming the object easy. However, children born without a corpus callosum – and therefore whose two brain hemispheres are separated – can often pass such tactile naming tests when they are old enough to take them. Their brain hemispheres are obviously communicating, but it wasn't clear how. © Copyright Reed Business Information Ltd
By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post
Erin Allday A gene variant that scientists already knew to be associated with longer life also seems to make people smarter, and may help offset the effects of normal cognitive decline in old age, according to a team of San Francisco researchers. The findings, published Thursday in the journal Cell Reports, are encouraging news for the roughly 1 in 5 people who have the genetic trait, which is a variant of the klotho gene. Beyond that, scientists hope the findings will help them develop tools for retaining, or even boosting, intelligence in people who have suffered cognitive losses, either from disease or through the normal course of aging. 'Cognitive enhancer' "What we've discovered is a cognitive enhancer," said Dr. Dena Dubal, an assistant professor of neurology at UCSF and lead author of the study, which was done with researchers from the Gladstone Institutes. "This may represent a new way to treat problems of cognition in the brain." The name of the gene comes from Greek mythology - Klotho is one of the three sisters of fate, and she spins the thread of life. The gene is responsible for secretions of the hormone klotho, which is thought to have effects on a variety of biological systems and has been shown to disrupt some processes associated with aging. © 2014 Hearst Communications, Inc.
By DAVID L. KIRP Whenever President Obama proposes a major federal investment in early education, as he did in his two most recent State of the Union addresses, critics have a two-word riposte: Head Start. Researchers have long cast doubt on that program’s effectiveness. The most damning evidence comes from a 2012 federal evaluation that used gold-standard methodology and concluded that children who participated in Head Start were not more successful in elementary school than others. That finding was catnip to the detractors. “Head Start’s impact is no better than random,” The Wall Street Journal editorialized. Why throw good money after bad? Though the faultfinders have a point, the claim that Head Start has failed overstates the case. For one thing, it has gotten considerably better in the past few years because of tougher quality standards. For another, researchers have identified a “sleeper effect” — many Head Start youngsters begin to flourish as teenagers, maybe because the program emphasizes character and social skills as well as the three R’s. Still, few would give Head Start high marks, and the bleak conclusion of the 2012 evaluation stands in sharp contrast to the impressive results from well-devised studies of state-financed prekindergartens. Head Start, a survivor of President Lyndon B. Johnson’s war on poverty, enrolls only poor kids. That’s a big part of the problem — as the adage goes, programs for the poor often become poor programs. Whether it’s health care (compare the trajectories of Medicare, for those 65 and older of all incomes, and Medicaid, only for the poor), education or housing, the sorry truth is that “we” don’t like subsidizing “them.” Head Start is no exception. It has been perpetually underfunded, never able to enroll more than half of eligible children or pay its teachers a decent wage. If Head Start is going to realize its potential, it has to break out of the antipoverty mold. One promising but unfortunately rarely used strategy is to encourage all youngsters, not just poor kids, to enroll, with poor families paying nothing and middle-class families contributing on a sliding scale. Another is to merge Head Start with high-quality state prekindergarten. © 2014 The New York Times Company