Chapter 7. Life-Span Development of the Brain and Behavior
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By CATHERINE SAINT LOUIS More than 50 children in 23 states have had mysterious episodes of paralysis to their arms or legs, according to data gathered by the Centers for Disease Control and Prevention. The cause is not known, although some doctors suspect the cases may be linked to infection with enterovirus 68, a respiratory virus that has sickened thousands of children in recent months. Concerned by a cluster of cases in Colorado, the C.D.C. last month asked doctors and state health officials nationwide to begin compiling detailed reports about cases of unusual limb weakness in children. Experts convened by the agency plan next week to release interim guidelines on managing the condition. That so many children have had full or partial paralysis in a short period is unusual, but officials said that the cases seemed to be extremely rare. “At the moment, it looks like whatever the chances are of getting this syndrome are less than one in a million,” said Mark A. Pallansch, the director of the division of viral diseases at the C.D.C. Some of the affected children have lost the use of a leg or an arm, and are having physical therapy to keep their muscles conditioned. Others have sustained more extensive damage and require help breathing. Marie, who asked to be identified by her middle name to protect her family’s privacy, said her 4-year-old son used to climb jungle gyms. But in late September, after the whole family had been sick with a respiratory illness, he started having trouble climbing onto the couch. He walked into Boston Children’s Hospital the day he was admitted. But soon his neck grew so weak, it “flopped completely back like he was a newborn,” Marie said. Typically, the time from when weakness begins until it reaches its worst is one to three days. But for her son, eight mornings in a row, he awoke with a "brand new deficit" until he had some degree of weakness in each limb and had trouble breathing. He was eventually transferred to a Spaulding rehabilitation center, where he is now. © 2014 The New York Times Company
By Virginia Morell Human fetuses are clever students, able to distinguish male from female voices and the voices of their mothers from those of strangers between 32 and 39 weeks after conception. Now, researchers have demonstrated that the embryos of the superb fairy-wren (Malurus cyaneus, pictured), an Australian songbird, also learn to discriminate among the calls they hear. The scientists played 1-minute recordings to 43 fairy-wren eggs collected from nests in the wild. The eggs were between days 9 and 13 of a 13- to 14-day incubation period. The sounds included white noise, a contact call of a winter wren, or a female fairy-wren’s incubation call. Those embryos that listened to the fairy-wrens’ incubation calls and the contact calls of the winter wrens lowered their heart rates, a sign that they were learning to discriminate between the calls of a different species and those of their own kind, the researchers report online today in the Proceedings of the Royal Society B. (None showed this response to the white noise.) Thus, even before hatching, these small birds’ brains are engaged in tasks requiring attention, learning, and possibly memory—the first time embryonic learning has been seen outside humans, the scientists say. The behavior is key because fairy-wren embryos must learn a password from their mothers’ incubation calls; otherwise, they’re less successful at soliciting food from their parents after hatching. © 2014 American Association for the Advancement of Science.
By Paula Span First, an acknowledgment: Insomnia bites. S. Bliss, a reader from Albuquerque, comments that even taking Ativan, he or she awakens at 4:30 a.m., can’t get back to sleep and suffers “a state of sleep deprivation and eventually a kind of walking exhaustion.” Molly from San Diego bemoans “confusion, anxiety, exhaustion, depression, loss of appetite, frankly a loss of will to go on,” all consequences of her sleeplessness. She memorably adds, “Give me Ambien or give me death.” Marciacornute reports that she’s turned to vodka (prompting another reader to wonder if Medicare will cover booze). After several rounds of similar laments here (and not only here; insomnia is prevalent among older adults), I found the results of a study by University of Chicago researchers particularly striking. What if people who report sleep problems are actually getting enough hours of sleep, overall? What if they’re not getting significantly less sleep than people who don’t complain of insomnia? Maybe there’s something else going on. It has always been difficult to ascertain how much people sleep; survey questions are unreliable (how can you tell when you’ve dozed off?), and wiring people with electrodes creates such an abnormal situation that the results may bear little resemblance to ordinary nightlife. Enter the actigraph, a wrist-motion monitor. “The machines have gotten better, smaller, less clunky and more reliable,” said Linda Waite, a sociologist and a co-author of the study. By having 727 older adults across the United States (average age: almost 72) wear actigraphs for three full days, Dr. Waite and her colleagues could tell when subjects were asleep and when they weren’t. Then they could compare their reported insomnia to their actual sleep patterns. Overall, in this random sample, taken from an ongoing national study of older adults, people didn’t appear sleep-deprived. They fell asleep at 10:27 p.m. on average, and awakened at 6:22 a.m. After subtracting wakeful periods during the night, they slept an average seven and a quarter hours. But averages don’t tell us much, so let’s look more closely at their reported insomnia. “What was surprising to us is that there’s very little association between people’s specific sleep problems and what the actigraph shows,” Dr. Waite said. © 2014 The New York Times Company
By Neuroskeptic A new paper threatens to turn the world of autism neuroscience upside down. Its title is Anatomical Abnormalities in Autism?, and it claims that, well, there aren’t very many. Published in Cerebral Cortex by Israeli researchers Shlomi Haar and colleagues, the new research reports that there are virtually no differences in brain anatomy between people with autism and those without. What makes Haar et al.’s essentially negative claims so powerful is that their study had a huge sample size: they included structural MRI scans from 539 people diagnosed with high-functioning autism spectrum disorder (ASD) and 573 controls. This makes the paper an order of magnitude bigger than a typical structural MRI anatomy study in this field. The age range was 6 to 35. The scans came from the public Autism Brain Imaging Data Exchange (ABIDE) database, a data sharing initiative which pools scans from 18 different neuroimaging centers. Haar et al. examined the neuroanatomy of the cases and controls using the popular FreeSurfer software package. What did they find? Well… not much. First off, the ASD group had no differences in overall brain size (intracranial volume). Nor were there any group differences in the volumes of most brain areas; the only significant finding here was an increased ventricle volume in the ASD group, but even this had a small effect size (d = 0.34). Enlarged ventricles is not specific to ASD by any means – the same thing has been reported in schizophrenia, dementia, and many other brain disorders.
by Neurobonkers A paper published in Nature Reviews Neuroscience last week addressed the prevalence of neuromyths among educators. The paper has been widely reported, but the lion's share of the coverage glossed over the impact that neuromyths have had in the real world. Your first thought after reading the neuromyths in the table below — which were widely believed by teachers — may well be, "so what?" It is true that some of the false beliefs are relatively harmless. For example, encouraging children to drink a little more water might perhaps result in the consumption of less sugary drinks. This may do little if anything to reduce hyperactivity but could encourage a more nutritious diet which might have impacts on problems such as Type II diabetes. So, what's the harm? The paper addressed a number of areas where neuromyths have had real world impacts on educators and policymakers, which may have resulted negatively on the provision of education. The graph above, reprinted in the Nature Reviews Neuroscience, paper has been included as empirical data in educational policy documents to provide evidence for an "allegedly scientific argument for withdrawing public funding of university education." The problem? The data is made up. The graph is in fact a model that is based on the false assumption that investment before the age of three will have many times the benefit of investment made in education later in life. The myth of three — the belief that there is a critical window to educate children before the age of three, after which point the trajectory is fixed — is one of the most persistent neuromyths. Viewed on another level, while some might say investment in early education can never be a bad thing, how about the implication that the potential of a child is fixed at such an early point in their life, when in reality their journey has just begun. © Copyright 2014, The Big Think, Inc
By CLIVE THOMPSON “You just crashed a little bit,” Adam Gazzaley said. It was true: I’d slammed my rocket-powered surfboard into an icy riverbank. This was at Gazzaley’s San Francisco lab, in a nook cluttered with multicolored skullcaps and wires that hooked up to an E.E.G. machine. The video game I was playing wasn’t the sort typically pitched at kids or even middle-aged, Gen X gamers. Indeed, its intended users include people over 60 — because the game might just help fend off the mental decline that accompanies aging. It was awfully hard to play, even for my Call of Duty-toughened brain. Project: Evo, as the game is called, was designed to tax several mental abilities at once. As I maneuvered the surfboard down winding river pathways, I was supposed to avoid hitting the sides, which required what Gazzaley said was “visual-motor tracking.” But I also had to watch out for targets: I was tasked with tapping the screen whenever a red fish jumped out of the water. The game increased in difficulty as I improved, making the river twistier and obliging me to remember turns I’d taken. (These were “working-memory challenges.”) Soon the targets became more confusing — I was trying to tap blue birds and green fish, but the game faked me out by mixing in green birds and blue fish. This was testing my “selective attention,” or how quickly I could assess a situation and react to it. The company behind Project: Evo is now seeking approval from the Food and Drug Administration for the game. If it gets that government stamp, it might become a sort of cognitive Lipitor or Viagra, a game that your doctor can prescribe for your aging mind. After only two minutes of play, I was making all manner of mistakes, stabbing frantically at the wrong fish as the game sped up. “It’s hard,” Gazzaley said, smiling broadly as he took back the iPad I was playing on. “It’s meant to really push it.” “Brain training” games like Project: Evo have become big business, with Americans spending an estimated $1.3 billion a year on them. They are also a source of controversy. © 2014 The New York Times Company
By Emily Underwood Aging baby boomers and seniors would be better off going for a hike than sitting down in front of one of the many video games designed to aid the brain, a group of nearly 70 researchers asserted this week in a critique of some of the claims made by the brain-training industry. With yearly subscriptions running as much as $120, an expanding panoply of commercial brain games promises to improve memory, processing speed, and problem-solving, and even, in some cases, to stave off Alzheimer’s disease. Many companies, such as Lumosity and Cogmed, describe their games as backed by solid scientific evidence and prominently note that neuroscientists at top universities and research centers helped design the programs. But the cited research is often “only tangentially related to the scientific claims of the company, and to the games they sell,” according to the statement released Monday by the Stanford Center on Longevity in Palo Alto, California, and the Max Planck Institute for Human Development in Berlin. Although the letter, whose signatories include many researchers outside those two organizations, doesn’t point to specific bad actors, it concludes that there is “little evidence that playing brain games improves underlying broad cognitive abilities, or that it enables one to better navigate a complex realm of everyday life.” A similar statement of concern was published in 2008 with a smaller number of signatories, says Ulman Lindenberger of the Max Planck Institute for Human Development, who helped organize both letters. Although Lindenberger says there was no particular trigger for the current statement, he calls it the “expression of a growing collective concern among a large number of cognitive psychologists and neuroscientists who study human cognitive aging.” © 2014 American Association for the Advancement of Science
By PAUL VITELLO Most adults do not remember anything before the age of 3 or 4, a gap that researchers had chalked up to the vagaries of the still-developing infant brain. By some accounts, the infant brain was just not equipped to remember much. Textbooks referred to the deficiency as infant amnesia. Carolyn Rovee-Collier, a developmental psychologist at Rutgers University who died on Oct. 2 at 72, challenged the theory, showing in a series of papers in the early 1980s that babies remember plenty. A 3-month-old can recall what he or she learned yesterday, she found, and a 9-month-old can remember a game for as long as a month and a half. She cited experiments suggesting that memory processes in adults and infants are virtually the same, and argued that infant memories were never lost. They just become increasingly harder to retrieve as the child grows, learns language and loses touch with the visual triggers that had kept those memories sharp — a view from between the bars of a crib, say, or the view of the floor as a crawler, not a toddler, sees it. Not all of Dr. Rovee-Collier’s theories won over the psychology establishment, which still uses the infant amnesia concept to explain why people do not remember life as a baby. But her insights about an infant’s short-term memory and ability to learn have been widely accepted, and have helped recast scientific thinking about the infant mind over the past 30 years. Since the first of her 200 papers was published, infant cognitive studies has undergone a boom in university programs around the country. It was a field that had been largely unexplored in any systematic way by the giants of psychological theory. Freud and Jean Piaget never directly addressed the subject of infant memory. William James, considered the father of American psychology, once hazarded a guess that the human baby’s mind was a place of “blooming, buzzing confusion.” © 2014 The New York Times Company
By Fergus Walsh Medical correspondent A paralysed man has been able to walk again after a pioneering therapy that involved transplanting cells from his nasal cavity into his spinal cord. Darek Fidyka, who was paralysed from the chest down in a knife attack in 2010, can now walk using a frame. The treatment, a world first, was carried out by surgeons in Poland in collaboration with scientists in London. Prof Wagih El Masri Consultant spinal injuries surgeon Details of the research are published in the journal Cell Transplantation. BBC One's Panorama programme had unique access to the project and spent a year charting the patient's rehabilitation. Darek Fidyka, 40, from Poland, was paralysed after being stabbed repeatedly in the back in the 2010 attack. He said walking again - with the support of a frame - was "an incredible feeling", adding: "When you can't feel almost half your body, you are helpless, but when it starts coming back it's like you were born again." He said what had been achieved was "more impressive than man walking on the moon". UK research team leader Prof Geoff Raisman: Paralysis treatment "has vast potential" The treatment used olfactory ensheathing cells (OECs) - specialist cells that form part of the sense of smell. OECs act as pathway cells that enable nerve fibres in the olfactory system to be continually renewed. In the first of two operations, surgeons removed one of the patient's olfactory bulbs and grew the cells in culture. Two weeks later they transplanted the OECs into the spinal cord, which had been cut through in the knife attack apart from a thin strip of scar tissue on the right. They had just a drop of material to work with - about 500,000 cells. About 100 micro-injections of OECs were made above and below the injury. BBC © 2014
By Paula Span Maybe it’s something else. That’s what you tell yourself, isn’t it, when an older person begins to lose her memory, repeat herself, see things that aren’t there, lose her way on streets she’s traveled for decades? Maybe it’s not dementia. And sometimes, thankfully, it is indeed some other problem, something that mimics the cognitive destruction of Alzheimer’s disease or another dementia — but, unlike them, is fixable. “It probably happens more often than people realize,” said Dr. P. Murali Doraiswamy, a neuroscientist at Duke University Medical Center. But, he added, it doesn’t happen nearly as often as family members hope. Several confounding cases have appeared at Duke: A woman who appeared to have Alzheimer’s actually was suffering the effects of alcoholism. Another patient’s symptoms resulted not from dementia but from chronic depression. Dr. Doraiswamy estimates that when doctors suspect Alzheimer’s, they’re right 50 to 60 percent of the time. (The accuracy of Alzheimer’s diagnoses, even in specialized medical centers, is more haphazard than you would hope.) Perhaps another 25 percent of patients actually have other types of dementia, like Lewy body or frontotemporal — scarcely happy news, but because these diseases have different trajectories and can be exacerbated by the wrong drugs, the distinction matters. The remaining 15 to 25 percent “usually have conditions that can be reversed or at least improved,” Dr. Doraiswamy said. © 2014 The New York Times Company
Link ID: 20227 - Posted: 10.22.2014
By Jane E. Brody Within a week of my grandsons’ first year in high school, getting enough sleep had already become an issue. Their concerned mother questioned whether lights out at midnight or 1 a.m. and awakening at 7 or 7:30 a.m. to get to school on time provided enough sleep for 14-year-olds to navigate a demanding school day. The boys, of course, said “yes,” especially since they could “catch up” by sleeping late on weekends. But the professional literature on the sleep needs of adolescents says otherwise. Few Americans these days get the hours of sleep optimal for their age, but experts agree that teenagers are more likely to fall short than anyone else. Researchers report that the average adolescent needs eight and a half to nine and a half hours of sleep each night. But in a poll taken in 2006 by the National Sleep Foundation, less than 20 percent reported getting that much rest on school nights. With the profusion of personal electronics, the current percentage is believed to be even worse. A study in Fairfax, Va., found that only 6 percent of children in the 10th grade and only 3 percent in the 12th grade get the recommended amount of sleep. Two in three teens were found to be severely sleep-deprived, losing two or more hours of sleep every night. The causes can be biological, behavioral or environmental. And the effect on the well-being of adolescents — on their health and academic potential — can be profound, according to a policy statement issued in August by the American Academy of Pediatrics. “Sleep is not optional. It’s a health imperative, like eating, breathing and physical activity,” Dr. Judith A. Owens, the statement’s lead author, said in an interview. “This is a huge issue for adolescents.” © 2014 The New York Times Company
By Catherine Saint Louis KATY, Tex. — Like many parents of children with autism, Nicole Brown feared she might never find a dentist willing and able to care for her daughter, Camryn Cunningham, now a lanky 13-year-old who uses words sparingly. Finishing a basic cleaning was a colossal challenge, because Camryn was bewildered by the lights in her face and the odd noises from instruments like the saliva suctioner — not to mention how utterly unfamiliar everything was to a girl accustomed to routine. Sometimes she’d panic and bolt from the office. Then in May, Ms. Brown, 45, a juvenile supervision officer, found Dr. Amy Luedemann-Lazar, a pediatric dentist in this suburb of Houston. Unlike previous dentists, Dr. Luedemann-Lazar didn’t suggest that Camryn would need to be sedated or immobilized. Instead, she suggested weekly visits to help her learn to be cooperative, step by step, with lots of breaks so she wouldn’t be overwhelmed. Bribery helped. If she sat calmly for 10 seconds, her reward was listening to a snippet of a Beyoncé song on her sister’s iPod. This month, Camryn sat still in the chair, hands crossed on her lap, for no less than 25 minutes through an entire cleaning — her second ever — even as purple-gloved hands hovered near her face, holding a noisy tooth polisher. At the end, Dr. Luedemann-Lazar examined Camryn’s teeth and declared her cavity-free and ready to see an orthodontist. “It was like a breakthrough,” Ms. Brown said, adding, “Dr. Amy didn’t just turn her away.” Parents of children with special needs have long struggled to find dentists who will treat them. In a 2005 study, nearly three-fifths of 208 randomly chosen general dentists in Michigan said they would not provide care for children on the autism spectrum; two-thirds said the same for adults. But as more and more children receive diagnoses of autism spectrum disorder, more dentists and dental hygienists are recognizing that with accommodations, many of them can become cooperative patients. © 2014 The New York Times Company
Link ID: 20222 - Posted: 10.21.2014
by Flora Graham This glowing blue web of neurons is usually what researchers examine when searching for a cure for Parkinson's. But a new study, part-funded by Parkinson's UK, hones in on the tiny yellow dots. These are the connections between brain cells known as synapses, has discovered a killer that targets these links, potentially paving the way for new treatments. Soledad Galli at University College London and her colleagues have found that the death of synapses in mice may be due to malfunctioning proteins called Wnt proteins. "If we confirm that Wnt is involved in the early stages of Parkinson's, this throws up exciting possibilities, not just for new treatment targets, but also for new ways to identify people with Parkinson's early on in their condition," says Galli. Most patients currently depend on the drug levodopa, which is over 50 years old and can have severe side-effects, in addition to becoming less effective over time. Moreover, it only masks the symptoms: there is no cure for Parkinson's and no way to stop its progression. Journal reference: Nature Communications, DOI: 10.1038/ncomms5992 © Copyright Reed Business Information Ltd
2014 by Andy Coghlan Seeing is definitely believing when it comes to stem cell therapy. A blind man has recovered enough sight to ride his horse. A woman who could see no letters at all on a standard eye test chart can now read the letters on the top four lines. Others have recovered the ability to see colour. All have had injections of specialised retinal cells in their eyes to replace ones lost through age or disease. A trial in 18 people with degenerative eye conditions is being hailed as the most promising yet for a treatment based on human embryonic stem cells. "We've been hearing about their potential for more than a decade, but the results have always been in mice and rats, and no one has shown they're safe or effective in humans long term," says Robert Lanza of Advanced Cell Technology in Marlborough, Massachusetts, the company that carried out the stem cell intervention. "Now, we've shown both that they're safe and that there's a real chance these cells can help people." Ten years ago, the team at Advanced Cell Technology announced that it had successfully converted human embryonic stem cells into retinal pigment epithelial cells. These cells help keep the eyes' light-detecting rods and cones healthy. But when retinal pigment epithelial cells deteriorate, blindness can occur. This happens in age-related macular degeneration and Stargardt's macular dystrophy. In a bid to reverse this, Lanza's team injected retinal cells into one of each of the 18 participants' eyes, half of whom had age-related macular degeneration and half had Stargardt's. A year later, 10 people's eyes had improved, and the eyes of the others had stabilised. Untreated eyes had continued to deteriorate. © Copyright Reed Business Information Ltd.
|By Jenni Laidman During the second and third trimester of pregnancy, the outer layer of the embryo's brain, the cortex, assembles itself into six distinct layers. But in autism, according to new research, this organization goes awry—marring parts of the brain associated with the abilities often impaired in the disorder, such as social skills and language development. Eric Courchesne, director of the Autism Center of Excellence at the University of California, San Diego, and his colleagues uncovered this developmental misstep in a small study that compared 11 brains of children with autism who died at ages two through 15 with 11 brains of kids who died without the diagnosis. The study employed a sophisticated genetic technique that looked for signatures of the activity of 25 genes in brain slices taken from the front of the brain—an area called the prefrontal cortex—as well as from the occipital cortex at the back of the brain and the temporal cortex near the temple. The researchers found disorganized patches, roughly a quarter of an inch across, in which gene expression indicated cells were not where they were supposed to be, amid the folds of tissue in the prefrontal cortex in 10 of 11 brains from children with autism. That part of the brain is associated with higher-order communication and social interactions. The team also found messy patches in the temporal cortices of autistic brains but no disorder at the back of the brain, which also matches typical symptom profiles. The patches appeared at seemingly random locations within the frontal and temporal cortices, which may help explain why symptoms can differ dramatically among individuals, says Rich Stoner, then at U.C. San Diego and the first author of the study, which appeared in the New England Journal of Medicine. © 2014 Scientific American
By JOSHUA A. KRISCH An old stucco house stands atop a grassy hill overlooking the Long Island Sound. Less than a mile down the road, the renowned Cold Spring Harbor Laboratory bustles with more than 600 researchers and technicians, regularly producing breakthroughs in genetics, cancer and neuroscience. But that old house, now a private residence on the outskirts of town, once held a facility whose very name evokes dark memories: the Eugenics Record Office. In its heyday, the office was the premier scientific enterprise at Cold Spring Harbor. There, bigoted scientists applied rudimentary genetics to singling out supposedly superior races and degrading minorities. By the mid-1920s, the office had become the center of the eugenics movement in America. Today, all that remains of it are files and photographs — reams of discredited research that once shaped anti-immigration laws, spurred forced-sterilization campaigns and barred refugees from entering Ellis Island. Now, historians and artists at New York University are bringing the eugenics office back into the public eye. “Haunted Files: The Eugenics Record Office,” a new exhibit at the university’s Asian/Pacific/American Institute, transports visitors to 1924, the height of the eugenics movement in the United States. Inside a dimly lit room, the sounds of an old typewriter click and clack, a teakettle whistles and papers shuffle. The office’s original file cabinets loom over reproduced desks and period knickknacks. Creaky cabinets slide open, and visitors are encouraged to thumb through copies of pseudoscientific papers. © 2014 The New York Times Company
Keyword: Genes & Behavior
Link ID: 20204 - Posted: 10.14.2014
By GINA KOLATA For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease. In doing so, they resolved a longstanding problem of how to study Alzheimer’s and search for drugs to treat it; the best they had until now were mice that developed an imperfect form of the disease. The key to their success, said the lead researcher, Rudolph E. Tanzi of Massachusetts General Hospital in Boston, was a suggestion by his colleague Doo Yeon Kim to grow human brain cells in a gel, where they formed networks as in an actual brain. They gave the neurons genes for Alzheimer’s disease. Within weeks they saw the hard Brillo-like clumps known as plaques and then the twisted spaghetti-like coils known as tangles — the defining features of Alzheimer’s disease. The work, which also offers strong support for an old idea about how the disease progresses, was published in Nature on Sunday. Leading researchers said it should have a big effect. “It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.” Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients. © 2014 The New York Times Company
Link ID: 20203 - Posted: 10.13.2014
By David Leonhardt and Amanda Cox Like so many other parts of health care, childbirth has become a more medically intense experience over the last two decades. The use of drugs to induce labor has become far more common, as have cesarean sections. Today, about half of all births in this country are hastened either by drugs or surgery, double the share in 1990. Crucial to the change has been a widely held belief that once fetuses pass a certain set of thresholds — often 39 weeks of gestation and five and a half pounds in weight — they’re as healthy as they can get. More time in the womb doesn’t do them much good, according to this thinking. For parents and doctors, meanwhile, scheduling a birth, rather than waiting for its random arrival, is clearly more convenient. But a huge new set of data, based on every child born in Florida over an 11-year span, is calling into question some of the most basic assumptions of our medicalized approach to childbirth. The results also play into a larger issue: the growing sense among many doctors and other experts that Americans would actually be healthier if our health care system were sometimes less aggressive. The new data suggest that the thresholds to maximize a child’s health seem to be higher, which means that many fetuses might benefit by staying longer in the womb, where they typically add at least a quarter-pound per week. Seven-pound babies appear to be healthier than six-pound babies — and to fare better in school as they age. The same goes for eight-pound babies compared with seven-pound babies, and nine-pound babies compared with eight-pound babies. Weight, of course, may partly be an indicator of broader fetal health, but it seems to be a meaningful one: The chunkier the baby, the better it does on average, all the way up to almost 10 pounds. “Birth weight matters, and it matters for everyone,” says David N. Figlio, a Northwestern University professor and co-author of the study, which will soon be published in the American Economic Review, one of the field’s top journals. © 2014 The New York Times Company
Ann Robinson Neuroscience research got a huge boost last week with news of Professor John O’Keefe’s Nobel prize for work on the “brain’s internal GPS system”. It is an exciting new part of the giant jigsaw puzzle of our brain and how it functions. But how does cutting-edge neuroscience research translate into practical advice about how to pass exams, remember names, tot up household bills and find where the hell you left the car in a crowded car park? O’Keefe’s prize was awarded jointly with Swedish husband and wife team Edvard and May-Britt Moser for their discovery of “place and grid cells” that allow rats to chart where they are. When rats run through a new environment, these cells show increased activity. The same activity happens much faster while the rats are asleep, as they replay the new route. We already knew that the part of the brain known as the hippocampus was involved in spatial awareness in birds and mammals, and this latest work on place cells sheds more light on how we know where we are and where we’re going. In 2000, researchers at University College London led by Dr Eleanor Maguire showed that London taxi drivers develop a pumped-up hippocampus after years of doing the knowledge and navigating the backstreets of the city. MRI scans showed that cabbies start off with bigger hippocampuses than average, and that the area gets bigger the longer they do the job. As driver David Cohen said at the time to BBC News: “I never noticed part of my brain growing – it makes you wonder what happened to the rest of it!” © 2014 Guardian News and Media Limited
For decades, scientists thought that neurons in the brain were born only during the early development period and could not be replenished. More recently, however, they discovered cells with the ability to divide and turn into new neurons in specific brain regions. The function of these neuroprogenitor cells remains an intense area of research. Scientists at the National Institutes of Health (NIH) report that newly formed brain cells in the mouse olfactory system — the area that processes smells — play a critical role in maintaining proper connections. The results were published in the October 8 issue of the Journal of Neuroscience. “This is a surprising new role for brain stem cells and changes the way we view them,” said Leonardo Belluscio, Ph.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and lead author of the study. The olfactory bulb is located in the front of the brain and receives information directly from the nose about odors in the environment. Neurons in the olfactory bulb sort that information and relay the signals to the rest of the brain, at which point we become aware of the smells we are experiencing. Olfactory loss is often an early symptom in a variety of neurological disorders, including Alzheimer’s and Parkinson’s diseases. In a process known as neurogenesis, adult-born neuroprogenitor cells are generated in the subventricular zone deep in the brain and migrate to the olfactory bulb where they assume their final positions. Once in place, they form connections with existing cells and are incorporated into the circuitry.