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Laura Sanders In growing brains, billions of nerve cells must make trillions of precise connections. As they snake through the brain, nerve cell tendrils called axons use the brain’s stiffness to guide them on their challenging journey, a study of frog nerve cells suggests. The results, described online September 19 in Nature Neuroscience, show that along with chemical guidance signals, the brain’s physical properties help shape its connections. That insight may be key to understanding how nerve cells wire the brain, says study coauthor Kristian Franze. “I strongly believe that it’s not enough to look at chemistry,” says Franze, a mechanobiologist at the University of Cambridge. “We need to look at environmental factors, too.” The notion that physical features help guide axons is gaining momentum, says neuroscientist Samantha Butler of UCLA. “It’s a really intriguing study.” A better understanding of how nerve cells find their targets could help scientists coax new cells to grow after a spinal cord injury or design better materials for nerve cell implants. Franze and colleagues studied nerve cells from the retina of frogs. Experiments on cells in dishes suggested that axons, signal-transmitting tendrils led by tiny pioneering structures called growth cones, grew differently on hard and soft material. Axons grew longer and straighter on stiff surfaces and seemed to meander more on softer material. © Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22672 - Posted: 09.20.2016

By JANE E. BRODY As a woman of a certain age who consumes a well-balanced diet of all the usual food groups, including reasonable amounts of animal protein, I tend to dismiss advice to take a multivitamin supplement. I’ve been told repeatedly by nutrition experts that the overuse of dietary supplements for “nutritional insurance” has given Americans the most expensive urine in the world. I do take a daily supplement of vitamin D, based on considerable evidence of its multiple health benefits, especially for older people. However, based on advice from the National Academy of Medicine and an examination of accumulating research, I’m prompted to consider also taking a vitamin B12 supplement in hopes of protecting my aging brain. Animal protein foods — meat, fish, milk, cheese and eggs — are the only reliable natural dietary sources of B12, and I do get ample amounts of several in my regular diet. But now at age 75, I wonder whether I’m still able to reap the full benefit of what I ingest. You see, the ability to absorb B12 naturally present in foods depends on the presence of adequate stomach acid, the enzyme pepsin and a gastric protein called intrinsic factor to release the vitamin from the food protein it is attached to. Only then can the vitamin be absorbed by the small intestine. As people age, acid-producing cells in the stomach may gradually cease to function, a condition called atrophic gastritis. A century ago, researchers discovered that some people — most likely including Mary Todd Lincoln — had a condition called pernicious anemia, a deficiency of red blood cells ultimately identified as an autoimmune disease that causes a loss of stomach cells needed for B12 absorption. Mrs. Lincoln was known to behave erratically and was ultimately committed to a mental hospital. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22634 - Posted: 09.06.2016

By PAM BELLUCK The images tell a heartbreaking story: Zika’s calamitous attack on the brains of babies — as seen from the inside. A study of brain scans and ultrasound pictures of 45 Brazilian babies whose mothers were infected with Zika in pregnancy shows that the virus can inflict serious damage to many different parts of the fetal brain beyond microcephaly, the condition of unusually small heads that has become the sinister signature of Zika. The images, published Tuesday in the journal Radiology, also suggest a grim possibility: Because some of the damage was seen in brain areas that continue to develop after birth, it may be that babies born without obvious impairment will experience problems as they grow. “It really brings to the forefront the importance of truly understanding the impact of Zika virus and the fact that we need to follow children who not only are exposed to Zika in pregnancy, but even those who don’t appear to have any complications at birth,” said Dr. Catherine Y. Spong, chief of the pregnancy and perinatology branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, who was not involved in the study. Most of the babies in the study were born with microcephaly, although three were not. Each also suffered other impairments, almost all of which emerge earlier than microcephaly because a smaller head is really a consequence of brain that has failed to develop fully or has been damaged along the way, experts said. “The brain that should be there is not there,” said Dr. Deborah Levine, an author of the study and a professor of radiology at Harvard Medical School in Boston. “The abnormalities that we see in the brain suggest a very early disruption of the brain development process.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22594 - Posted: 08.24.2016

By Virginia Morell Scientists have long worried whether animals can respond to the planet’s changing climate. Now, a new study reports that at least one species of songbird—and likely many more—already knows how to prep its chicks for a warming world. They do so by emitting special calls to the embryos inside their eggs, which can hear and learn external sounds. This is the first time scientists have found animals using sound to affect the growth, development, behavior, and reproductive success of their offspring, and adds to a growing body of research revealing that birds can “doctor” their eggs. “The study is novel, surprising, and fascinating, and is sure to lead to much more work on parent-embryo communication,” says Robert Magrath, a behavioral ecologist at the Australian National University in Canberra who was not involved in the study. The idea that the zebra finch (Taeniopygia guttata) parents were “talking to their eggs” occurred to Mylene Mariette, a behavioral ecologist at Deakin University in Waurn Ponds, Australia, while recording the birds’ sounds at an outdoor aviary. She noticed that sometimes when a parent was alone, it would make a rapid, high-pitched series of calls while sitting on the eggs. Mariette and her co-author, Katherine Buchanan, recorded the incubation calls of 61 female and 61 male finches inside the aviary. They found that parents of both sexes uttered these calls only during the end of the incubation period and when the maximum daily temperature rose above 26°C (78.8°F). © 2016 American Association for the Advancement of Scienc

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22579 - Posted: 08.20.2016

By Emily Underwood In 2010, neurobiologist Beth Stevens had completed a remarkable rise from laboratory technician to star researcher. Then 40, she was in her second year as a principal investigator at Boston Children’s Hospital with a joint faculty position at Harvard Medical School. She had a sleek, newly built lab and a team of eager postdoctoral investigators. Her credentials were impeccable, with high-profile collaborators and her name on an impressive number of papers in well-respected journals. But like many young researchers, Stevens feared she was on the brink of scientific failure. Rather than choosing a small, manageable project, she had set her sights on tackling an ambitious, unifying hypothesis linking the brain and the immune system to explain both normal brain development and disease. Although the preliminary data she’d gathered as a postdoc at Stanford University in Palo Alto, California, were promising, their implications were still murky. “I thought, ‘What if my model is just a model, and I let all these people down?’” she says. Stevens, along with her mentor at Stanford, Ben Barres, had proposed that brain cells called microglia prune neuronal connections during embryonic and later development in response to a signal from a branch of the immune system known as the classical complement pathway. If a glitch in the complement system causes microglia to prune too many or too few connections, called synapses, they’d hypothesized, it could lead to both developmental and degenerative disorders. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 22576 - Posted: 08.20.2016

Meghan Rosen Zika may harm grown-up brains. The virus, which can cause brain damage in infants infected in the womb, kills stem cells and stunts their numbers in the brains of adult mice, researchers report August 18 in Cell Stem Cell. Though scientists have considered Zika primarily a threat to unborn babies, the new findings suggest that the virus may cause unknown — and potentially long-term — damage to adults as well. In adults, Zika has been linked to Guillain-Barré syndrome, a rare neurological disorder (SN: 4/2/16, p. 29). But for most people, infection is typically mild: a headache, fever and rash lasting up to a week, or no symptoms at all. In pregnant women, though, the virus can lodge in the brain of a fetus and kill off newly developing cells (SN: 4/13/16). If Zika targets newborn brain cells, adults may be at risk, too, reasoned neuroscientist Joseph Gleeson of Rockefeller University in New York City and colleagues. Parts of the forebrain and the hippocampus, which plays a crucial role in learning and memory, continue to generate nerve cells in adult brains. In mice infected with Zika, the virus hit these brain regions hard. Nerve cells died and the regions generated one-fifth to one-half as many new cells compared with those of uninfected mice. The results might not translate to humans; the mice were genetically engineered to have weak immune systems, making them susceptible to Zika. But Zika could potentially harm immunocompromised people and perhaps even healthy people in a similar way, the authors write. © Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22575 - Posted: 08.20.2016

By Nicholas Bakalar Taking antipsychotic medicines during pregnancy does not increase the risk for birth defects, a large new study has found. Antipsychotics are used to treat schizophrenia, bipolar disorder, depression and other psychiatric disorders. Previous studies of their use during pregnancy have been small and have had mixed results. This study, in JAMA Psychiatry, reviewed records of 1,341,715 pregnant women, of whom 9,258 filled prescriptions for the newer atypical antipsychotics like quetiapine (Seroquel) or aripiprazole (Abilify), and 733 for older typical antipsychotics such as haloperidol (Haldol). All prescriptions were filled in the first trimester of pregnancy. After controlling for race, number of pregnancies, smoking, alcohol use, psychiatric conditions, additional medications and other variables, there was no difference in the risk for birth defects between those who took the drugs and those who did not. One possible exception was a marginal increase in risk with one drug, risperidone (Risperdal), which the authors said will require further study. “These findings suggest that the use of antipsychotics during the first trimester does not seem to increase congenital malformation,” or birth defects, said the lead author, Krista F. Huybrechts, an assistant professor of medicine at Harvard. But, she added, “we only looked at congenital malformation, not other possible negative outcomes for women and their children.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22574 - Posted: 08.20.2016

Dean Burnett On July 31st 2016, this blog will have been in existence for four years exactly. A huge thanks to everyone who’s made the effort to read it in that time (an alarming number of you). Normally there’d be a post on the day to mark the occasion, but this year the 31st is a) a Sunday, and b) my birthday, so even if I could be bothered to work that day, it’s unlikely anyone would want to read it. However, today also marks the ridiculously-unlikely-but-here-we-are American release of my book. How did it get to this point? I’ve been a “professional” science writer now for four years, and I’ve been involved in neuroscience, in one guise or another, since 2000, the year I started my undergraduate degree. In that time, I’ve heard/encountered some seriously bizarre claims about how the brain works. Oftentimes it was me not understanding what was being said, or misinterpreting a paper, or just my own lack of competence. Sometimes, it was just a media exaggeration. However, there have been occasions when a claim made about the brain thwarts all my efforts to find published evidence or even a rational basis for it, leaving me scratching my head and wondering “where the hell did THAT come from?” Here are some of my favourites. In the past, one terabyte of storage capacity would have seemed incredibly impressive. But Moore’s law has put paid to that. My home desktop PC presently has 1.5 TB of storage space, and that’s over seven years old. Could my own clunky desktop be, in terms of information capacity, smarter than me? Apparently. Some estimates put the capacity of the human brain as low as 1TB. A lifetimes worth of memories wouldn’t fill a modern-day hard drive? That seems far-fetched, at least at an intuitive level.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 22477 - Posted: 07.26.2016

By Dave Dormer, Transporting babies deprived of oxygen at birth to a neonatal intensive care unit in Calgary will soon be safer thanks to a new portable cooling device. The Foothills hospital is one of the first facilities in Canada to acquire one and doctors hope it will help prevent brain injuries, as reducing a baby's temperature can prevent damage to brain tissue and promote healing. The reduction in temperature is called therapeutic hypothermia, and it can help prevent damage to brain tissue and promote healing. (Evelyne Asselin/CBC) "The period immediately following birth is critical. We have about a six-hour window to lower these babies' temperatures to prevent neurological damage," said Dr. Khorshid Mohammad, the neonatal neurocritical care project lead who spearheaded the initiative. "The sooner we can do so, and the more consistent we can make the temperature, the more protective it is and the better their chances of surviving without injury." Since about 2008, doctors used cooling blankets and gel packs to lower a baby's temperature to 33.5 C from the normal 37 C for 72 hours in order to prevent brain damage. "With those methods, it can be difficult to maintain a stable temperature," said Mohammad. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22476 - Posted: 07.26.2016

By Andy Coghlan The final brain edit before adulthood has been observed for the first time. MRI scans of 300 adolescents and young adults have shown how the teenage brain upgrades itself to become quicker – but that errors in this process may lead to schizophrenia in later life. The editing process that takes place in teen years seems to select the brain’s best connections and networks, says Kirstie Whitaker at the University of Cambridge. “The result is a brain that’s sleeker and more efficient.” When Whitaker and her team scanned brains from people between the ages of 14 and 24, they found that two major changes take place in the outer layer of the brain – the cortex – at this time. As adolescence progresses, this layer of grey matter gets thinner – probably because unwanted or unused connections between neurons – called synapses – are pruned back. At the same time, important neurons are upgraded. The parts of these cells that carry signals down towards synapses are given a sheath that helps them transmit signals more quickly – a process called myelination. “It may be that pruning and myelination are part of the maturation of the brain,” says Steven McCarroll at Harvard Medical School. “Pruning involves removing the connections that are not used, and myelination takes the ones that are left and makes them faster,” he says. McCarroll describes this as a trade-off – by pruning connections, we lose some flexibility in the brain, but the proficiency of signal transmission improves. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 22474 - Posted: 07.26.2016

Helen Haste The American psychologist and educationist Jerome Bruner, who has died aged 100, repeatedly challenged orthodoxies and generated novel directions. His elegant, accessible writing reached wide audiences. His colleague Rom Harré described his lectures as inspiring: “He darted all over the place, one topic suggested another and so on through a thrilling zigzag.” To the charge that he was always asking impossible questions, Jerry replied: “They are pretty much impossible, but the search for the impossible is part of what intelligence is about.” He was willing to engage with controversy, both on academic issues and in education politics. Blind at birth because of cataracts, Jerry gained his sight after surgery at the age of two. He credited this for his sense that we actively interpret and organise our world rather than passively react to it – a theme that he continued to develop in different ways. His first work lay in perception, when he resumed research at Harvard after the second world war. He found that children’s judgments of the size of coins and coin-like disks varied: poorer children overestimated the size of the coins. This contributed to the emerging “new look” movement in psychology, involving values, intentions and interpretation in contrast to the then dominant behaviourist focus on passive learning, reward and punishment. His professorship at Harvard came in 1952, and by the middle of the decade a computer metaphor began to influence psychology – the “cognitive revolution”. With Jacqueline Goodnow and George Austin, Jerry published A Study of Thinking (1956). © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 22445 - Posted: 07.16.2016

Laura Sanders If you’ve ever watched a baby purse her lips to hoot for the first time, or flash a big, gummy grin when she sees you, or surprise herself by rolling over, you’ve glimpsed the developing brain in action. A baby’s brain constructs itself into something that controls the body, learns and connects socially. Spending time with an older person, you may notice signs of slippage. An elderly man might forget why he went into the kitchen, or fail to anticipate the cyclist crossing the road, or muddle medications with awkward and unfamiliar names. These are the signs of the gentle yet unrelenting neural erosion that comes with normal aging. These two seemingly distinct processes — development and aging — may actually be linked. Hidden in the brain-building process, some scientists now suspect, are the blueprints for the brain’s demise. The way the brain is built, recent research suggests, informs how it will decline in old age. That the end can be traced to the beginning sounds absurd: A sturdily constructed brain stays strong for decades. During childhood, neural pathways make connections in a carefully choreographed order. But in old age, this sequence plays in reverse, brain scans reveal. In both appearance and behavior, old brains seem to drift backward toward earlier stages of development. What’s more, some of the same cellular tools are involved in both processes. © Society for Science & the Public 2000 - 2016

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22440 - Posted: 07.14.2016

By Louise Whiteley It’s an appealing idea: the notion that understanding the learning brain will tell us how to maximise children’s potential, bypassing the knotty complexities of education research. But promises to replace sociological complexity with biological certainty should always be treated with caution. Hilary and Steven Rose are deeply sceptical of claims that neuroscience can inform education and early intervention policy, and deeply concerned about the use of such claims to support neoliberal agendas. They argue that focusing on the brain encourages a focus on the individual divorced from their social context, and that this is easily aligned with a view of poor achievement as a personal moral failing, rather than a practical consequence of poverty and inequality. Whether or not you end up cheerleading for the book’s political agenda, its deconstruction of faulty claims about how neuroscience translates into the classroom is relevant to anyone interested in education. The authors tear apart the scientific logic of policy documents, interrogate brain-based interventions and dismantle prevalent neuro-myths. One of the book’s meatiest chapters deals with government reports advocating early intervention to increase “mental capital”, and thus reduce the future economic burden of deprived, underachieving brains. As we discover, the neuroscientific foundations of these reports are shaky. For instance, they tend to assume that the more synaptic connections between brain cells the better, and that poor environment in a critical early period permanently reduces the number of synapses. This makes early intervention focusing on the individual child and “poor parenting” seem like the obvious solution. But pruning of synapses is just as important to brain development, and learning involves the continual forming and reforming of synaptic connections. More is not necessarily better. And while an initial explosion in synapses can be irreversibly disrupted by extreme neglect, the evidence just isn’t there yet for extrapolating this to the more common kinds of childhood deprivation that such reports address.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 22409 - Posted: 07.08.2016

By Amina Zafar, CBC News The Zika virus can cause devastating brain defects in newborns with microcephaly, but also in babies with normal-sized heads and those born to women infected late in pregnancy, Brazilian doctors say. In Wednesday's issue of the journal The Lancet, researchers said that of 602 babies born in Brazil with definite or probable Zika cases one in five had head circumferences in the normal range. Dr. Cesar Victora of the Federal University of Pelotas in Rio Grande do Sul, Brazil, and his team say the current focus on screening for microcephaly or small head circumference alone is too narrow. "We should not equate Zika congenital infection with microcephaly," Victora said in an interview from Washington. "We could well have many babies with normal head size who are affected. We will need to think about other exams to screen these babies, such as improving the diagnostic test we have for Zika and also possibly in areas that are undergoing an epidemic, doing ultrasound of the brains of these babies as soon as they are born." The epidemic in the worst-hit northeastern regions of the country peaked in November 2015. While the current season is cooler and mosquitoes aren't reproducing in Brazil, public health authorities continue to advise pregnant women to avoid travel to countries with Zika outbreaks. Countries in South Asia, the Western Pacific Islands, and South and Central America also have outbreaks. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22384 - Posted: 07.01.2016

Laura Sanders Busy nerve cells in the brain are hungry and beckon oxygen-rich blood to replenish themselves. But active nerve cells in newborn mouse brains can’t yet make this request, and their silence leaves them hungry, scientists report June 22 in the Journal of Neuroscience. Instead of being a dismal starvation diet, this lean time may actually spur the brain to develop properly. The new results, though, muddy the interpretation of the brain imaging technique called functional MRI when it is used on infants. Most people assume that all busy nerve cells, or neurons, signal nearby blood vessels to replenish themselves. But there were hints from fMRI studies of young children that their brains don’t always follow this rule. “The newborn brain is doing something weird,” says study coauthor Elizabeth Hillman of Columbia University. That weirdness, she suspected, might be explained by an immature communication system in young brains. To find out, she and her colleagues looked for neuron-blood connections in mice as they grew. “What we’re trying to do is create a road map for what we think you actually should see,” Hillman says. When 7-day-old mice were touched on their hind paws, a small group of neurons in the brain responded instantly, firing off messages in a flurry of activity. Despite this action, no fresh blood arrived, the team found. By 13 days, the nerve cell reaction got bigger, spreading across a wider stretch of the brain. Still the blood didn’t come. But by the time the mice reached adulthood, neural activity prompted an influx of blood. The results show that young mouse brains lack the ability to send blood to busy neurons, a skill that influences how the brain operates (SN: 11/14/15, p. 22). © Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22348 - Posted: 06.22.2016

Bentley Yoder was born with his brain outside his skull. Doctors said he didn’t have a chance, but he not only survived—he thrived. Now, some seven months later, Bentley has undergone reconstructive surgery to move his brain back into his skull. Bentley’s parents, Sierra and Dustin, both 25, found out something was wrong when they went in for a routine ultrasound at 22 weeks. Still in the womb, he was diagnosed with a rare condition called encephalocele, or cranium bifidum, in which parts of the brain protrude outside of gaps that have formed in the developing skull. The parents were told that their baby likely wouldn’t survive very long after birth, or that if he did he wouldn’t have any brain function; he was simply “incompatible with life.” As Sierra told the Washington Post, “We had no hope whatsoever.” The parents were unwilling to terminate the pregnancy, saying they wanted at least one chance to meet him before saying goodbye. To virtually everyone’s surprise, Bentley came out on his due date, October 31, 2015, kicking and screaming. After the first 36 hours, Sierra and Dustin had to take him home wearing the only onesie they bothered to purchase. Over the course of the next few weeks and months, Bentley continued to march on, save for a staph infection in his lungs. Aside from the large sac containing critical parts of his brain atop his head, Bentley developed normally. He continued to grow, and cried when he was hungry. The doctors were incredulous, and insisted that the growth above his head was just “damaged tissue,” and that “there’s no way it could be functioning,” but Bentley’s behaviors and normal developmental trajectory suggested otherwise.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22347 - Posted: 06.22.2016

By Gretchen Reynolds Physical activity is good for our brains. A wealth of science supports that idea. But precisely how exercise alters and improves the brain remains somewhat mysterious. A new study with mice fills in one piece of that puzzle. It shows that, in rodents at least, strenuous exercise seems to beneficially change how certain genes work inside the brain. Though the study was in mice, and not people, there are encouraging hints that similar things may be going on inside our own skulls. For years, scientists have known that the brains of animals and people who regularly exercise are different than the brains of those who are sedentary. Experiments in animals show that, for instance, exercise induces the creation of many new cells in the hippocampus, which is a part of the brain essential for memory and learning, and also improves the survival of those fragile, newborn neurons. Researchers believe that exercise performs these feats at least in part by goosing the body’s production of a substance called brain-derived neurotropic factor, or B.D.N.F., which is a protein that scientists sometimes refer to as “Miracle-Gro” for the brain. B.D.N.F. helps neurons to grow and remain vigorous and also strengthens the synapses that connect neurons, allowing the brain to function better. Low levels of B.D.N.F. have been associated with cognitive decline in both people and animals. Exercise increases levels of B.D.N.F. in brain tissue. But scientists have not understood just what it is about exercise that prompts the brain to start pumping out additional B.D.N.F. So for the new study, which was published this month in the journal eLIFE, researchers with New York University’s Langone Medical Center and other institutions decided to microscopically examine and reverse engineer the steps that lead to a surge in B.D.N.F. after exercise. They began by gathering healthy mice. Half of the animals were put into cages that contained running wheels. The others were housed without wheels. For a month, all of the animals were allowed to get on with their lives. Those living with wheels ran often, generally covering several miles a day, since mice like to run. The others remained sedentary. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22325 - Posted: 06.15.2016

By Brady Dennis In one city after another, the tests showed startling numbers of children with unsafe blood lead levels: Poughkeepsie and Syracuse and Buffalo. Erie and Reading. Cleveland and Cincinnati. In those cities and others around the country, 14 percent of kids — and in some cases more — have troubling amounts of the toxic metal in their blood, according to new research published Wednesday. The findings underscore how despite long-running public health efforts to reduce lead exposure, many U.S. children still live in environments where they're likely to encounter a substance that can lead to lasting behavioral, mental and physical problems. "We've been making progress for decades, but we have a ways to go," said Harvey Kaufman, senior medical director at Quest Diagnostics and a co-author of the study, which was published in the Journal of Pediatrics. "With blood [lead] levels in kids, there is no safe level." Kaufman and two colleagues at Quest, the nation's largest lab testing provider, examined more than 5.2 million blood tests for infants and children under age 6 that were taken between 2009 and 2015. The results spanned every state and the District of Columbia. The researchers found that while blood lead levels declined nationally overall during that period, roughly 3 percent of children across the country had levels that exceed five micrograms per deciliter — the threshold that the Centers for Disease Control and Prevention considers cause for concern. But in some places and among particular demographics, those figures are much higher.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22322 - Posted: 06.15.2016

By BENEDICT CAREY Jerome S. Bruner, whose theories about perception, child development and learning informed education policy for generations and helped launch the modern study of creative problem solving, known as the cognitive revolution, died on Sunday at his home in Manhattan. He was 100. His death was confirmed by his partner, Eleanor M. Fox. Dr. Bruner was a researcher at Harvard in the 1940s when he became impatient with behaviorism, then a widely held theory, which viewed learning in terms of stimulus and response: the chime of a bell before mealtime and salivation, in Ivan Pavlov’s famous dog experiments. Dr. Bruner believed that behaviorism, rooted in animal experiments, ignored many dimensions of human mental experience. In one 1947 experiment, he found that children from low-income households perceived a coin to be larger than it actually was — their desires apparently shaping not only their thinking but also the physical dimensions of what they saw. In subsequent work, he argued that the mind is not a passive learner — not a stimulus-response machine — but an active one, bringing a full complement of motives, instincts and intentions to shape comprehension, as well as perception. His writings — in particular the book “A Study of Thinking” (1956), written with Jacqueline J. Goodnow and George A. Austin — inspired a generation of psychologists and helped break the hold of behaviorism on the field. To build a more complete theory, he and the experimentalist George A. Miller, a Harvard colleague, founded the Center for Cognitive Studies, which supported investigation into the inner workings of human thought. Much later, this shift in focus from behavior to information processing came to be known as the cognitive revolution. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22300 - Posted: 06.09.2016

James Gorman Fruit flies are far from human, but not as far as you might think. They do many of the same things people do, like seek food, fight and woo mates. And their brains, although tiny and not set up like those of humans or other mammals, do many of the same things that all brains do — make and use memories, integrate information from the senses, and allow the creature to navigate both the physical and the social world. Consequently, scientists who study how all brains work like to use flies because it’s easier for them to do invasive research that isn’t allowed on humans. The technology of neuroscience is sophisticated enough to genetically engineer fly brains, and to then use fluorescent chemicals to indicate which neurons are active. But there are some remaining problems, like how to watch the brain of a fly that is moving around freely. It is one thing to record what is going on in a fly’s brain if the insect’s movement is restricted, but quite another to try to catch the light flash of brain cells from a fly that is walking around. Takeo Katsuki, an assistant project scientist at the Kavli Institute at the University of California, San Diego, is interested in courtship. And, he said, fruit flies simply won’t engage in courtship when they are tethered. So he and Dhruv Grover, another assistant project scientist, and Ralph J. Greenspan, in whose lab they both work, set out to develop a method for recording the brain activity of a walking fly. One challenge was to track the fly as it moved. They solved that problem with three cameras to follow the fly and a laser to activate the fluorescent chemicals in the brain. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 22290 - Posted: 06.06.2016