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Erika Check Hayden Physicians may soon have a lot more help in treating newborns. Neuroscientists and physicians have embarked on what they hope will be a revolution in treatments to prevent brain damage in newborn babies. As many as 800,000 babies die each year when blood and oxygen stop flowing to the brain around the time of birth. And thousands develop brain damage that causes long-lasting mental or physical disabilities, such as cerebral palsy. Physicians have few tools to prevent this, but they are optimistic that clinical trials now under way will change things. The trials were sparked by neuroscientists’ realization in the 1990s that some brain injuries can be repaired. That discovery spurred a flurry of basic research that is just now coming to fruition in the clinic. In January, a US study will start to test whether the hormone erythropoietin, or EPO, can prevent brain damage hours after birth when combined with hypothermia, in which babies are cooled to 33.5 °C. A trial in Australia is already testing this treatment. Physicians in countries including the United States, China and Switzerland are testing EPO in premature babies, as well as other treatments, such as melatonin, xenon, argon, magnesium, allopurinol and cord blood in full-term babies. “The world has really changed for us,” says neurologist Janet Soul at Boston Children’s Hospital in Massachusetts. Therapeutic hypothermia was the first success: clinical trials over the past decade have shown that it decreases the risk of death and of major brain-development disorders by as much as 60%. It is now standard treatment for babies in developed countries whose brains are deprived of blood and oxygen during birth. © 2016 Macmillan Publishers Limited,

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: 22935 - Posted: 11.30.2016

By Dwayne Godwin, Jorge Cham © 2016 Scientific American,

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: 22914 - Posted: 11.26.2016

By PAM BELLUCK It is the news that doctors and families in the heart of Zika territory had feared: Some babies not born with the unusually small heads that are the most severe hallmark of brain damage as a result of the virus have developed the condition, called microcephaly, as they have grown older. The findings were reported in a study of 13 babies in Brazil that was published Tuesday in Morbidity and Mortality Weekly Report. At birth, none of the babies had heads small enough to receive a diagnosis of microcephaly, but months later, 11 of them did. For most of those babies, brain scans soon after birth showed significant abnormalities, and researchers found that as the babies aged, their brains did not grow or develop enough for their age and body size. The new study echoes another published this fall, in which three babies were found to have microcephaly later in their first year. As they closed in on their first birthdays, many of the babies also had some of the other developmental and medical problems caused by Zika infection, a range of disabilities now being called congenital Zika syndrome. The impairments resemble characteristics of cerebral palsy and include epileptic seizures, muscle and joint problems and difficulties swallowing food. “There are some areas of great deficiency in the babies,” said Dr. Cynthia Moore, the director of the division of congenital and developmental disorders for the Centers for Disease Control and Prevention and an author of the new study. “They certainly are going to have a lot of impairment.” Dr. Deborah Levine, a professor of radiology at Harvard Medical School who has studied Zika but was not involved in either study, said there would most likely be other waves of children whose brains were affected by the Zika infection, but not severely enough to be noticed in their first year. © 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: 22903 - Posted: 11.23.2016

Laura Sanders Harmful factors circulating in old blood may be partly responsible for the mental decline that can come with age, a small study in mice suggests. Irina Conboy of the University of California, Berkeley and colleagues devised a new way to mingle blood in two mice that didn’t involve stitching their bodies together, as in previous experiments (SN: 5/31/14, p. 8). Instead, researchers used a microfluidic device to shuttle blood, a process that precisely controlled the timing and amount of blood transferred between the mice. The method, reported online November 22 in Nature Communications, allows more precise tests of blood’s influence on aging, the researchers believe. Old mice benefited in some ways from infusions of young blood, experiments with four young-old pairs of mice revealed. With young blood around, old muscles were better able to recover after an injury. And young blood seemed to improve old livers in some tests. But young blood didn’t seem to help one measure of brain health. After transfusions of young blood, old mice still had lower numbers of newborn nerve cells in the hippocampus, a brain structure important for learning and memory. What’s more, old blood reduced the number of newborn nerve cells in young mice. This damage happened quickly, after just one blood exchange, the researchers found. The results suggest that old blood contains components that harm brain cells, an insight that makes scientists eager to identify those factors. |© 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: 22898 - Posted: 11.23.2016

Laura Sanders SAN DIEGO — Mice raised in cages bombarded with glowing lights and sounds have profound brain abnormalities and behavioral trouble. Hours of daily stimulation led to behaviors reminiscent of attention-deficit/hyperactivity disorder, scientists reported November 14 at the annual meeting of the Society for Neuroscience. Certain kinds of sensory stimulation, such as sights and sounds, are known to help the brain develop correctly. But scientists from Seattle Children’s Research Institute wondered whether too much stimulation or stimulation of the wrong sort could have negative effects on the growing brain. To mimic extreme screen exposure, mice were blasted with flashing lights and TV audio for six hours a day. The cacophony began when the mice were 10 days old and lasted for six weeks. After the end of the ordeal, scientists examined the mice’s brains. “We found dramatic changes everywhere in the brain,” said study coauthor Jan-Marino Ramirez. Mice that had been stimulated had fewer newborn nerve cells in the hippocampus, a brain structure important for learning and memory, than unstimulated mice, Ramirez said. The stimulation also made certain nerve cells more active in general. Stimulated mice also displayed behaviors similar to some associated with ADHD in children. These mice were noticeably more active and had trouble remembering whether they had encountered an object. The mice also seemed more inclined to take risks, venturing into open areas that mice normally shy away from, for instance. |© Society for Science & the Public 2000 - 2016.

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: 22876 - Posted: 11.16.2016

Anesthesia during early childhood surgery poses little risk for intelligence and academics later on, the largest study of its kind suggests. The results were found in research on nearly 200,000 Swedish teens. School grades were only marginally lower in kids who'd had one or more common surgeries with anesthesia before age 4, compared with those who'd had no anesthesia during those early years. Whether the results apply to sicker children who have riskier surgeries with anesthesia is not known. But the researchers from Sweden's Karolinska Institute and doctors elsewhere called the new results reassuring, given experiments in young animals linking anesthesia drugs with brain damage. Previous studies of children have been relatively small, with conflicting results. The new findings, published Monday in JAMA Pediatrics, don't provide a definitive answer and other research is ongoing. The study authors and other doctors say the harms from postponing surgery must be considered when evaluating any potential risks from anesthesia in young children. The most common procedures in the study were hernia repairs; ear, nose or throat surgeries; and abdominal operations. The researchers say the operations likely lasted an hour or less. The study did not include children with other serious health problems and those who had more complex or risky operations, including brain, heart and cancer surgeries. The research involved about 33,500 teens who'd had surgery before age 4 and nearly 160,000 who did not. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 22842 - Posted: 11.08.2016

By Marian Vidal-Fernandez, Ana Nuevo-Chiquero, The title of this article might trigger self-satisfied smiles among first-borns, and some concerns among the rest of us. Many studies show children born earlier in the family enjoy better wages and more education, but until now we didn’t really know why. Our recently published findings are the first to suggest advantages of first born siblings start very early in life—around zero to three years old! We observe parents changing their behaviour as new children are born, and offering less cognitive stimulation to children of higher birth order. It now seems clear that for those born and raised in high-income countries such as the United States, the UK and Norway, earlier-born children enjoy higher wages and education as adults—known as the “birth order effect”. Comparing two siblings, the greater the difference in their birth order, the greater the relative benefit to the older child. However, to date we’ve had no evidence that explains where such differences come from. We know it’s not an effect of family size, because the effect remains when comparing siblings within the same family and families with the same number of children. While it makes sense that parents earn more money and gain experience as they get older and have more children, they also need to divide their economic resources and attention among any children that arrive after the first born. We wondered where in childhood these differences began, and what the cause or causes might be. © 2016 Scientific American,

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: 22835 - Posted: 11.05.2016

Tina Hesman Saey VANCOUVER — Zika virus’s tricks for interfering with human brain cell development may also be the virus’s undoing. Zika infection interferes with DNA replication and repair machinery and also prevents production of some proteins needed for proper brain growth, geneticist Feiran Zhang of Emory University in Atlanta reported October 19 at the annual meeting of the American Society of Human Genetics. Levels of a protein called p53, which helps control cell growth and death, shot up by 80 percent in human brain cells infected with the Asian Zika virus strain responsible for the Zika epidemic in the Americas, Zhang said. The lab dish results are also reported in the Oct. 14 Nucleic Acids Research. Increased levels of the protein stop developing brain cells from growing and may cause the cells to commit suicide. A drug that inactivates p53 stopped brain cells from dying, Zhang said. Such p53 inhibitors could help protect developing brains in babies infected with Zika. But researchers would need to be careful giving such drugs because too little p53 can lead to cancer. Zika also makes small RNA molecules that interfere with production of proteins needed for DNA replication, cell growth and brain development, Zhang said. In particular, a small viral RNA called vsRNA-21 reduced the amount of microcephalin 1 protein made in human brain cells in lab dishes. The researchers confirmed the results in mouse experiments. That protein is needed for brain growth; not enough leads to the small heads seen in babies with microcephaly. Inhibitors of the viral RNAs might also be used in therapies, Zhang suggested. |© 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: 22770 - Posted: 10.20.2016

By MARC SANTORA The morning after Christine Grounds gave birth to her son Nicholas, she awoke to find a neurologist examining her baby. It was summer 2006, and Nicholas was her first child. There had been no indication that anything was wrong during her pregnancy, but it was soon clear that there was a problem. “Did you know he has microcephaly?” she remembers the doctor asking matter-of-factly. Confused, she replied, “What is microcephaly?” This was before the Zika virus had spread from Brazil across South and Central America and the Caribbean and reached Florida. It was before doctors had determined that the virus could cause microcephaly, a birth defect in which children have malformed heads and severely stunted brain development. And it was before people had seen the devastating pictures of scores of newborns with the condition in Brazil and elsewhere that shocked the world this year. Ms. Grounds, a 45-year-old psychotherapist, and her husband, Jon Mir, who live in Manhattan, had no idea what microcephaly would mean for them or for their child. “We had a diagnosis but no prognosis,” recalled Mr. Mir, 44, who works in finance. The doctors could offer few answers. “We don’t know if he will walk,” the couple recalled being told. “We don’t know if he will talk. He might be in a vegetative state.” But the truth was, even the doctors did not know. As mosquito season draws to a close in much of the country, taking with it the major risk of new Zika infections, there are still more than 2,600 pregnant women who have tested positive for the virus in the United States and its territories, according to the Centers for Disease Control and Prevention. They, and thousands more around the world, face the prospect of giving birth to a child with microcephaly. © 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: 22766 - Posted: 10.19.2016

Erin Ross The teenage brain has been characterized as a risk-taking machine, looking for quick rewards and thrills instead of acting responsibly. But these behaviors could actually make teens better than adults at certain kinds of learning. "In neuroscience, we tend to think that if healthy brains act in a certain way, there should be a reason for it," says Juliet Davidow, a postdoctoral researcher at Harvard University in the Affective Neuroscience and Development Lab and the lead author of the study, which was published Wednesday in the journal Neuron. But scientists and the public often focus on the negatives of teen behavior, so she and her colleagues set out to test the hypothesis that teenagers' drive for rewards, and the risk-taking that comes from it, exist for a reason. When it comes to what drives reward-seeking in teens, fingers have always been pointed at the striatum, a lobster-claw-shape structure in the brain. When something surprising and good happens — say, you find $20 on the street — your body produces the pleasure-related hormone dopamine, and the striatum responds. "Research shows that the teenage striatum is very active," says Davidow. This suggests that teens are hard-wired to seek immediate rewards. But, she adds, it's also shown that their prefrontal cortex, which helps with impulse control, isn't fully developed. Combined, these two things have given teens their risky rep. But the striatum isn't just involved in reward-seeking. It's also involved in learning from rewards, explains Daphna Shohamy, a cognitive neuroscientist at the Zuckerman Mind Brain Behavior Institute at Columbia University who worked on the study. She wanted to see if teenagers would be better at this type of learning than adults would. © 2016 npr

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: 22738 - Posted: 10.10.2016

Richard A. Friedman There’s a reason adults don’t pick up Japanese or learn how to kite surf. It’s ridiculously hard. In stark contrast, young people can learn the most difficult things relatively easily. Polynomials, Chinese, skateboarding — no problem! Neuroplasticity — the brain’s ability to form new neural connections and be influenced by the environment — is greatest in childhood and adolescence, when the brain is still a work in progress. But this window of opportunity is finite. Eventually it slams shut. Or so we thought. Until recently, the conventional wisdom within the fields of neuroscience and psychiatry has been that development is a one-way street, and once a person has passed through his formative years, experiences and abilities are very hard, if not impossible, to change. What if we could turn back the clock in the brain and recapture its earlier plasticity? This possibility is the focus of recent research in animals and humans. The basic idea is that during critical periods of brain development, the neural circuits that help give rise to mental states and behaviors are being sculpted and are particularly sensitive to the effects of experience. If we can understand what starts and stops these periods, perhaps we can restart them. Think of the brain’s sensitive periods as blown glass: The molten glass is very malleable, but you have a relatively brief time before it cools and becomes crystalline. Put it back into the furnace, and it can once again change shape. © 2016 The New York Times Company

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: 22737 - Posted: 10.10.2016

By Anna Azvolinsky _The human cerebral cortex experiences a burst of growth late in fetal development thanks to the expansion and migration of progenitor cells that ultimately form excitatory neurons. For a fully functional brain, in addition to excitatory neurons, inhibitory ones (called interneurons) are also necessary. Yet scientists have not been able to account for the increase in inhibitory neurons that occurs after birth. Now, in a paper published today (October 6) in Science, researchers from the University of California, San Francisco (UCSF), have shown that there is a reserve of young neurons that continue to migrate and integrate into the frontal lobes of infants. “It was thought previously that addition of new neurons to the human cortex [mostly] happens only during fetal development. This new study shows that young neurons continue to migrate on a large scale into the cerebral cortex of infants,” Benedikt Berninger, who studies brain development at the Johannes Gutenberg University of Mainz, Germany, and was not involved in the work, wrote in an email to The Scientist. “This implies that experience during the first few months could affect this migration and thereby contribute to brain plasticity.” Aside from the migration of neurons into the olfactory bulb in infants, “this is the first time anyone has been able to catch neurons in the act of moving into the cortex,” said New York University neuroscientist Gord Fishell who penned an accompanying editorial but was not involved in the work. “We kept expecting these interneurons to be new cells but, in fact, they are immature ones hanging around and taking the long road from the bottom of the brain to the cortex.” © 1986-2016 The Scientist

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: 22734 - Posted: 10.08.2016

Hannah Devlin Science correspondent Scientists have found the most definitive evidence yet that some people are destined to age quicker and die younger than others - regardless of their lifestyle. The findings could explain the seemingly random and unfair way that death is sometimes dealt out, and raise the intriguing future possibility of being able to extend the natural human lifespan. “You get people who are vegan, sleep 10 hours a day, have a low-stress job, and still end up dying young,” said Steve Horvath, a biostatistician who led the research at the University of California, Los Angeles. “We’ve shown some people have a faster innate ageing rate.” A higher biological age, regardless of actual age, was consistently linked to an earlier death, the study found. For the 5% of the population who age fastest, this translated to a roughly 50% greater than average risk of death at any age. Intriguingly, the biological changes linked to ageing are potentially reversible, raising the prospect of future treatments that could arrest the ageing process and extend the human lifespan. “The great hope is that we find anti-ageing interventions that would slow your innate ageing rate,” said Horvath. “This is an important milestone to realising this dream.” Horvath’s ageing “clock” relies on measuring subtle chemical changes, in which methyl compounds attach or detach from the genome without altering the underlying code of our DNA. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 22708 - Posted: 09.29.2016

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