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By Mitch Leslie If these sweltering summer days prompt you to reach for a cold drink, you can thank your hypothalamus, a region of the brain that helps us regulate body temperature and other internal conditions. But the region may fail us when we get older. A new study in mice suggests that the hypothalamus promotes aging, hastening physical and mental decline as its stem cells die off. “It’s a pretty stunning paper,” says Charles Mobbs, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York City. The new aging mechanism “is totally novel and quite unexpected,” adds neuroendocrinologist Marianna Sadagurski of Wayne State University in Detroit, Michigan. Tucked away deep in the brain, the hypothalamus monitors and maintains our blood concentration, our body temperature, and other physiological variables. Researchers have also suspected that it plays a role in aging. The hypothalamus becomes inflamed as we get older, and 4 years ago a team led by neurodendocrinologist Dongsheng Cai of Albert Einstein College of Medicine in New York City showed that quelling this inflammation delays physical deterioration and boosts life span in mice. In the new study, the team turned its attention to the hypothalamus’s stem cells, which in young animals divide to produce replacements for dead and damaged cells. As mice get older, the scientists found, the number of stem cells in the hypothalamus plunges. By later ages they are “basically all gone,” Cai says. © 2017 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23886 - Posted: 07.27.2017

Sara Reardon Mice aged more slowly when injected with stem cells from the brains of newborns. Stem cells in the brain could be the key to extending life and slowing ageing. These cells — which are located in the hypothalamus, a region that produces hormones and other signalling molecules — can re­invigorate declining brain function and muscle strength in middle-aged mice, according to a study published on 26 July in Nature1. Previous studies have suggested that the hypothalamus is involved in ageing, but the latest research shows that stem cells in this region can slow the process. That makes sense, because the hypothalamus is involved in many bodily functions, including inflammation and appetite, says Dongsheng Cai, a neuroendocrinologist at Albert Einstein College of Medicine in New York City. In their study, Cai and his colleagues found that stem cells in the hypothalamus disappear as mice grow older. When the researchers injected their mice with viruses that destroy these cells, the animals seemed to grow older faster, experiencing declines in memory, muscle strength, endurance and coordination. They also died sooner than untreated mice of the same age. Next, the team injected stem cells taken from the hypothalami of newborn mice into the brains of middle-aged mice. After four months, these animals had better cognitive and muscular function than untreated mice of the same age. They also lived about 10% longer, on average. © 2017 Macmillan Publishers Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23885 - Posted: 07.27.2017

Carina Storrs In the late 1960s, a team of researchers began doling out a nutritional supplement to families with young children in rural Guatemala. They were testing the assumption that providing enough protein in the first few years of life would reduce the incidence of stunted growth. It did. Children who got supplements grew 1 to 2 centimetres taller than those in a control group. But the benefits didn't stop there. The children who received added nutrition went on to score higher on reading and knowledge tests as adolescents, and when researchers returned in the early 2000s, women who had received the supplements in the first three years of life completed more years of schooling and men had higher incomes1. “Had there not been these follow-ups, this study probably would have been largely forgotten,” says Reynaldo Martorell, a specialist in maternal and child nutrition at Emory University in Atlanta, Georgia, who led the follow-up studies. Instead, he says, the findings made financial institutions such as the World Bank think of early nutritional interventions as long-term investments in human health. Since the Guatemalan research, studies around the world — in Brazil, Peru, Jamaica, the Philippines, Kenya and Zimbabwe — have all associated poor or stunted growth in young children with lower cognitive test scores and worse school achievement2. A picture slowly emerged that being too short early in life is a sign of adverse conditions — such as poor diet and regular bouts of diarrhoeal disease — and a predictor for intellectual deficits and mortality. But not all stunted growth, which affects an estimated 160 million children worldwide, is connected with these bad outcomes. Now, researchers are trying to untangle the links between growth and neurological development. Is bad nutrition alone the culprit? What about emotional neglect, infectious disease or other challenges? © 2017 Macmillan Publishers Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23831 - Posted: 07.13.2017

Ewen Callaway For 18 months in the early 1980s, John Sulston spent his days watching worms grow. Working in twin 4-hour shifts each day, Sulston would train a light microscope on a single Caenorhabditis elegans embryo and sketch what he saw at 5-minute intervals, as a fertilized egg morphed into two cells, then four, eight and so on. He worked alone and in silence in a tiny room at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, solving a Rubik's cube between turns at the microscope. “I did find myself little distractions,” the retired Nobel prize-winning biologist once recalled. His hundreds of drawings revealed the rigid choreography of early worm development, encompassing the births of precisely 671 cells, and the deaths of 111 (or 113, depending on the worm’s sex). Every cell could be traced to its immediate forebear and then to the one before that in a series of invariant steps. From these maps and others, Sulston and his collaborators were able to draw up the first, and so far the only, complete ‘cell-lineage tree’ of a multicellular organism1. Although the desire to record an organism’s development in such exquisite detail preceded Sulston by at least a century, the ability to do so in more-complex animals has been limited. No one could ever track the fates of billions of cells in a mouse or a human with just a microscope and a Rubik’s cube to pass the time. But there are other ways. Revolutions in biologists’ ability to edit genomes and sequence them at the level of a single cell have sparked a renaissance in cell-lineage tracing. © 2017 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: 23812 - Posted: 07.07.2017

Mike Mariani With its bright colors, anthropomorphic animal motif, and nautical-themed puzzle play mat, Dr. Kimberly Noble’s laboratory at Columbia University looks like your typical day care center—save for the team of cognitive neuroscientists observing kids from behind a large two-way mirror. The Neurocognition, Early Experience, and Development Lab is home to cutting-edge research on how poverty affects young brains, and I’ve come here to learn how Noble and her colleagues could soon definitively prove that growing up poor can keep a child’s brain from developing. Noble, a 40-year-old from outside of Philadelphia who discusses her work with a mix of enthusiasm and clinical restraint, is among the handful of neuroscientists and pediatricians who’ve seen increasing evidence that poverty itself—and not factors like nutrition, language exposure, family stability, or prenatal issues, as previously thought—may diminish the growth of a child’s brain. Now she’s in the middle of planning a five-year, nationwide study that could establish a causal link between poverty and brain development—and, in the process, suggest a path forward for helping our poorest children. It’s the culmination of years of work for Noble, who helped jump-start this fledgling field in the early 2000s when, as a University of Pennsylvania graduate student, she and renowned cognitive neuroscientist Martha Farah began exploring the observation that poor kids tended to perform worse academically than their better-off peers. They wanted to investigate the neurocognitive underpinnings of this relationship—to trace the long-standing correlation between socioeconomic status and academic performance back to specific parts of the brain. “There have been decades of work from social scientists, looking at socioeconomic disparities in broad cognitive outcomes—things like IQ or high school graduation rate,” she says. “But there’s no high school graduation part of the brain.” ©2017 Mother Jones and the Foundation for National Progress.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23805 - Posted: 07.04.2017

Heidi Ledford By 13 weeks of gestation, human fetuses have developed a much more unusual immune system than previously thought. A human fetus in its second trimester is extraordinarily busy. It is developing skin and bones, the ability to hear and swallow, and working on its first bowel movement. Now, a study published on 14 June in Nature finds that fetuses are also acquiring a functioning immune system — one that can recognize foreign proteins, but is less inclined than a mature immune system to go on the attack (N. McGovern et al. Nature http://dx.doi.org/10.1038/nature22795; 2017). The results add to a growing body of literature showing that the fetal immune system is more active than previously appreciated. “In general textbooks, you see this concept of a non-responsive fetus is still prevailing,” says immunologist Jakob Michaelsson at the Karolinska Institute in Stockholm. But the fetal immune system is unique, he says. “It’s not just immature, it’s special.” A developing fetus is constantly exposed to foreign proteins and cells, which are transferred from the mother through the placenta. In humans, this exposure is more extensive than in many other mammals, says immunologist Mike McCune at the University of California, San Francisco. As a result, laboratory mice have proved a poor model for studying the developing human fetal immune system. But fully understanding that development could reveal the reasons for some miscarriages, as well as explain conditions such as pre-eclampsia, which is associated with abnormal immune responses to pregnancy and causes up to 40% of premature births. © 2017 Macmillan Publishers Limited,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23746 - Posted: 06.15.2017

Maria Temming Fascination with faces is nature, not nurture, suggests a new study of third-trimester fetuses. Scientists have long known that babies like looking at faces more than other objects. But research published online June 8 in Current Biology offers evidence that this preference develops before birth. In the first-ever study of prenatal visual perception, fetuses were more likely to move their heads to track facelike configurations of light projected into the womb than nonfacelike shapes. Past research has shown that newborns pay special attention to faces, even if a “face” is stripped down to its bare essentials — for instance, a triangle of three dots: two up top for eyes, one below for a mouth or nose. This preoccupation with faces is considered crucial to social development. “The basic tendency to pick out a face as being different from other things in your environment, and then to actually look at it, is the first step to learning who the important people are in your world,” says Scott Johnson, a developmental psychologist at UCLA who was not involved in the study. Using a 4-D ultrasound, the researchers watched how 34-week-old fetuses reacted to seeing facelike triangles compared with seeing triangles with one dot above and two below. They projected triangles of red light in both configurations through a mother’s abdomen into the fetus’s peripheral vision. Then, they slid the light across the mom’s belly, away from the fetus’s line of sight, to see if it would turn its head to continue looking at the image. |© Society for Science & the Public 2000 - 2017

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 23726 - Posted: 06.09.2017

By Jessica Hamzelou Drinking even small amounts of alcohol when pregnant seems to have subtle effects on how a baby’s face develops – including the shape of their eyes, nose and lips. This isn’t necessarily harmful, though. “We don’t know if the small changes in the children’s facial shape are connected in any way to differences in their development,” says Jane Halliday of the Murdoch Children’s Research Institute in Victoria, Australia, who led the research. “We plan to look at this as the children grow.” Heavy drinking during pregnancy can cause fetal alcohol syndrome, which is characterised by distinctive facial features, such as small eye openings, a short up-turned nose, and a smooth philtrum over the upper lip. Children with this condition are likely to have attention and behavioural disorders, as well as a lower IQ, says Halliday. To find out whether low levels of alcohol consumption, which are more common in pregnancy, might also affect developing fetuses, Halliday’s team studied 1570 women throughout their pregnancies and births. Of these women, 27 per cent said they continued to drink at least some alcohol while pregnant. When the children were 1 year old, Halliday’s team took photos of 415 of the babies’ faces with multiple cameras from different angles. When the team stitched these images together using computer software, the resulting 3D photographs detailed almost 70,000 points on each baby’s face. Analysing these revealed subtle differences in the faces of babies whose mothers had drunk alcohol compared with those whose mothers hadn’t. These included a slightly shorter, more-upturned nose. © Copyright New Scientist Ltd.

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: 23714 - Posted: 06.06.2017

By JANE E. BRODY Harding Senior High, a public school in St. Paul, Minn., has long been known as a 90-90-90 school: 90 percent of students are minorities, nearly 90 percent come from poor or struggling families and, until recently, 90 percent graduate (now about 80 percent) to go on to college or a career. Impressive statistics, to be sure. But perhaps most amazing about this school is that it recognizes and acts on the critical contribution that adequate food and good nutrition make to academic success. Accordingly, it provides three balanced meals a day to all its students, some of whom might otherwise have little else to eat on school days. For those who can’t get to school in time for early breakfast, a substitute meal is offered after first period, to be eaten during the second period. Every student can pick up dinner at the end of the school day, and those who play sports after school can take the dinner with them to practices and games. To Jennifer Funkhauser, a French teacher at Harding and hands-on participant in the meal program, making sure the students are well fed is paramount to their ability to succeed academically. Ms. Funkhauser and the staff at Harding are well aware of the many studies showing that children who are hungry or malnourished have a hard time learning. After she noticed that some youngsters were uncomfortable eating with hundreds of others in a large, noisy lunchroom, Ms. Funkhauser created a more private, quieter “lunch bunch” option for them. The attitude and atmosphere at Harding are in stark contrast to the humiliating lunchroom experiences suffered by students at some schools, where youngsters are sometimes shamed in front of their classmates and their meals confiscated and dumped in the garbage when parents have an unpaid lunch bill. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23706 - Posted: 06.05.2017

Irwin Feinberg, One of the grand strategies nature uses to construct nervous systems is to overproduce neural elements, such as neurons, axons and synapses, and then prune the excess. In fact, this overproduction is so substantial that only about half of the neurons mammalian embryos generate will survive until birth. Why do some neural connections persist, whereas others do not? A common misconception is that neurons that do not make the cut are defective. Although some may indeed be damaged, most simply fail to connect to their chemically defined targets. In a series of brilliant studies performed during the latter half of the 20th century, researchers discovered how pruning works. They found that newborn neurons migrate along chemically defined routes and that when the neurons arrive at their genetically assigned locations, they compete with their “sibling” neurons to connect with predetermined targets. Victorious neurons receive trophic, or nourishing, factors that allow their survival; unsuccessful neurons fade away in a process called apoptosis, or cell death. The timing of cell death is genetically programmed and occurs at different points in the embryonic development of each species. For decades neuroscientists believed that neural pruning ended shortly after birth. But in 1979 the late Peter Huttenlocher, a neurologist at the University of Chicago, demonstrated that this excess production and pruning strategy actually continues for synapses long after birth. Using electron microscopy to analyze carefully selected autopsied human brains, he showed that synapses—the tiny connections between neurons—proliferate after birth, reaching twice their neonatal levels by mid- to late childhood, and then decrease precipitously during adolescence. © 2017 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: 23676 - Posted: 05.30.2017

By Diana Kwon Age as a state of mind is not just the stuff of birthday card clichés. In recent years, scientists have plumbed the molecular depths of the body and surfaced with tell-tale biomarkers of aging, some of which extend to the brain. Now, researchers are harnessing another tool, neuroimaging, to measure the organ’s age, and using that to predict how long a person will live. “People are searching for the tree rings of humans,” James Cole, a research associate at Imperial College London, told The Scientist. Cole and his colleagues recently devised their own technique of predicting the biological age of people’s brains using a combination of machine learning and magnetic resonance imaging (MRI) scans. In a study published last month (April 25) in Molecular Psychiatry, the team reported that this technique was able to predict mortality in humans—people with “older” brains, they found, had greater risk of dying before age 80. To create this marker of brain aging, the researchers first trained a machine-learning algorithm to analyze structural brain scans from a healthy reference sample containing 2,001 individuals between 18 and 90 years old. Then, they used this tool to predict brain age in the Lothian Birth Cohort, a group of 669 adults, all born in 1936. Based on the algorithm’s assessment, individuals who had brains that were “older” than their actual, chronological age also tended to have an increased risk of dying sooner and lower performance on various fitness measures, such as lung function, walking speed, and fluid intelligence. © 1986-2017 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: 23654 - Posted: 05.24.2017

Tina Hesman Saey Face-to-face, a human and a chimpanzee are easy to tell apart. The two species share a common primate ancestor, but over millions of years, their characteristics have morphed into easily distinguishable features. Chimps developed prominent brow ridges, flat noses, low-crowned heads and protruding muzzles. Human noses jut from relatively flat faces under high-domed crowns. Those facial features diverged with the help of genetic parasites, mobile bits of genetic material that insert themselves into their hosts’ DNA. These parasites go by many names, including “jumping genes,” “transposable elements” and “transposons.” Some are relics of former viruses assimilated into a host’s genome, or genetic instruction book. Others are self-perpetuating pieces of genetic material whose origins are shrouded in the mists of time. “Transposable elements have been with us since the beginning of evolution. Bacteria have transposable elements,” says evolutionary biologist Josefa González. She doesn’t think of transposons as foreign DNA. They are parts of our genomes — like genes. “You cannot understand the genome without understanding what transposable elements are doing,” says González, of the Institute of Evolutionary Biology in Barcelona. She studies how jumping genes have influenced fruit fly evolution. Genomes of most organisms are littered with the carcasses of transposons, says Cédric Feschotte, an evolutionary geneticist at the University of Utah in Salt Lake City. Fossils of the DNA parasites build up like the remains of ancient algae that formed the white cliffs of Dover. One strain of maize, the organism in which Nobel laureate Barbara McClintock first discovered transposable elements in the 1940s, is nearly 85 percent transposable elements (SN: 12/19/09, p. 9). Corn is an extreme example, but humans have plenty, too: Transposable elements make up nearly half of the human genome. |© Society for Science & the Public 2000 - 2017

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23627 - Posted: 05.17.2017

Katherine Hobson American Indian and Alaska Native families are much more likely to have an infant die suddenly and unexpectedly, and that risk has remained higher than in other ethnic groups since public health efforts were launched to prevent sudden infant death syndrome in the 1990s. African-American babies also face a higher risk, a study finds. American Indians and Alaska Natives had a rate of 177.6 sudden unexplained infant deaths per 100,000 live births in 2013 (down from 237.5 per 100,000 in 1995) compared with 172.4 for non-Hispanic blacks (down from 203), 84.5 for non-Hispanic whites (down from 93), 49.3 for Hispanics (down from 62.7) and 28.3 for Asians and Pacific Islanders (down from 59.3). The declines were statistically significant only among non-Hispanic blacks, Hispanics and Asians/Pacific Islanders. "There are still significant gaps and disparities between races and ethnicities," says Lori Feldman-Winter, a professor of pediatrics at Cooper University Health Care in Camden, N.J., who wasn't involved with this study but was a co-author of the most recent sleep guidelines from the American Academy of Pediatrics, released in the fall. Overall rates of sudden unexpected infant death, which includes sudden infant death syndrome as well as accidental suffocation or strangulation in bed and other unexplained deaths, declined sharply in the five or so years after a national campaign was launched in 1994 to encourage caregivers to put babies to sleep on their backs. But the rates have not declined since 2000. Researchers at the Centers for Disease Control and Prevention wanted to know whether those changes were uniform across racial and ethnic groups. © 2017 npr

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 23616 - Posted: 05.16.2017

by Laura Sanders One of the most pressing and perplexing questions parents have to answer is what to do about screen time for little ones. Even scientists and doctors are stumped. That’s because no one knows how digital media such as smartphones, iPads and other screens affect children. The American Academy of Pediatrics recently put out guidelines, but that advice was based on a frustratingly slim body of scientific evidence, as I’ve covered. Scientists are just scratching the surface of how screen time might influence growing bodies and minds. Two recent studies point out how hard these answers are to get. But the studies also hint that the answers might be important. In the first study, Julia Ma at the University of Toronto and colleagues found that, in children younger than 2, the more time spent with a handheld screen, such as a smartphone or tablet, the more likely the child was to show signs of a speech delay. Ma presented the work May 6 at the 2017 Pediatric Academic Societies Meeting in San Francisco. The team used information gleaned from nearly 900 children’s 18-month checkups. Parents answered a questionnaire about their child’s mobile media use and then filled out a checklist designed to identify heightened risk of speech problems. This checklist is a screening tool that picks up potential signs of trouble; it doesn’t offer a diagnosis of a language delay, points out study coauthor Catherine Birken, a pediatrician at The Hospital for Sick Children in Toronto. Going into the study, the researchers didn’t have expectations about how many of these toddlers were using handheld screens. “We had very little clues, because there is almost no literature on the topic,” Birken says. “There’s just really not a lot there.” |© Society for Science & the Public 2000 - 2017

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 23608 - Posted: 05.13.2017

Ian Sample Science editor A landmark project to map the wiring of the human brain from womb to birth has released thousands of images that will help scientists unravel how conditions such as autism, cerebral palsy and attention deficit disorders arise in the brain. The first tranche of images come from 40 newborn babies who were scanned in their sleep to produce stunning high-resolution pictures of early brain anatomy and the intricate neural wiring that ferries some of the earliest signals around the organ. The initial batch of brain scans are intended to give researchers a first chance to analyse the data and provide feedback to the senior scientists at King’s College London, Oxford University and Imperial College London who are leading the Developing Human Connectome Project, which is funded by €15m (£12.5m) from the EU. The images show the intricate neural wiring that ferries some of the earliest signals around the brain. Hundreds of thousands more images will be released in the coming months and years. Most will come from a thousand sleeping babies, but another 500 have had their brains scanned while still in the womb. “The challenge is that you are imaging one person inside another person and both of them move,” said Jo Hajnal, professor of imaging science at King’s College London, who developed new MRI technology for the project. Taking brain scans of sleeping babies is hard enough. At the start of the project in 2013, more than 10% of the scans failed when babies woke up in the middle of the two to three hour procedure. Now the babies are fed and prepared for their scans at their mother’s side before they are carried to the scanner. To cut the odds of the babies waking, scientists tweaked the scanner software to stop it making sudden noises.

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: 23599 - Posted: 05.10.2017

By Simon Makin The past few decades have seen intensive efforts to find the genetic roots of neurological disorders, from schizophrenia to autism. But the genes singled out so far have provided only sketchy clues. Even the most important genetic risk factors identified for autism, for example, may only account for a few percent of all cases. Much frustration stems from the realization that the key mutations elevating disease risk tend to be rare, because they are less likely to be passed on to offspring. More common mutations confer only small risks (although those risks become more significant when calculated across an entire population). There are several other places to look for the missing burden of risk, and one surprising possible source has recently emerged—an idea that overturns a fundamental tenet of biology and has many researchers excited about a completely new avenue of inquiry. Accepted dogma holds that—although every cell in the body contains its own DNA—the genetic instructions in each cell nucleus are identical. But new research has now proved this assumption wrong. There are actually several sources of spontaneous mutation in somatic (nonsex) cells, resulting in every individual containing a multitude of genomes—a situation researchers term somatic mosaicism. “The idea is something that 10 years ago would have been science fiction,” says biochemist James Eberwine of the University of Pennsylvania. “We were taught that every cell has the same DNA, but that's not true.” There are reasons to think somatic mosaicism may be particularly important in the brain, not least because neural genes are very active. © 2017 Scientific American

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: 23565 - Posted: 05.04.2017

By Ruth Williams | When the immune system has eliminated the last traces of Zika virus from the blood, low-level infection may continue at certain sites around the body. A study published in Cell today (April 27) reveals that the cerebrospinal fluid (CSF) is one such sanctuary, which, if also true for infected humans, may have implications for long-term neurological health. “Up until now, everyone was focused on the acute [infection]—what happens when a person gets infected initially by a mosquito bite. But what this paper tells us is that maybe, two months down the line, symptoms could manifest from this later stage of virus replication in the central nervous system and other sites,” said microbiologist and immunologist Andres Pekosz of the Johns Hopkins Bloomberg School of Public Health in Baltimore who was not involved in the research. “Right now, we may be missing some of the disease associated with infection because we’re not looking far enough down the path.” Zika virus infection generally causes a short acute illness of fever, fatigue, headache and other mild symptoms, or can be entirely asymptomatic. But, in pregnant women, infection can cause grievous fetal abnormalities, including microcephaly. In rare cases, Zika can also induce Guillain-Barré syndrome and other neurological symptoms in adults. © 1986-2017 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: 23550 - Posted: 04.29.2017

By Olga Mecking When I was a new mother, the parenting books I read encouraged me to treat child-rearing like a science project. I was told to pay particular attention to my baby’s developing brain, which was malleable and awe-inspiring, but also fragile. I thought I was supposed to provide an optimal environment for my children’s brain growth, because didn’t they deserve the very best? And the earlier I started the better, because the stakes were high. If I failed, my children could develop any number of mental disorders. At least, that was my impression after having read nearly every parenting book on the market. I also expected to spontaneously and intuitively know how to care for my babies. But I didn’t have a clue, and articles like these made me feel like a failure. Was it so unnatural for a mother to want time to herself, or to not want to become one with her baby? It seemed that way, but Jan Macvarish, author of the recent book, “Neuroparenting: The Expert Invasion of Family Life,” disagrees. Macvarish is deeply concerned about this ultra-scientific approach to parenting, in part because it reduces everything to the mother-child relationship. “To talk about parenting in this way is untruthful because this isn’t the way that any child is raised,” she says. “There are always other people involved.” And she’s right. I felt that I was solely responsible for my children’s well-being, and that pressure started to get to me. What kind of mother was I if I couldn’t take care of my babies’ developing brains properly? © 1996-2017 The Washington Post

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: 23547 - Posted: 04.28.2017

Jon Hamilton Tiny, 3-D clusters of human brain cells grown in a petri dish are providing hints about the origins of disorders like autism and epilepsy. An experiment using these cell clusters — which are only about the size of the head of a pin — found that a genetic mutation associated with both autism and epilepsy kept developing cells from migrating normally from one cluster of brain cells to another, researchers report in the journal Nature. "They were sort of left behind," says Dr. Sergiu Pasca, an assistant professor of psychiatry and behavioral sciences at Stanford. And that type of delay could be enough to disrupt the precise timing required for an actual brain to develop normally, he says. The clusters — often called minibrains, organoids or spheroids — are created by transforming skin cells from a person into neural stem cells. These stem cells can then grow into structures like those found in the brain and even form networks of communicating cells. Brain organoids cannot grow beyond a few millimeters in size or perform the functions of a complete brain. But they give scientists a way to study how parts of the brain develop during pregnancy. "One can really understand both a process of normal human brain development, which we frankly don't understand very well, [and] also what goes wrong in the brain of patients affected by diseases," says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard who was not involved in the cell migration study. Arlotta is an author of a second paper in Nature about creating a wide variety of brain cells in brain organoids. © 2017 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 23545 - Posted: 04.27.2017

Laura Sanders Plasma taken from human umbilical cords can rejuvenate old mice’s brains and improve their memories, a new study suggests. The results, published online April 19 in Nature, may ultimately help scientists develop ways to stave off aging. Earlier studies have turned up youthful effects of young mice’s blood on old mice (SN: 12/27/14, p. 21). Human plasma, the new results suggest, confers similar benefits, says study coauthor Joseph Castellano, a neuroscientist at Stanford University. The study also identifies a protein that’s particularly important for the youthful effects, a detail that “adds a nice piece to the puzzle,” Castellano says. Identifying the exact components responsible for rejuvenating effects is important, says geroscientist Matt Kaeberlein of the University of Washington in Seattle. That knowledge will bring scientists closer to understanding how old tissues can be rejuvenated. And having the precise compounds in hand means that scientists might have an easier time translating therapies to people. Kaeberlein cautions that the benefits were in mice, not people. Still, he says, “there is good reason to be optimistic that some of these approaches will have similar effects on health span in people.” Like people, as mice age, brain performance begins to slip. Compared with younger generations, elderly mice perform worse on some tests of learning and memory, taking longer to remember the location of an escape route out of a maze, for instance. Researchers suspect that these deficits come from age-related trouble in the hippocampus, a brain structure important for learning and memory. |© Society for Science & the Public 2000 - 2017

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: 23517 - Posted: 04.20.2017