Chapter 7. Life-Span Development of the Brain and Behavior
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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
By NICHOLAS BAKALAR A new study links diet soft drinks to an increased risk for stroke and dementia. Researchers studied more than 4,000 people over 45 who had filled out food-frequency questionnaires and had periodic health examinations between 1991 and 2001. The scientists tracked their health over the next 10 years and found 97 cases of stroke and 81 cases of dementia. The study, in the journal Stroke, found that compared with those who did not drink diet soda, people who drank one to six artificially sweetened drinks a week had twice the risk of stroke. There were similar, although weaker, associations for dementia risk. The reasons for the link remain unknown. The study adjusted for age, sex, education, physical activity, diabetes, smoking and many other characteristics that might affect the risks. But the senior author, Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine, said that there were additional variables the study could not address. For example, she said, people might have switched to diet soda because they already had cardiovascular problems. Still, she added, there are health benefits associated with some drinks, like tea or coffee, “but not with soda of any kind, either diet or not.” © 2017 The New York Times Company
By Debra W. Soh The reasons behind why people are gay, straight, or bisexual have long been a source of public fascination. Indeed, research on the topic of sexual orientation offers a powerful window into understanding human sexuality. The Archives of Sexual Behavior recently published a special edition devoted to research in this area, titled “The Puzzle of Sexual Orientation.” One study, conducted by scientists at the University of Lethbridge in Alberta, Canada, offers compelling, cross-cultural evidence that common genetic factors underlie same-sex, sexual preference in men. In southern Mexico, individuals who are biologically male and sexually attracted to men are known as muxes. They are recognized as a third gender: Muxe nguiiu tend to be masculine in their appearance and behavior, while muxe gunaa are feminine. In Western cultures, they would be considered gay men and transgender women, respectively. Several correlates of male androphilia — biological males who are sexually attracted to men — have been shown across different cultures, which is suggestive of a common biological foundation among them. For example, the fraternal birth order effect—the phenomenon whereby male androphilia is predicted by having a higher number of biological older brothers—is evident in both Western and Samoan cultures. Interestingly, in Western society, homosexual men, compared with heterosexual men, tend to recall higher levels of separation anxiety — the distress resulting from being separated from major attachment figures, like one’s primary caregiver or close family members. Research in Samoa has similarly demonstrated that third-gender fa’afafine—individuals who are feminine in appearance, biologically male, and attracted to men—also recall greater childhood separation anxiety when compared with heterosexual Samoan men. Thus, if a similar pattern regarding separation anxiety were to be found in a third, disparate culture—in the case, the Istmo region of Oaxaca, Mexico—it would add to the evidence that male androphilia has biological underpinnings. © 2017 Scientific American
By NICHOLAS BAKALAR Drinking sugary beverages is associated with markers of accelerated aging and early signs of Alzheimer’s disease, a new study reports. Researchers used data on more than 4,000 people over 30, examining their brains with M.R.I. and measuring memory with psychological tests. All completed well-validated food frequency questionnaires. Sugary beverage intake is an indirect measure of how much sugar we get in our diets, which is difficult to measure precisely. The authors defined “sugary beverage” to include sodas as well as fruit juices, which may contain added sugars. The study, in Alzheimer’s & Dementia, found that on average, the more sugary drinks consumed, the lower the total brain volume and the lower the scores on memory tests. Brain shrinkage is tied to an increased risk of Alzheimer’s disease. Compared with those who drank no sugary drinks, those who drank one or two a day had a reduced brain volume equivalent to 1.6 years of normal aging, and lower memory scores equivalent to 5.8 years of aging. Those who drank more than two had decreased brain volume equivalent to two years of normal aging and lower memory scores by the equivalent of 11 years. The researchers controlled for diabetes, blood pressure, cholesterol, smoking and many other health and behavioral characteristics. “Although we can’t prove cause and effect, these data suggest that we should be cautious about drinking sugary beverages,” said the lead author, Matthew P. Pase, a senior research fellow at Boston University. “They’re empty calories that contribute to weight gain and metabolic disease.” © 2017 The New York Times Company
Doing moderate exercise several times a week is the best way to keep the mind sharp if you're over 50, research suggests. Thinking and memory skills were most improved when people exercised the heart and muscles on a regular basis, a review of 39 studies found. This remained true in those who already showed signs of cognitive decline. Taking up exercise at any age was worthwhile for the mind and body, the Australian researchers said. Exercises such as T'ai Chi were recommended for people over the age of 50 who couldn't manage other more challenging forms of exercise, the study in the British Journal of Sports Medicine said. Physical activity has long been known to reduce the risk of a number of diseases, including type-2 diabetes and some cancers, and it is thought to play a role in warding off the brain's natural decline as we enter middle age. The theory is that through exercise the brain receives a greater supply of blood, oxygen and nutrients that boost its health as well as a growth hormone that helps the formation of new neurons and connections. In this analysis of previous studies, researchers from the University of Canberra looked at the effects of at least four weeks of structured physical exercise on the brain function of adults. In a variety of brain tests, they found evidence of aerobic exercise improving cognitive abilities, such as thinking, reading, learning and reasoning, while muscle training - for example, using weights - had a significant effect on memory and the brain's ability to plan and organise, the so-called executive functions. Joe Northey, study author and researcher from the Research Institute for Sport and Exercise at Canberra, said the findings were convincing enough to enable both types of exercise to be prescribed to improve brain health in the over-50s. © 2017 BBC.
Link ID: 23532 - Posted: 04.25.2017
By Lauren Gravitz, Connor was diagnosed with autism early — when he was just 18 months old. His condition was already obvious by then. “He was lining things up, switching lights on and off, on and off,” says his mother, Melissa. He was bright, but he didn’t speak much until age 3, and he was easily frustrated. Once he started school, he couldn’t sit still in class, called out answers without raising his hand and got visibly upset when he couldn’t master a math concept or a handwriting task quickly enough. “One time, he rolled himself up into the carpet like a burrito and wouldn’t come out until I got there,” Melissa recalls. (All families in this story are identified by first name only, to protect their privacy.) Connor was prescribed his first psychiatric drug, methylphenidate (Ritalin), at age 6. That didn’t last long, but when he was 7, his parents tried again. A psychiatrist suggested a low dose of amphetamine and dextroamphetamine (Adderall), a stimulant commonly used to treat attention deficit hyperactivity disorder (ADHD). The drug seemed to improve his time at school: He was able to sit still for longer periods of time and focus on what his teachers were saying. His chicken-scratch handwriting became legible. Then, it became neat. Then perfect. And then it became something Connor began to obsess over. “We were told that these are the gives and takes; if it’s helping him enough to get through school, you have to decide if it’s worth it,” Melissa says. It was worth it — for a while. © 2017 Scientific American
Link ID: 23531 - Posted: 04.25.2017
By Clare Wilson Could fasting boost your brainpower? A stomach hormone that stimulates appetite seems to promote the growth of new brain cells and protect them from the effects of ageing – and may explain why some people say that fasting makes them feel mentally sharper. When ghrelin was first discovered, it became known as the hunger hormone. It is made by the stomach when it gets empty, and whenever we go a few hours without food its levels rise in our blood. But there is also evidence that ghrelin can enhance cognition. Animals that have reduced-calorie diets have better mental abilities, and ghrelin might be part of the reason why. Injecting the hormone into mice improves their performance in learning and memory tests, and seems to boost the number of neuron connections in their brains. Now Jeffrey Davies at Swansea University, UK, and his team have found further evidence that ghrelin can stimulate brain cells to divide and multiply, a process called neurogenesis. When they added the hormone to mouse brain cells grown in a dish, it switched on a gene known to trigger neurogenesis, called fibroblast growth factor. If the same effect happens in animals, this could be how ghrelin exerts its effects on memory, says Davies, whose work was presented at the British Neuroscience Association conference this month. © Copyright Reed Business Information Ltd.
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
Keyword: Development of the Brain
Link ID: 23517 - Posted: 04.20.2017
Tara García Mathewson You saw the pictures in science class—a profile view of the human brain, sectioned by function. The piece at the very front, right behind where a forehead would be if the brain were actually in someone’s head, is the pre-frontal cortex. It handles problem-solving, goal-setting, and task execution. And it works with the limbic system, which is connected and sits closer to the center of the brain. The limbic system processes emotions and triggers emotional responses, in part because of its storage of long-term memory. When a person lives in poverty, a growing body of research suggests the limbic system is constantly sending fear and stress messages to the prefrontal cortex, which overloads its ability to solve problems, set goals, and complete tasks in the most efficient ways. This happens to everyone at some point, regardless of social class. The overload can be prompted by any number of things, including an overly stressful day at work or a family emergency. People in poverty, however, have the added burden of ever-present stress. They are constantly struggling to make ends meet and often bracing themselves against class bias that adds extra strain or even trauma to their daily lives. And the science is clear—when brain capacity is used up on these worries and fears, there simply isn’t as much bandwidth for other things. Economic Mobility Pathways, or EMPath, has built its whole service-delivery model around this science, which it described in its 2014 report, “Using Brain Science to Design New Pathways Out of Poverty.” The Boston nonprofit started out as Crittenton Women’s Union, a merger of two of the city’s oldest women-serving organizations, both of which focused on improving the economic self-sufficiency of families. It continues that work with a new name and a burgeoning focus on intergenerational mobility. © 2017 by The Atlantic Monthly Group.
By James Gallagher Health and science reporter, Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia. In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world. But the compound used was unsuitable for people, as it caused organ damage. Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people. "It's really exciting," said Prof Giovanna Mallucci, from the MRC Toxicology Unit in Leicester. She wants to start human clinical trials on dementia patients soon and expects to know whether the drugs work within two to three years. Why might they work? The novel approach is focused on the natural defence mechanisms built into brain cells. When a virus hijacks a brain cell it leads to a build-up of viral proteins. Cells respond by shutting down nearly all protein production in order to halt the virus's spread. Many neurodegenerative diseases involve the production of faulty proteins that activate the same defences, but with more severe consequences. The brain cells shut down production for so long that they eventually starve themselves to death. This process, repeated in neurons throughout the brain, can destroy movement, memory or even kill, depending on the disease. It is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases. In the initial study, the researchers used a compound that prevented the defence mechanism kicking in. © 2017 BBC.
Link ID: 23512 - Posted: 04.20.2017
By Grace Rubenstein, North Dakota’s sparse geography has long made it a natural frontier: Pioneers here pushed the boundaries of westward expansion, then agriculture, and recently domestic oil drilling. Now the state finds itself on the leading edge of a new boom that it never would have chosen: Alzheimer’s disease. Cases are rocketing up across the United States, and especially in North Dakota, which has the country’s second highest death rate from the disease. While Alzheimer’s is the sixth leading cause of death nationally, it already ranks third here. “Everybody knows somebody” affected by the disease, said Kendra Binger, a program manager with the Alzheimer’s Association of Minnesota and North Dakota. As public awareness rises along with the numbers of cases, “it’s hard to ignore anymore.” This makes the state an ideal laboratory to glimpse at the future of Alzheimer’s in America, and to identify strategies that could help the rest of the country cope. The devastating disease has strained families and the state budget. So North Dakota — a place that prides itself on personal independence and financial parsimony — has found new ways to support its residents and a new consensus to spend money on prevention. The state’s primary strategy is to assist family caregivers — the estimated 30,000 North Dakota spouses, siblings, sons, and daughters looking after loved ones with dementia. A half-dozen consultants roam the state to evaluate families’ needs, train caregivers, connect them to services, and offer advice. Studies show the program has helped families keep their loved ones out of nursing homes and save the state money. © 2017 Scientific American,
Link ID: 23508 - Posted: 04.19.2017
By TIM REQUARTH SAN FRANCISCO — On a cloudy afternoon in the Bayview district, Shaquille, 21, was riding in his sister’s 1991 Acura when another car ran a stop sign, narrowly missing them. Both cars screeched to a halt, and Shaquille and the other driver got out. “I just wanted to talk,” he recalls. But the talk became an argument, and the argument ended when Shaquille sent the other driver to the pavement with a left hook. Later that day, he was arrested and charged with felony assault. He already had a misdemeanor assault conviction — for a fight in a laundromat when he was 19. This time he might land in prison. Instead, Shaquille — who spoke on condition that his full name not be used, lest his record jeopardize his chances of finding a job — wound up in San Francisco’s Young Adult Court, which offered him an alternative. For about a year, he would go to the court weekly to check in with Judge Bruce E. Chan. Court administrators would coordinate employment, housing and education support for him. He would attend weekly therapy sessions and life-skills classes. In return, he would avoid trial and, on successful completion of the program, the felony charge would be reduced to a misdemeanor. This was important, because a felony record would make it nearly impossible for him to get a job. “These are transitional-age youth,” said Carole McKindley-Alvarez, who oversees case management for the court. “They’re supposed to make some kind of screwed-up choices. We all did. That’s how you learn.” © 2017 The New York Times Company
Keyword: Development of the Brain
Link ID: 23502 - Posted: 04.18.2017
By Jia Naqvi The rate of stroke among young people has apparently been rising steadily since 1995, according to a study published this week. Hospitalization rates for stroke increased for women between the ages of 18 and 44, and nearly doubled for men in that age range from 1995 through 2012. Using more-detailed data for 2003 through 2012, the researchers found that rates of hospitalizations for acute ischemic stroke increased by nearly 42 percent for men 35 to 44, while rates for women of the same age group increased by 30 percent over the same time, the study published in the JAMA, the Journal of the American Medical Association. Across all adults, including those in older age ranges, stroke was the fifth leading cause of death in 2013. Overall mortality rates from strokes have significantly decreased over the past 50 years due to multiple factors, including better treatment for hypertension and increased use of aspirin, even as incidence of acute ischemic stroke among young adults has been on the rise. The study also looked at stroke risk factors and whether there were any changes in their prevalence from 2003 to 2012. The likelihood of having three or more of five common risk factors — diabetes, hypertension, lipid disorders, obesity and tobacco use — doubled in men and women hospitalized for acute ischemic strokes. © 1996-2017 The Washington Post=
Tina Hesman Saey Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs. Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs. Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck. Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature. Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional. |© Society for Science & the Public 2000 - 2017.
Laura Sanders Soon after systems biologist Juergen Hahn published a paper describing a way to predict whether a child has autism from a blood sample, the notes from parents began arriving. “I have a bunch of parents writing me now who want to test their kids,” says Hahn, of Rensselaer Polytechnic Institute in Troy, N.Y. “I can’t do that.” That’s because despite their promise, his group’s results, reported March 16 in PLOS Computational Biology, are preliminary — nowhere close to a debut in a clinical setting. The test will need to be confirmed and repeated in different children before it can be used to help diagnose autism. Still, the work of Hahn and colleagues, along with other recent papers, illustrates how the hunt for a concrete biological signature of autism, a biomarker, is gaining speed. Currently, pediatricians, child psychologists and therapists rely on behavioral observations and questionnaires, measures with limitations. Barring genetic tests for a handful of rare mutations, there are no blood draws, brain scans or other biological tests that can reveal whether a child has — or will get — autism. Objective tests would be incredibly useful, helping provide an early diagnosis that could lead to therapy in the first year of life, when the brain is the most malleable. A reliable biomarker might also help distinguish various types of autism, divisions that could reveal who would benefit from certain therapies. And some biomarkers may reveal a deeper understanding of how the brain normally develops. |© Society for Science & the Public 2000 - 2017
By Jef Akst | Previous research has shown that high doses of broad-spectrum antibiotics can affect the behavior of adult animals, and numerous epidemiological studies have begun to link early-life antibiotic use to diverse ailments in humans. A study published last week (April 4) in Nature Communications adds to this growing literature, demonstrating that even low, clinically relevant doses of the classic narrow-spectrum antibiotic penicillin can trigger changes in the gut microbiome, in the blood-brain barrier and brain chemistry, and in the behaviors of mice exposed at a young age. Treating the mice with Lactobacillus rhamnosus bacteria, however, helped protect the mice against the effects of early-life, low-dose penicillin exposure. “There are almost no babies in North America that haven’t received a course of antibiotics in their first year of life,” McMaster University coauthor John Bienenstock, who is also the director of the Brain-Body Institute at St. Joseph’s Healthcare Hamilton, said in a press release. “In this paper, we report that low-dose penicillin taken late in pregnancy and in early life of mice offspring, changes behavior and the balance of microbes in the gut. While these studies have been performed in mice, they point to popular increasing concerns about the long-term effects of antibiotics. Furthermore, our results suggest that a probiotic might be effective in preventing the detrimental effects of the penicillin.” Bienenstock and colleagues gave pregnant female mice low doses of penicillin during their last week of gestation, and continued to treat their pups until they weaned a few weeks after birth. At six weeks old, mice exposed to the antibiotic were less social, slightly less anxious, and more aggressive than unexposed mice, the team reported. In the animals’ brains, the researchers found evidence of a thinned blood-brain barrier, as well as increased production of cytokines and heightened activity of a gene that has been linked to aggressive behavior. © 1986-2017 The Scientist
Nicola Davis Sitting in a padded car seat, a small black and white bullseye stuck to his cheek, four-month-old Teo Bosten-Lam gazes at a computer. The screen is a mottled grey, like the snow on a old-fashioned television, but in the top right-hand corner is a deep blue circle. Teo has spotted it. He glances at the circle and, as he does so, it morphs into a smiley face and a triumphant jingle fills the darkened room. Buoyed by the reaction, he looks around. Suddenly a black and white spinning disc appears on the screen, issuing a sound that can only be described as “boing”. “Babies can’t resist the black and white swirl things,” says researcher Alice Skelton. “When they look away we play it and it brings them back to the screen.” A PhD student in the baby lab at the University of Sussex, Skelton is attempting to unpick a conundrum that has fascinated parents and scientists alike: when it comes to colour, exactly what can babies can see? It’s a mission that takes technology: Teo’s ability to pick up on colour is being probed with an eye-tracking system. The sticker on his cheek directs the camera to his face, while his corneal reflections and the position of his pupils are automatically detected. “What we are looking to see is, do you have to have a more saturated blue for a baby to see it than you would for a red, for example,” says Skelton. If Teo can see a colour, the novelty will attract his attention, triggering the smiley face and jingle. And this isn’t the only ingenious idea. At the first sound that indicates our participant is becoming fed up with this science lark, the screen flashes to a clip from the 1980s cartoon Dogtanian. Teo, once again, is transfixed.
Ed Yong 12:00 PM ET Science Octopuses have three hearts, parrot-like beaks, venomous bites, and eight semi-autonomous arms that can taste the world. They squirt ink, contort through the tiniest of spaces, and melt into the world by changing both color and texture. They are incredibly intelligent, capable of wielding tools, solving problems, and sabotaging equipment. As Sy Montgomery once wrote, “no sci-fi alien is so startlingly strange” as an octopus. But their disarming otherness doesn’t end with their bodies. Their genes are also really weird. A team of scientists led by Joshua Rosenthal at the Marine Biological Laboratory and Eli Eisenberg at Tel Aviv University have shown that octopuses and their relatives—the cephalopods—practice a type of genetic alteration called RNA editing that’s very rare in the rest of the animal kingdom. They use it to fine-tune the information encoded by their genes without altering the genes themselves. And they do so extensively, to a far greater degree than any other animal group. “They presented this work at a recent conference, and it was a big surprise to everyone,” says Kazuka Nishikura from the Wistar Institute. “I study RNA editing in mice and humans, where it’s very restricted. The situation is very different here. I wonder if it has to do with their extremely developed brains.” It certainly seems that way. Rosenthal and Eisenberg found that RNA editing is especially rife in the neurons of cephalopods. They use it to re-code genes that are important for their nervous systems—the genes that, as Rosenthal says, “make a nerve cell a nerve cell.” And only the intelligent coleoid cephalopods—octopuses, squid, and cuttlefish—do so. The relatively dumber nautiluses do not. “Humans don’t have this. Monkeys don’t. Nothing has this except the coleoids,” says Rosenthal.
By JENNIFER MALIA In “Meet Julia,” an episode of “Sesame Street” that will air April 10 on PBS and HBO, Elmo and Abby Cadabby introduce Big Bird to Julia, a new muppet character with autism. Big Bird says, “Hi, Julia, I’m Big Bird. Nice to meet you.” But Julia continues painting without making eye contact or responding to Big Bird. On “60 Minutes,” Big Bird tells Lesley Stahl, who was on the set when “Sesame Street” was filming the new Muppet’s debut, that he thought Julia didn’t like him at first. Elmo then explains, “Julia has autism so sometimes it takes her a little longer to do things.” I can relate. When my daughter started preschool, she would run laps around the perimeter of the fenced-in playground without responding to kids who said “hi” as she passed by. One day, she stopped in her tracks to pick up a jacket that had fallen to the ground, handed it to a girl without saying a word, and continued running. The kids on the playground probably assumed she didn’t like them — just as Big Bird did. Within the past year, my daughter, who is now 3, my 2-year-old son and I were all given diagnoses of autism spectrum disorder because of our repetitive behaviors, obsessive interests, sensory issues and difficulty with social interactions and pragmatic communication skills. My kids are on the mild to moderate part of the spectrum, having language, but not intellectual, impairments. (I also have a 4-year-old daughter who does not have a diagnosis.) Julia gives me hope that my children and their peers will grow up in a world where autism is normalized, rather than stigmatized. Preschoolers are the primary audience for “Sesame Street,” an educational television program where young children watching Julia’s interactions with her peers can learn by example to support autism acceptance. Since one in 68 American children have an autism diagnosis, wider understanding of the condition is valuable for them as well as for their peers. © 2017 The New York Times Company
Link ID: 23462 - Posted: 04.07.2017
By Tracy Vence Last year, 5 percent of the babies born to nearly 1,000 mothers in the U.S. who showed signs of Zika virus infection during their pregnancies had birth defects, the US Centers for Disease Control and Prevention (CDC) reported this week (April 3). Among babies born to the 250 US mothers with confirmed Zika infection during their pregnancies, just shy of 10 percent had birth defects. The agency’s latest analysis is based on data from the US Zika Pregnancy Registry, which does not include information from Puerto Rico (where CDC has a separate database). During a press briefing, CDC Acting Director Anne Schuchat told reporters that researchers and clinicians have observed a variety of brain-related birth defects in babies with congenital Zika infection, beyond microcephaly. “Some seemingly healthy babies . . . may have developmental problems that become evident months after birth,” she said. “Although we’re still learning about the full range of birth defects that can occur when a women is infected with Zika during pregnancy, we’ve seen that it can cause brain abnormalities, vision problems, hearing problems, and other consequences of brain damage that might require lifelong specialized care.” Schuchat described cases of congenital Zika infection in which babies experienced seizures, reduced motor control, feeding difficulties, missed developmental milestones (like sitting up), or inconsolable crying. “These circumstances are just heartbreaking,” she said. © 1986-2017 The Scientist
Keyword: Development of the Brain
Link ID: 23461 - Posted: 04.07.2017