Chapter 7. Life-Span Development of the Brain and Behavior

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Jon Hamilton Brain scientists are offering a new reason to control blood sugar levels: It might help lower your risk of developing Alzheimer's disease. "There's many reasons to get [blood sugar] under control," says David Holtzman, chairman of neurology at Washington University in St. Louis. "But this is certainly one." Holtzman moderated a panel Sunday at the Society for Neuroscience meeting in Chicago that featured new research exploring the links between Alzheimer's and diabetes. "The risk for dementia is elevated about twofold in people who have diabetes or metabolic syndrome (a group of risk factors that often precedes diabetes)," Holtzman says. "But what's not been clear is, what's the connection?" One possibility involves the way the brain metabolizes sugar, says Liqin Zhao, an associate professor in the school of pharmacy at the University of Kansas. Zhao wanted to know why people whose bodies produce a protein called ApoE2 are less likely to get Alzheimer's. Previous research has shown that these people are less likely to develop the sticky plaques in the brain associated with the disease. But Zhao looked at how ApoE2 affects glycolysis, a part of the process that allows brain cells to turn sugar into energy. So she gave ApoE2 to mice that develop a form of Alzheimer's. And sure enough, Zhao says, the substance not only improved energy production in brain cells but made the cells healthier overall. "All of this together increased the brain's resilience against Alzheimer's disease," she says. © 2019 npr

Keyword: Alzheimers; Obesity
Link ID: 26728 - Posted: 10.22.2019

By Austin Frakt To ward off age-related cognitive decline, you may be tempted to turn to brain training apps. Last year, consumers spent nearly $2 billion on them, some of which claim to improve cognitive skills. Evidence suggests you’d be better off spending more time exercising and less time staring at your phone. This year the World Health Organization released evidence-based guidelines on reducing risks of cognitive decline and dementia. Although it pointed to some systematic reviews that reported positive cognitive effects of brain training, the W.H.O. judged the studies to be of low quality. Among the studies’ limitations is that they measure only short-term effects and in areas targeted by the training. There is no long-term evidence of general improvement in cognitive performance. Instead of mind games, moving your body is among the most helpful things you can do. At least 150 minutes of moderate physical activity per week, including strength training, yields not just physical benefits but cognitive ones as well. But to be most effective, you need to do it before cognitive decline starts, according to the W.H.O. Some evidence to support this recommendation comes from short-term studies. Several randomized studies of tai chi for older adults found it yielded cognitive benefits. Likewise, randomized studies of aerobic exercise for older adults found short-term improvements in cognitive performance. A systematic review published this year in PLOS One examined 36 randomized studies of exercise programs that were as short as four weeks and as long as a year. It found cognitive benefits of activities such as bicycling, walking, jogging, swimming and weight training. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26727 - Posted: 10.21.2019

by Emily Anthes The Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, launched by the U.S. National Institutes of Health (NIH) in 2013, has a lofty goal: to unravel the cellular basis of cognition and behavior. Since the initiative’s launch, the NIH has doled out about $1 billion to researchers who are developing tools and technologies to map, measure and observe the brain’s neural circuits. Along the way, the agency has also tried to explore the ethical implications of this research. Khara Ramos, who directs the neuroethics program at the NIH’s National Institute of Neurological Disorders and Stroke, described the emerging field of neuroethics today at the 2019 Society for Neuroscience annual meeting in Chicago, Illinois. Spectrum: Was discussion about ethics part of the BRAIN Initiative from the beginning? Khara Ramos: We knew that we needed to do something with neuroethics, but it took time for us to figure out what exactly, in part because neuroethics is a relatively new field. Bioethics is a broad field that covers all aspects of biomedicine, but there isn’t specialization of bioethics in kidney research or pulmonary research the way there is in neuroscience research, and that’s really because the brain is so intimately connected with who we are. Neuroscience research raises these unique ethical questions, such as: How might new neurotechnologies alter fundamental notions of agency or autonomy or identity? We’re starting to focus on data sharing and privacy from a philosophical, conceptual perspective: Is there something unique about brain data that is different from, for instance, genetic data? How do researchers themselves feel about data sharing and privacy? And how does the public view it? For instance, is my social security number more or less sensitive than the kinds of neural data that somebody might be able to get if I were participating in a clinical trial? © 2019 Simons Foundation

Keyword: Autism; Attention
Link ID: 26725 - Posted: 10.21.2019

By Nicholas Bakalar Your personality in high school may help predict your risk of dementia decades later. Researchers reached this conclusion using a 150-item personality inventory given to a national sample of teenagers in 1960. The survey assessed character traits — sociability, calmness, empathy, maturity, conscientiousness, self-confidence and others — using scores ranging from low to high. For their study, in JAMA Psychiatry, scientists linked the scores of 82,232 of the test-takers to Medicare data on diagnoses of dementia from 2011 to 2013. They found that high extroversion, an energetic disposition, calmness and maturity were associated with a lower risk of dementia an average of 54 years later, though the association did not hold for students with low socioeconomic status. Calmness and maturity have been linked to lower levels of stress, which may help explain the association. Lower socioeconomic status, which often increases chronic stress, may negate the apparent benefits of those personality traits. “The study was not set up to discern a causal link,” said the lead author, Benjamin P. Chapman, an associate professor of psychiatry at the University of Rochester. “Most likely these traits lead to all kinds of other things over 50 years that culminate in a diagnosis of dementia. We tried to rule out as many other factors as possible, but our findings are suggestive, and we don’t want to draw strong conclusions about causation.” © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26716 - Posted: 10.18.2019

By Laura Sanders Brainlike blobs made from chimpanzee cells mature faster than those grown from human cells. That finding, described October 16 in Nature along with other clues to human brain development, is one of the latest insights from studies of cerebral organoids — three-dimensional clumps of cells that can mimic aspects of early brain growth (SN: 2/20/18). The new study “draws interesting parallels, but also highlights important differences” in the way that the brains of humans and chimpanzees develop, says Paola Arlotta, a neurobiologist at Harvard University who was not involved in the study. While “it’s still early days in the organoid world,” the results represent an important step toward understanding the particulars of the human brain, she says. To make cerebral organoids from chimpanzees, researchers use cells in blood left over from veterinarians’ routine blood draws. In the vials were white blood cells that could be reprogrammed into stem cells, which themselves were then coaxed into blobs of brain cells. “From that, we get something that really looks a lot like the early brain,” says Gray Camp, a stem cell biologist at the Institute of Molecular and Clinical Ophthalmology Basel in Switzerland. There were no obvious differences in appearance between the chimpanzee organoids and the human organoids, Camp says. But a close look at how genes behaved in the two organoids — and how that behavior changed over time — turned up a big difference in pacing. Chimpanzee organoids seemed to grow up faster than their human counterparts. © Society for Science & the Public 2000–2019

Keyword: Development of the Brain; Evolution
Link ID: 26713 - Posted: 10.17.2019

National Institutes of Health scientists have developed an ultrasensitive new test to detect abnormal forms of the protein tau associated with uncommon types of neurodegenerative diseases called tauopathies. As they describe in Acta Neuropathologica, this advance gives them hope of using cerebrospinal fluid, or CSF—an accessible patient sample—to diagnose these and perhaps other, more common neurological diseases, such as Alzheimer’s disease. Scientists have linked the abnormal deposition of tau in the brain to at least 25 different neurodegenerative diseases. However, to accurately diagnose these diseases, brain tissue often must be analyzed after the patient has died. For their study, the researchers used the same test concept they developed when using post-mortem brain tissue samples to detect the abnormal tau types associated with Pick disease, Alzheimer’s disease and chronic traumatic encephalopathy (CTE). They adapted the test to use CSF for the detection of abnormal tau of progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and other less common tauopathies. They detected abnormal tau in CSF from both living and deceased patients. In one case, the test led to a corrected diagnosis in a patient who had died from CBD, but who was initially diagnosed with PSP. The new test is called 4R RT-QuIC—which stands for 4-repeat tau protein amplified in a real-time, quaking-induced conversion process.

Keyword: Alzheimers
Link ID: 26711 - Posted: 10.17.2019

Diana Kwon There are approximately 5.6 million people over the age of 65 living with Alzheimer’s disease in the United States. With the population aging, that number is projected to grow to 7.1 million by 2025. Researchers know that age, a family history of the disease, and carrying a genetic variant known as APOE4 are all associated with a higher chance of developing the condition. But the biological mechanisms leading to Alzheimer’s are still largely a mystery. Over the last decade, scientists have amassed evidence for a hypothesis that, prior to developing full-blown Alzheimer’s disease, patients experience a period of hyperactivity and hyperconnectivity in the brain. Several functional magnetic resonance imaging studies have reported that people with mild cognitive impairment (MCI), a condition that often precedes Alzheimer’s, appear to have higher brain activity levels than their age-matched counterparts. Researchers have also found signs of such changes in healthy people carrying the APOE4 allele, as well as in presymptomatic stages of Alzheimer’s in rodent models of the disease. Krishna Singh, a physicist and imaging neuroscientist at the Cardiff University Brain Research Imaging Center (CUBRIC) in the UK, and his colleagues wanted to investigate this theory further. Previous studies of brain activity in young APOE4 carriers were mostly conducted using small sample sizes, according to Singh. But by the mid-2010s, his team had access to neuroimaging data from close to 200 participants studied at CUBRIC as part of an effort to build a massive dataset of healthy brains. So the researchers decided to use the data to search for signs of unusual brain activity and connectivity in people with the APOE4 allele. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26709 - Posted: 10.16.2019

Sandra G. Boodman The July day wasn’t too steamy — a rarity in Madison, Ala. — and her toddler’s physical therapy session wasn’t scheduled for another hour, so Jeannette Vega thought she’d take 26-month-old Tiana outside to play in their yard. Immediately, she was struck by her younger daughter’s difficulty climbing up the sturdy low-slung plastic slide, something Tiana had been able to do with ease only a week earlier. To distract her, Jeannette opened the door of the family’s truck. “Come on, let’s get in and buckle up,” she remembers saying. Tiana took particular delight in clambering into her car seat and fastening her seat belt. Not this time. The little girl seemed rooted to the ground, impervious to her mother's encouragement. "It wasn't that she wouldn't [comply]," Jeannette recalled of the 2015 incident. "I could tell she just couldn't." Later that afternoon, she mentioned Tiana's difficulties to the physical therapist who had been working with the little girl for more than a year to try to overcome her significant, unexplained developmental delays. “This isn’t normal, to regress after so many months of therapy,” Jeannette, now 37, remembers the therapist telling her. She mentioned a disorder Jeannette had never heard of and suggested it might be the cause. Jeannette did a quick search, dismissed the possibility and said she “forgot about it.” But the first anguished words she blurted out nearly a half-year later on that shattering day in the specialist’s office when she learned what was wrong, was that the therapist had been right.

Keyword: Autism
Link ID: 26697 - Posted: 10.14.2019

Jef Akst In the past few years, a number of high-profile studies have linked parental age at birth, and paternal age in particular, with a child’s autism risk. Walid Yassin, a neuropsychiatric researcher at the University of Tokyo, wanted to know if having older parents correlated with characteristics of the brain that have been linked to autism. When Yassin and his colleagues examined the brain scans of 39 adult males with high-functioning autism spectrum disorder (ASD) and of 37 typically developing males, they found that paternal age correlated with characteristics of the white matter in regions of the brain responsible for social interactions in analyses of all 76 individuals. Specifically, in the men with older fathers, these areas had higher radial diffusivity, a measure of water diffusing toward the axonal membrane instead of along the axon, suggesting damage to nerve cells’ myelin sheaths, says Yassin. “And such difference in radial diffusivity has been previously reported in ASD.” Magdalena Janecka, an epidemiologist who specializes in autism at the Icahn School of Medicine at Mount Sinai in New York, applauds the study’s focus on the brain. “We have a lot of epidemiological associations . . . but what [underlies them] is still very much underexplored,” she says. “The authors did a great job at exploring the mechanism that could connect the two.” But Janecka adds that the results can’t distinguish whether the link between age and autism is due to an accumulation of mutations in the sperm of older men, or if men who choose to have children later in life are enriched for certain traits associated with autism. “Is the effect we’re observing due to age or is it due to some underlying propensity of men who delay fatherhood?” she asks. © 1986–2019 The Scientist.

Keyword: Autism; Epigenetics
Link ID: 26690 - Posted: 10.11.2019

Jessica Wright Delicate lines dance across a screen mounted on the wall of the operating room. Their peaks and valleys become pronounced, suddenly flatten into a straight line—and then return, stronger than before. These digital traces represent the buzz of neurons in 12-year-old Kevin Lightner, read by two thin electrodes that surgeons have inserted deep into his brain. Kevin, who has autism and has had seizures since he was 8 years old, lies uncharacteristically still in the center of the room, draped under a blue sheet, his tiger-print pajamas neatly folded on a nearby shelf. What’s happening in this room may be the last chance to bring Kevin’s seizures under control. An hour and a half ago, neurosurgeon Saadi Ghatan removed a roughly 2-inch by 1-inch piece of the top of Kevin’s skull. He replaced it with a rectangular metal device, carefully screwed into the newly exposed edges of bone. The implant, a “responsive neurostimulation device,” is now transmitting signals from the electrodes planted in Kevin’s thalamus. The surgeons’ hope is that the device will learn to recognize what kind of brain activity precedes Kevin’s seizures and discharge electrical pulses to prevent them—like a “defibrillator for the brain,” as Ghatan puts it. If it works, it could save Kevin’s life. Ghatan projects the device’s readout to the screen by gently placing a black wand over the exposed metal in Kevin’s skull. The signal on the screen is surprisingly strong, given that it stems from the thalamus, a brain region that reveals its activity only weakly, if at all—and so is rarely the choice for monitoring seizures. © 1986–2019 The Scientist.

Keyword: Autism; Epilepsy
Link ID: 26687 - Posted: 10.10.2019

Ashley Yeager In March 2018, researchers reported evidence suggesting that adult humans do not generate new neurons in the hippocampus—the brain’s epicenter of learning and memory. The result contradicted two decades of work that said human adults actually do grow new neurons there, and revealed a need for new and better tools to study neurogenesis, Salk Institute President Fred Gage, who generated foundational evidence for adult human neurogenesis, told The Scientist at the time. Since that study was published, several other teams have used similar techniques—but have come to different conclusions, publishing evidence that adult humans do indeed grow new hippocampal neurons, even at the age of 99. Despite the equivocal results, Maura Boldrini, a neuroscientist at Columbia University, and a number of other neuroscientists tell The Scientist they think neurogenesis does occur in the adult human brain, bolstering learning and memory and possibly also our stress and emotional responses. Neurogenesis is “fundamentally important for the brain to react to all sorts of different insults and prevent neurological and psychiatric problems,” Boldrini says. Because of its role in brain function, researchers want to learn how neurogenesis works to potentially use it to treat brain trauma, neurodegeneration, psychiatric disorders, such as depression, and possibly even the ill effects of aging. The growth of new neurons is well studied in newborn and adult animals, especially rodents. There’s prolific neurogenesis as the brain develops, which then drops off and plateaus in adulthood, only occurring in particular areas of the brain. Examinations of human postmortem tissue suggest that the process is similar in people, based on antibody markers that label neural progenitors and young neurons. But those signals can be hard to detect in preserved cells, and the gap in time between the death of a donor and when her tissue is fixed and analyzed can affect the reliability of the markers, scientists say, which might explain the disparities in findings between different studies. © 1986–2019 The Scientist

Keyword: Neurogenesis
Link ID: 26685 - Posted: 10.09.2019

Allison Aubrey The condition strikes young children. It can start with run-of-the-mill virus symptoms, like fever or sniffles. But, then the kids lose control of their limbs, may have trouble swallowing or breathing, or even end up paralyzed. This terrifying experience happened to more than 570 families since 2014, whose children were struck with an illness called acute flaccid myelitis, or AFM. "It was really scary," says Susan Coyne, the mother of a son, Evan Mazanec, who developed AFM back in 2014 when he was 7 years old. "When this first started, no one really knew what it was," she says. It came on quickly, starting with a fever and an ear infection. Coyne says the limb weakness and paralysis began several days later — just as Evan was getting over the fever. He lost control of his arms and legs. "He couldn't move them, he couldn't lift them, he couldn't walk," Coyne says. He spent a year and a half in intensive rehab. He had to learn to walk and move his arms again. "It set him back years," Coyne says. Scientists have struggled to understand what causes this rare childhood disease. Now, one theory is gaining ground. A paper published Monday in the journal Pediatrics finds the condition may be triggered by a virus. The disease follows a pattern: Scientists have documented outbreaks every other year, beginning in 2014, and again in 2016 and 2018. Last year, there were 233 cases in the U.S. It strikes young kids, average age of 6. And, it can lead to long-term paralysis. © 2019 npr

Keyword: Movement Disorders; Development of the Brain
Link ID: 26684 - Posted: 10.09.2019

Angela Saini How should we remember historical figures who we know have done terrible things? It’s a dilemma we face more often, as universities and public institutions critically examine their histories, reassessing the past with 21st-century eyes. And over the last year, University College London has been in the midst of a historical inquiry into its role as the institutional birthplace of eugenics – the debunked “science” that claimed that by selectively breeding humans we could improve racial quality. We tend to associate eugenics with Nazi Germany and the Holocaust, but it was in fact developed in London. Its founder was Francis Galton, who established a laboratory at UCL in 1904. Already, some students and staff have called on the university to rename its Galton lecture theatre. Galton’s seductive promise was of a bold new world filled only with beautiful, intelligent, productive people. The scientists in its thrall claimed this could be achieved by controlling reproduction, policing borders to prevent certain types of immigrants, and locking away “undesirables”, including disabled people. University College London is investigating its role as the birthplace of eugenics. In hindsight, it’s easy to say that only a moral abyss could have given rise to such a pseudo-scientific plan, not least because we have borne witness to its horrifying consequences through the 20th century, when it was used to justify genocide and mass sterilisations. And by the standards of today, Galton does resemble a monster. He was a brilliant statistician but also a racist (not just my assessment, but that of Veronica van Heyningen, the current president of the Galton Institute). He was obsessed with human difference, and determined to remove from British society those he considered inferior. © 2019 Guardian News & Media Limited

Keyword: Genes & Behavior; Intelligence
Link ID: 26683 - Posted: 10.09.2019

By Nicholas Bakalar During pregnancy, sleeping on your back may be a bad idea. Previous studies have found that sleeping in a supine position causes compression of veins and arteries that can lead to a reduction in blood flow to the placenta severe enough to double the risk for stillbirth after 28 weeks of gestation. Now a new study, in JAMA Network Open, concludes that supine sleeping is also associated with low birth weight in full-term babies. Of 1,760 pregnant women in the analysis, 57 went to sleep lying on their backs. (The initial sleep position is the one maintained for the longest time during the night.) After controlling for age, body mass index, previous pregnancies, hypertension, diabetes and other factors, they found that compared with those sleeping in other positions, women who slept on their backs had babies who were three times as likely to be in the lowest 10th percentile for birth weight. “It’s a small number of pregnant women who go to sleep on their backs — only about 3 percent,” said the lead author, Dr. Ngaire H. Anderson, a senior lecturer in obstetrics and gynecology at the University of Auckland. “But we are keen to encourage the message that sleeping on one’s side is a way to optimize the baby’s health, both in reducing stillbirth and optimizing the baby’s growth.” © 2019 The New York Times Company

Keyword: Sleep; Development of the Brain
Link ID: 26677 - Posted: 10.08.2019

Ariana Eunjung Cha After Danielle Rizzo’s first son and then her second were diagnosed with autism, she has struggled with the how and why. She wondered whether she could have prevented the condition in her second child by putting him on a gluten-free and casein-free diet. Did she have her children, born 14 months apart, too close together? She even held off on vaccinating her younger son before he, too, was diagnosed not long after the first. (The supposed link between vaccines and autism has been debunked by extensive research. The American Academy of Pediatrics; National Academies of Sciences, Engineering and Medicine; Centers for Disease Control and Prevention; and other medical groups have compiled some of the many scientific papers.) Rizzo came to suspect a genetic link involving the sperm donor for both children, after finding several other children conceived with the same donor’s sperm who have also been diagnosed with autism or related developmental challenges. A geneticist with expertise in autism identified possible autism-risk genes carried by the children. Her story, in a report published by The Washington Post on Sept. 14, prompted an outpouring of comments and questions — legal, scientific and ethical — about her case. While there is no central database of donors and their children in the United States, some sperm banks try to mitigate risks of donors passing on genetic conditions by testing them for up to 400 common heritable conditions. However, genetic testing is not required and is by no means comprehensive, as evident by the case studies reported in medical journals regularly.

Keyword: Autism; Genes & Behavior
Link ID: 26671 - Posted: 10.04.2019

By Jonathan Lambert Your dog’s ability to learn new tricks may be less a product of your extensive training than their underlying genetics. Among 101 dog breeds, scientists found that certain behavioral traits such as trainability or aggression were more likely to be shared by genetically similar breeds. While past studies have looked into the genetic underpinnings of dog behaviors for certain breeds, this research — published October 1 in the Proceedings of the Royal Society B — is the first to investigate a wide swath of breed diversity and find a strong genetic signal. “Anecdotally, everyone knows that different dogs have different behavioral traits,” says Noah Snyder-Mackler, a geneticist at the University of Washington in Seattle. “But we didn’t know how much or why.” Humans and dogs have lived together for at least 15,000 years (SN: 7/6/17). But only within the last 300 years or so have breeders produced varieties such as Chihuahuas and Great Danes. So, Snyder-Mackler and his colleagues considered how 101 dog breeds behave while searching for genetic similarities among breeds sharing certain personality traits. Data came from two dog genotype databases and from C-BARQ, a survey that asks owners to rank their pure-bred dog’s propensity for certain behaviors, like chasing or aggressiveness toward strangers. As a result, the study didn’t have genetic and behavioral data from the same canine individuals, which could help highlight rare genetic variants that may be nonetheless important to diversity in behaviors. © Society for Science & the Public 2000–2019

Keyword: Aggression; Genes & Behavior
Link ID: 26667 - Posted: 10.03.2019

Catherine Offord When Lilian Calderón-Garcidueñas discovered abundant hallmarks of Alzheimer’s disease in a batch of human brain samples a few years ago, she initially wasn’t sure what to make of it. The University of Montana neuropathologist had been studying the brains as part of her research on environmental effects on neural development, and this particular set of samples came from autopsy examinations carried out on people who had died suddenly in Mexico City, where she used to work as a researcher and physician. Although Calderón-Garcidueñas had collected much of the tissue herself while attending the autopsies in Mexico, the light-microscope slides she was analyzing had been prepared by her colleagues, so she was in the dark about what patient each sample came from. By the end of the project, she’d identified accumulations of the Alzheimer’s disease–associated proteins amyloid-ß and hyperphosphorylated tau in almost all of the 203 brains she studied. “When I started opening envelopes to see who [each sample] belonged to . . . I was devastated,” she says. The people whose brains she’d been studying were not only adults, but teens and even children. The youngest was 11 months old. “My first thought was, ‘What am I going to do with this? What am I going to tell people?’” she says. “I was not expecting such a devastating, extreme pathology.” Despite her shock, Calderón-Garcidueñas had a reason to be on the lookout for signs of a disease usually associated with the elderly in these samples. For the last three decades, she’d been studying the health effects of Mexico City’s notoriously polluted air—a blight that earned the capital the dubious distinction of most polluted megacity on the planet from the United Nations in 1992. During that time, she’s discovered many links between exposure to air pollution and signs of neural damage in animals and humans. Although her findings are observational, and the pathology of proteins such as amyloid-ß is not fully understood, Calderón-Garcidueñas argues that air pollution is the most likely culprit behind the development of the abnormalities she saw in her postmortem samples—plus many other detrimental changes to the brains of Mexico City’s residents. © 1986–2019 The Scientist

Keyword: Neurotoxins; Alzheimers
Link ID: 26665 - Posted: 10.02.2019

Saba Salman As a graduate in the 1980s, Simon Baron‑Cohen taught autistic children at a special school in London. Little was known about autism then, and people often misheard him, assuming he taught “artistic children”. “People would be ashamed if they had an autistic child, or ashamed of saying, ‘I am autistic’, whereas now it’s treated as more ordinary and there’s less judgment,” he says. “In the 1980s, autism was seen as categorical, so ‘you either have it or you don’t’ … nowadays, we talk about a spectrum.” Today, Baron-Cohen, 61, is a world expert on autism, a Cambridge professor and director of the university’s influential Autism Research Centre. There is also greater awareness of autism, a lifelong condition affecting how people interact or process information. Estimates suggest one in every 100 people is on the autism spectrum (700,000 adults and children), from those with severe developmental disabilities needing intense support, to those with milder traits. Well-known autistic people include campaigner Greta Thunberg (who calls her “difference” a superpower). As a cognitive neuroscientist, Baron-Cohen has helped focus attention, from his pioneering psychological studies (autism was first diagnosed in the 1960s in the UK) to founding the UK’s first diagnosis clinic in Cambridge 20 years ago with charitable funding (today the centre is NHS-run). Yet his latest research reflects how improved awareness and understanding of autism have not led to improvements in the lives of people with autism. In the studyexploring how autistic adults experience disproportionately more “negative life events”, 45% of the 426 participants say they often lack money to meet basic needs (compared with 25% of non-autistic people) and 20% have been sexually abused by a partner (compared with 9%). The research, involving questionnaires created with autistic people, suggests why those with autism may experience more depression. © 2019 Guardian News & Media Limited

Keyword: Autism
Link ID: 26664 - Posted: 10.02.2019

By Gretchen Reynolds Physically fit young adults have healthier white matter in their brains and better thinking skills than young people who are out of shape, according to a large-scale new study of the links between aerobic fitness and brain health. The findings suggest that even when people are youthful and presumably at the peak of their mental prowess, fitness — or the lack of it — may influence how well their brains and minds work. We already have plenty of tantalizing evidence that aerobic fitness can beneficently shape our brains and cognition. In animal experiments, mice and rats that run on wheels or treadmills produce far more new neurons in their brains than sedentary animals and perform better on tests of rodent intelligence and memory. Similarly, studies involving people show strong relationships between being physically active or fit and having greater brain volume and stronger thinking abilities than people with low fitness or who rarely exercise. But most of these past studies focused on middle-aged or older adults, whose brains often are starting to sputter and contract with age. For them, fitness and exercise are believed to help slow any decline, keeping brain tissue and function relatively youthful. Much less has been known about whether fitness likewise might be related to the structure and function of healthy, younger people’s brains. So, for the new study, which was published last month in Scientific Reports, scientists at the University of Münster in Germany decided to look inside the skulls of a large group of young adults. They began by turning to a hefty trove of data gathered as part of the Human Connectome Project, an international collaborative effort that aims to help map much of the human brain and tease out how it works. © 2019 The New York Times Company

Keyword: Development of the Brain
Link ID: 26662 - Posted: 10.02.2019

Patti Neighmond Many American teenagers try to put in a full day of school, homework, after-school activities, sports and college prep on too little sleep. As evidence grows that chronic sleep deprivation puts teens at risk for physical and mental health problems, there is increasing pressure on school districts around the country to consider a later start time. In Seattle, school and city officials recently made the shift. Beginning with the 2016-2017 school year, the district moved the official start times for middle and high schools nearly an hour later, from 7:50 a.m. to 8:45 a.m. This was no easy feat; it meant rescheduling extracurricular activities and bus routes. But the bottom line goal was met: Teenagers used the extra time to sleep in. Researchers at the University of Washington studied the high school students both before and after the start-time change. Their findings appear in a study published Wednesday in the journal Science Advances. They found students got 34 minutes more sleep on average with the later school start time. This boosted their total nightly sleep from 6 hours and 50 minutes to 7 hours and 24 minutes. "This study shows a significant improvement in the sleep duration of students, all by delaying school start times so they're more in line with the natural wake-up times of adolescents," says senior author Horacio de la Iglesia, a University of Washington researcher and professor of biology. The study also found an improvement in grades and a reduction in tardiness and absences.

Keyword: Biological Rhythms; Development of the Brain
Link ID: 26660 - Posted: 10.01.2019