Links for Keyword: Autism

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By Aiyana Bailin To my dismay, Simon Baron-Cohen’s recent article “The Concept of Neurodiversity is Dividing the Autism Community” perpetuates a common misunderstanding of the neurodiversity movement: that it views autism as a difference but not a disability. Baron-Cohen presents the issue as one of opposing sides: the medical model, which sees autism as a set of symptoms and deficits to be cured or treated, and the neurodiversity model, which he believes ignores any disabling aspects of autism. Unfortunately, this confuses the neurodiversity movement with the social model of disability, and it is an incomplete understanding of the social model at that. Before I go into details, let me summarize what the neurodiversity movement does believe: Autism and other neurological variations (learning disabilities, ADHD, etc.) may be disabilities, but they are not flaws. People with neurological differences are not broken or incomplete versions of normal people. Disability, no matter how profound, does not diminish personhood. People with atypical brains are fully human, with inalienable human rights, just like everyone else. People with disabilities can live rich, meaningful lives. Neurological variations are a vital part of humanity, as much as variations in size, shape, skin color and personality. None of us has the right (or the wisdom) to try and improve upon our species by deciding which characteristics to keep and which to discard. Every person is valuable. Disability is a complicated thing. Often, it’s defined more by society’s expectations than by individual conditions. Not always, but often. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26310 - Posted: 06.07.2019

by Jessica Wright Spontaneous mutations that occur between genes are as important in autism as those within genes, a new study suggests1. The study, published today in Nature Genetics, is the first to look at the impact of these ‘noncoding’ mutations across the whole genomes of autistic people. Many teams over the past three years have sequenced the DNA of autistic people both within and between genes. Yet sorting through the hundreds of thousands of mutations between genes had seemed nearly impossible because researchers know so little about these genetic segments. The new study overcomes this challenge by using a machine-learning approach. The researchers created an algorithm that predicts whether a particular noncoding mutation alters any gene’s expression. It assigns each mutation a score based on how likely it is to do so — and to be harmful. “The unique approach here is that instead of just counting mutations, we’re using the deep-learning-based frameworks to look at their regulatory impacts,” says co-lead author Olga Troyanskaya, professor of integrative genomics at Princeton University in New Jersey. “All mutations are not created equal, and all effects are not created equal.” (Troyanskaya also holds a position at the Simons Foundation, Spectrum’s parent organization.) A strength of the study is that it looks at spontaneous mutations across the entire genome, experts say. © 2019 Simons Foundation

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26291 - Posted: 06.03.2019

By Kelly Servick Genes are a powerful driver of risk for autism, but some researchers suspect another factor is also at play: the set of bacteria that inhabits the gut. That idea has been controversial, but a new study offers support for this gut-brain link. It reveals that mice develop autismlike behaviors when they are colonized by microbes from the feces of people with autism. The result doesn’t prove that gut bacteria can cause autism. But it suggests that, at least in mice, the makeup of the gut can contribute to some hallmark features of the disorder. “It’s quite an encouraging paper,” says John Cryan, a neuroscientist at University College Cork in Ireland who was not involved in the research. The idea that metabolites—the molecules produced by bacterial digestion—can influence brain activity “is plausible, it makes sense, and it will help push the field forward.” Many studies have found differences between the composition of the gut microbiomes in people with and without autism. But those studies can’t determine whether a microbial imbalance is responsible for autism symptoms or is a result of having the condition. To test the effect of the gut microbiome on behavior, Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena, and collaborators put fecal samples from children with and without autism into the stomachs of germ-free mice, which had no microbiomes of their own. The researchers then mated pairs of mice colonized with the same microbiomes, so their offspring would be exposed to a set of human microbes early in development. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: 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: 26283 - Posted: 05.31.2019

By George Musser, Even the slightest touch can consume Kirsten Lindsmith’s attention. When someone shakes her hand or her cat snuggles up against her, for example, it becomes hard for her to think about anything else. “I’m taken out of the moment for however long the sensation lasts,” she says. Some everyday sensations, such as getting her hands wet, can feel like torture: “I usually compare it to the visceral, repulsive feeling you’d get plunging your hand into a pile of rotting garbage,” says the 27-year-old autistic writer. Stephanie Dehennin, an autistic illustrator who lives in Belgium, detests gentle touches but doesn’t mind firm hugs. “I will feel actual rage if someone strokes me or touches me very lightly,” she says. Dehennin seeks out deep pressure to relieve her stress. “I’ll sit between my bed and my nightstand, for example — squeezed between furniture.” Strong reactions to touch are remarkably widespread among people who have autism, despite the condition’s famed heterogeneity. “The touch thing is as close to universal as they come,” says Gavin Bollard, an autistic blogger who lives in Australia and writes about his and his autistic sons’ experiences. These responses are often described as a general hypersensitivity, but they are more complex than that: Sometimes autistic people crave touch; sometimes they cringe from it. For many people on the spectrum, these sensations are so intense that they take measures to shape their ‘touchscape.’ Some pile on heavy blankets at night for the extra weight; others cut off their clothing tags. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: 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: 26281 - Posted: 05.30.2019

by C.L. Lynch Everyone knows that autism is a spectrum. People bring it up all the time. “My son is on the severe end of the autism spectrum.” “We’re all a little autistic– it’s a spectrum.” “I’m not autistic but I’m definitely ‘on the spectrum.'” If only people knew what a spectrum is… because they are talking about autism all wrong. Let’s use the visible spectrum as an example. As you can see, the various parts of the spectrum are noticeably different from each other. Blue looks very different from red, but they are both on the visible light spectrum. Red is not “more blue” than blue is. Red is not “more spectrum” than blue is. When people discuss colours, they don’t talk about how “far along” the spectrum a colour is. They don’t say “my walls are on the high end of the spectrum” or “I look best in colours that are on the low end of the spectrum.” But when people talk about autism they talk as if it were a gradient, not a spectrum at all. People think you can be “a little autistic” or “extremely autistic,” the way a paint colour could be a little red or extremely red. An image of a colour gradient moving from white to red. The lightest zone is labelled How people think the spectrum looks But autism isn’t that simple. Autism isn’t a set of defined symptoms that collectively worsen as you move “up” the spectrum.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26254 - Posted: 05.21.2019

Ruth Williams Sequencing the nuclear RNA of more than 100,000 individual postmortem brain cells from people with and without autism spectrum disorder indicates the types of genes dysregulated in the condition and the types of cells in which such dysregulation occurs. The results, reported in Science today (May 16), help narrow the focus of future ASD studies to the most likely molecular and cellular anomalies, say researchers. “It’s using the latest technology, it’s looking at the single cell level, and it validates and extends previous observations,” says autism researcher Daniel Geschwind of the University of California, Los Angeles, who was not involved in the research. “It takes the previous work and brings it to a level of resolution that we didn’t have before.” “This was an experiment that needed to be done,” adds geneticist Stephan Sanders of the University of California, San Francisco, writing in an email to The Scientist. “At the tissue level, it broadly replicates previous data in autism. Then, [it] provides a first look at which cell types are responsible for the differences.” ASD, which currently affects somewhere around 1 in 60 children in the United States, includes a broad range of conditions that are characterized by an impaired ability to communicate and interact socially. The heterogeneous nature of ASD has made studies of its molecular pathology difficult. Nevertheless, gene expression studies carried out on postmortem brain tissue from ASD patients have pointed to commonly affected pathways, including synapse function, says Dmitry Velmeshev, an author of the study and postdoc in the lab of neurologist Arnold Kriegstein, also an author. © 1986–2019 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26245 - Posted: 05.18.2019

By Jessica Wright, Clinicians can reliably diagnose autism in some toddlers roughly two years earlier than the typical age of diagnosis, a new study suggests. The researchers assessed more than 1,200 toddlers for autism at least twice using standard diagnostic tools. They diagnosed roughly one in three with the condition by age 2; 84 percent of these toddlers retained the label at their last visit, which was at age 3 on average. The finding suggests clinicians should take autism traits in toddlers seriously, says co-lead researcher Karen Pierce, professor of neurosciences at the University of California, San Diego. “If children meet criteria and they do show signs and symptoms, don’t wait; let’s get them the help and the treatment that they need,” Pierce says. Experts are divided on whether autism can reliably be diagnosed before age 3. The American Academy of Pediatrics recommends screening for autism starting at 18 months. However, the U.S. Preventive Services Task Force—a government panel that makes recommendations about preventive medicine—has said there is insufficient evidence to recommend universal screening before 3. The new study suggests that early screening and diagnosis may benefit some proportion of children: It indicates that some toddlers are likely to have clear enough signs of autism to warrant a diagnosis before 2 years of age, says Zachary Warren, associate professor of pediatrics, psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. “The study shows that well-trained, expert teams evaluating young kids with autism are able to pick up concerns at fairly young ages for some kids,” says Warren, who was not involved in the work. “It’s an interesting and creative approach to understanding screening and diagnosis.” © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26243 - Posted: 05.17.2019

By Nicholette Zeliadt, Two drugs that alter the activity of the hormone vasopressin seem to improve social communication in people with autism. The findings come from two independent clinical trials published today in Science Translational Medicine. The results are encouraging, but some experts urge caution, saying the methods used to assess the drugs were not designed for that purpose. Vasopressin is related to oxytocin, a hormone thought to govern social bonding. But vasopressin’s link to autism is far from simple: There’s evidence implicating both too little and too much of the hormone in people with the condition. Advertisement The two drugs also target vasopressin in opposite ways. One of them, balovaptan, blocks a receptor for vasopressin in the brain and dampens the hormone’s activity. The other is a nasal spray containing vasopressin. Despite their opposing modes of action, both drugs appear to boost social function in autistic people; neither has serious side effects. The findings are noteworthy because no drugs are available to treat autism’s core traits, says Eric Hollander, professor of psychiatry and behavioral sciences at Albert Einstein College of Medicine in New York, who was not involved in either study. “These two studies provide important information that the vasopressin or vasopressin and oxytocin systems are important in social communication,” he says. “Different agents affecting these systems may ultimately be helpful in terms of new treatments for autism.” © 2019 Scientific American

Related chapters from BN8e: Chapter 5: Hormones and the Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 13: Memory, Learning, and Development
Link ID: 26202 - Posted: 05.03.2019

By Kelly Servick Many people with autism have trouble making eye contact, reading the emotions in other faces, and sharing affection. And no drugs are approved to treat such social impairments. Now, results from a small academic clinical trial suggest boosting levels of vasopressin—a hormone active in the brain that’s known to promote bonding in many animals—can improve social deficits in children with autism. But in a confusing twist, a larger, company-sponsored trial that took the reverse approach, tamping down vasopressin’s effects, also found some improvements in adults with autism. “I’ve never seen this before,” Kevin Pelphrey, a neuroscientist who studies autism at the University of Virginia in Charlottesville, says of the conflicting results. He and others say the vasopressin-blocking approach doesn’t have much support from previous animal research. The new study showed some benefits but failed to meet the main endpoint set out by investigators. Still, he says, both studies suggest vasopressin’s signaling in the brain plays a key role in autism and “give me a lot of renewed excitement” for treating the condition. Though vasopressin seems to stimulate social bonding in animals, the hormone’s activity in the brain isn’t fully understood, and its effects vary by species and context. Blocking its activity in the brains of some rodents prevents them from forming an attraction to a mate. But in a species of asocial hamster, injecting it into a male’s brain seems to stimulate aggression. © 2019 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26197 - Posted: 05.02.2019

By Simon Baron-Cohen At the annual meeting of the International Society for Autism Research (INSAR) in Montreal, Canada, this week, one topic likely to be widely debated is the concept of neurodiversity. It is dividing the autism community, but it doesn’t have to. The term “neurodiversity” gained popular currency in recent years but was first used by Judy Singer, an Australian social scientist, herself autistic, and first appeared in print in the Atlantic in 1998. Neurodiversity is related to the more familiar concept of biodiversity, and both are respectful ways of thinking about our planet and our communities. The notion of neurodiversity is very compatible with the civil rights plea for minorities to be accorded dignity and acceptance, and not to be pathologized. And whilst the neurodiversity movement acknowledges that parents or autistic people may choose to try different interventions for specific symptoms that may be causing suffering, it challenges the default assumption that autism itself is a disease or disorder that needs to be eradicated, prevented, treated or cured. Many autistic people—especially those who have intact language and no learning difficulties such that they can self-advocate—have adopted the neurodiversity framework, coining the term “neurotypical” to describe the majority brain and seeing autism as an example of diversity in the set of all possible diverse brains, none of which is “normal” and all of which are simply different. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26185 - Posted: 04.30.2019

Jessica Wright Sequencing can identify mutations linked to autism even before a child’s birth—especially in cases where doctors suspect problems, two new studies suggest. In the studies, scientists sequenced fetal DNA only when ultrasounds revealed atypical development of limbs or other organs, and they gave families only the results that seemed to explain those problems But there is a real risk that others might use the technique to test for mutations in any fetus—and to relay all the results to parents—without proper oversight, says Ronald Wapner, professor of obstetrics and gynecology at the Columbia Institute for Genomic Medicine, who led one of the studies. “Not everybody should be doing this; it should be in the hands of people that have expertise,” he says. Other types of analyses already detect mutations in a fetus: Some detect large DNA segments that are swapped between chromosomes, and others can pick up on missing or duplicated copies of DNA fragments. The new studies are among the first to scan for mutations across the fetal exome—essentially, the collection of genes in a genome. The field is fraught with ethical questions, including whether parents might choose to terminate a pregnancy based on the results. But the researchers note that most of the mutations they found pose serious health risks, which could be treated at birth or in utero. © 1986 - 2019 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26168 - Posted: 04.24.2019

By Perri Klass, M.D. Every pediatrician knows that it’s important to diagnose autism when a child is as young as possible, because when younger children get help and intensive therapy, their developmental outcomes improve, as measured in everything from improved language, cognition and social skills to normalized brain activity. “The signs and symptoms for most children are there between 12 and 24 months,” said Dr. Paul S. Carbone, an associate professor of pediatrics at the University of Utah and a co-author of “Autism Spectrum Disorder: What Every Parent Needs to Know,” published by the American Academy of Pediatrics. “If we can get them in for evaluation by then, the therapies are available as young as those ages, you can easily start by 2,” he said. “We’d like to give kids the benefit of getting started early.” That means taking parents seriously when they bring up concerns about what they regard as strange behaviors and interactions on the part of babies and toddlers, and it also means that we try to screen all our patients, often with a checklist for parents to complete, like the Modified Checklist for Autism in Toddlers, or M-CHAT. Children whose scores indicate a concern are then supposed to be referred on for a full developmental assessment. The Centers for Disease Control and Prevention’s website lists developmental milestones to look for; missing them may be an early sign of autism. So we all know this is important. We also know that we are not, collectively, doing a very good job of screening all children, that the questionnaires often over-identify children who don’t actually need full assessments, and that the referral process can be plagued with long waits (and when a young child has to wait months for the assessment, that works against the benefit of early diagnosis). Children in minority groups are diagnosed at an older average age than white children, and therefore get therapy later, contributing to increased disparities. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26160 - Posted: 04.22.2019

By Tiffany Hsu Amazon has removed the online listings for two books that claim to contain cures for autism, a move that follows recent efforts by several social media sites to limit the availability of anti-vaccination and other pseudoscientific material. The books, “Healing the Symptoms Known as Autism” and “Fight Autism and Win,” which had previously been listed for sale in Amazon’s marketplace, were not available on Wednesday. The company confirmed that the listings had been removed, but declined to discuss why or whether similar books would be taken down in the future. Several such books were still listed on Wednesday. In an article published this week, Wired magazine noted that Amazon is crowded with titles promoting unproven treatments for autism that include “sex, yoga, camel milk, electroconvulsive therapy and veganism.” There is no cure for autism spectrum disorder, but there are medications that can help address associated symptoms like high energy levels and depression, according to the Centers for Disease Control and Prevention. The agency has found that as many as a third of parents with an autistic child have tried treatments that most pediatricians do not recommend, and that up to 10 percent may be using potentially dangerous tactics. The books that were listed on Amazon were both written more than five years ago and have together generated more than 600 customer reviews. “Healing the Symptoms Known as Autism” recommends that autistic children drink and bathe in chlorine dioxide, a compound often referred to as “Miracle Mineral Solution.” In 2010, the Food and Drug Administration described it as “a potent bleach used for stripping textiles and industrial water treatment” that “can cause nausea, vomiting, diarrhea, and symptoms of severe dehydration.” Representative Adam Schiff, Democrat of California, wrote an open letter this month to Jeff Bezos, Amazon’s chief executive, chiding the company about the failure of its algorithms to “distinguish quality information from misinformation or misleading information.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26033 - Posted: 03.14.2019

By Frank Bruni How many studies do you have to throw at the vaccine hysterics before they quit? How much of a scientific consensus, how many unimpeachable experts and how exquisitely rational an argument must you present? That’s a trick question, of course. There’s no magic number. There’s no number, period. And that’s because the anti-vaccine crowd (or anti-vaxxers) aren’t trafficking in anything as concrete, mundane and quaint as facts. They’re not really engaged in a debate about medicine. They’re immersed in a world of conspiracies, in the dark shadows where no data can be trusted, nothing is what it seems and those who buy the party line are pitiable sheep. And, boy, are they living at the right time, when so much information and misinformation swirl by so quickly that it’s easy to confuse the two and even easier to grab hold and convince yourself of whatever it is you prefer to believe. With Google searches, you find the ostensible proof you seek. On social media, you bask in all the affirmation you could possibly want. The parents who are worried or sure about grave risks from vaccines reflect a broader horror that has flickered or flared in everything from the birther movement to “Pizzagate,” that nonsense about children as Democratic sex slaves in the imagined basement of a Washington pizza joint. Their recklessness and the attendant re-emergence of measles aren’t just a public health crisis. They’re a public sanity one, emblematic of too many people’s willful disregard of evidence, proud suspicion of expertise and estrangement from reason. Again and again, until blue in the face, medical authorities have debunked the renegade assertion that there’s a link between the M.M.R. vaccine, so named because it inoculates against measles, mumps and rubella, and autism. On Tuesday, a group of Danish researchers who looked at more than 650,000 children over 10 years announced that they had found no such association. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26025 - Posted: 03.11.2019

Rob Stein There's strong new evidence that a common childhood vaccine is safe. A large study released Monday finds no evidence that the vaccine that protects against measles, mumps and rubella increases the risk of autism. The study of children born in Denmark is one of the largest ever of the MMR vaccine. "The study strongly supports that MMR vaccination does not increase the risk for autism," the authors write in the Annals of Internal Medicine. "We believe our results offer reassurance and provide reliable data." The study's first author, epidemiologist Anders Hviid of the Staten Serum Institute in Copenhagen, added in an email: "MMR does not cause autism." In the study, researchers analyzed data collected from all children born in Denmark to Danish-born mothers between 1999 and 2010. Among the 657,461 children included in the analysis, 6,517 were diagnosed with autism over the next decade. But there was no overall increased risk for the developmental disorder among those who received the MMR vaccine when compared with those who had not gotten the vaccine, the researchers found. The researchers also found no increased risk among subgroups of children who might be unusually susceptible to autism, such as those with a brother or sister with the disorder. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26009 - Posted: 03.06.2019

By Daisy Yuhas, Spectrum Steve Slavin was 48 years old when a visit to a psychologist’s office sent him down an unexpected path. At the time, he was a father of two with a career in the music industry, composing scores for advertisements and chart toppers. But he was having a difficult year. He had fewer clients than usual, his mother had been diagnosed with cancer, and he was battling anxiety and depression, leading him to shutter his recording studio. Slavin’s anxiety—which often manifested as negative thoughts and routines characteristic of obsessive-compulsive disorder (OCD)—was nothing new. As a child, he had often felt compelled to swallow an even number of times before entering a room, or to swallow and count—one foot in the air—to four, six or eight before stepping on a paving stone. As an adult, he frequently became distressed in crowds, and he washed his hands over and over to avoid being contaminated by other people’s germs or personalities. His depression, too, was familiar—and had caused him to withdraw from friends and colleagues. This time, as Slavin’s depression and anxiety worsened, his doctor referred him to a psychologist. “I had had an appointment booked for weeks and weeks and months,” he recalls. But about 10 minutes into his first session, the psychologist suddenly changed course: Instead of continuing to ask him about his childhood or existing mental-health issues, she wanted to know whether anyone had ever talked to him about autism.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25996 - Posted: 03.01.2019

Sarah DeWeerdt An analysis of four mouse models negates certain assumptions underlying the “signaling imbalance theory,” a popular hypothesis about autism’s origins in the brain. The findings suggest that the imbalance is a compensatory response to other problems in the brain, rather than the underlying cause of autism. The signaling imbalance theory holds that the brains of autistic people have too much excitatory brain activity and not enough inhibitory signals to counteract it. This imbalance then causes neurons to fire too often, the theory goes, and contributes to motor problems, sensory hypersensitivity and other autism traits. This hypothesis, first suggested in 2003, is so popular that it is often cited as fact. The new study questions its underlying assumptions, however. The researchers did find a skewed signaling balance but not the unusually high rate of neuronal firing, or “spikes.” “It’s not as straightforward as the classic hypothesis is worded,” says study leader Dan Feldman, professor of neurobiology at the University of California, Berkeley. “The [signals] are changing in a way that stabilizes brain function rather than creates excess spikes.” Feldman’s team found this pattern in four popular models of autism: mice lacking the genes CNTNAP2 or FMR1, or missing one copy of TSC2 or a region of chromosome 16 called 16p11.2. © 1986 - 2019 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 25992 - Posted: 02.28.2019

Rachel Zamzow Patterns of brain activity in people with autism are unusually consistent over seconds—and even years, two new studies suggest. One study shows that patterns of connectivity remain stable in autistic adolescents, whereas they tend to change and specialize in controls. The other study found that connections remain fixed longer in people with autism than in controls. Both focused on so-called “functional connectivity,” the extent to which the activity of pairs of brain areas is synchronized. Together, the studies may help untangle seemingly contradictory findings on connectivity in autism: reports of both underconnectivity and overconnectivity in the brain. “Maybe the primary abnormality isn’t just that things are too weakly or strongly connected, that it has more to do with the timing of brain connections,” says Jeff Anderson, professor of radiology at the University of Utah, who led the second study. The studies also highlight the importance of measuring brain activity over varying time periods and at different ages. Researchers who home in on a single age may overlook differences that appear over time, says Mirella Dapretto, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, and lead researcher on the adolescent study. “You miss some of the bigger picture.” Studying brain activity over time provides a rare window into the development of connectivity. © 1986 - 2019 The Scientist

Related chapters from BN8e: 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: 25879 - Posted: 01.19.2019

Laura Sanders Young nerve cells derived from people with autism are precocious, growing bigger and developing sooner than cells taken from people without autism, a new study shows. The results, described January 7 in Nature Neuroscience, hint that in some cases nerve cells veer off course early in brain development to ultimately cause the disorder. As a proxy of brain growth, researchers led by Simon Schafer of the Salk Institute in La Jolla, Calif., transformed skin cells from people with and without autism into stem cells that then developed into nerve cells in the lab. Along the way, the scientists monitored the cells’ growth and the behavior of their genes. Compared with cells derived from five people without autism, cells from eight people with autism grew bigger, with longer and more elaborate branches, the researchers found. Three-dimensional balls called organoids made of the autism-derived cells were bulkier, too. In addition to this physical development, a group of genes important for brain development switched on sooner. Trouble in the autism-derived cells, however, actually began a bit earlier, just as the cells were on the cusp of becoming nerve cells. At the neural stem cell stage, certain spots of these cells’ chromatin — tightly packed genetic material — were more open and accessible than they should have been, an unfolding that can lead to abnormally active genes. The results show that open chromatin “can have major effects on neuronal development,” says neuroscientist David Amaral of the University of California, Davis. |© Society for Science & the Public 2000 - 2018.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 25856 - Posted: 01.11.2019

By Lina Zeldovich, It was 1924 when the 12-year-old boy was brought to the Moscow clinic for an evaluation. By all accounts, he was different from his peers. Other people did not interest him much, and he preferred the company of adults to that of children his own age. He never played with toys: He had taught himself to read by age 5 and spent his days reading everything he could instead. Thin and slouching, the boy moved slowly and awkwardly. He also suffered from anxiety and frequent stomachaches. At the clinic, a gifted young doctor, Grunya Efimovna Sukhareva, saw the boy. Caring and attentive, she observed him with a keen eye, noting that he was “highly intelligent” and liked to engage in philosophical discussions. By way of a diagnosis, she described him as “an introverted type, with an autistic proclivity into himself.” ‘Autistic’ was a relatively new adjective in psychiatry at the time. About a decade earlier, Swiss psychiatrist Eugen Bleuler had coined the term to describe the social withdrawal and detachment from reality often seen in children with schizophrenia. Sukhareva’s characterization came nearly two decades before Austrian doctors Leo Kanner and Hans Asperger published what have long been considered to be the first clinical accounts of autism. At first, Sukhareva used ‘autistic’ in the same way Bleuler did—but as she started to see other children with this trait, she decided to try to characterize it more fully. Over the course of the following year, she identified five more boys with what she described as “autistic tendencies.” All five also showed a preference for their own inner world, yet each had his own peculiarities or talents. One was an extraordinarily gifted violinist but struggled socially; another had an exceptional memory for numbers but could not recognize faces; yet another had imaginary friends who lived in the fireplace. None were popular with other children, she noted, and some saw peer interaction as useless: “They are too loud,” one boy said. “They hinder my thinking.” © 2018 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 25668 - Posted: 11.12.2018