Links for Keyword: Autism

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Most of the genetic risk for autism comes from versions of genes that are common in the population rather than from rare variants or spontaneous glitches, researchers funded by the National Institutes of Health have found. Heritability also outweighed other risk factors in this largest study of its kind to date. About 52 percent of the risk for autism was traced to common and rare inherited variation, with spontaneous mutations contributing a modest 2.6 percent of the total risk. “Genetic variation likely accounts for roughly 60 percent of the liability for autism, with common variants comprising the bulk of its genetic architecture,” explained Joseph Buxbaum, Ph.D., of the Icahn School of Medicine at Mount Sinai (ISMMS), New York City. “Although each exerts just a tiny effect individually, these common variations in the genetic code add up to substantial impact, taken together.” Buxbaum, and colleagues of the Population-Based Autism Genetics and Environment Study (PAGES) Consortium, report on their findings in a unique Swedish sample in the journal Nature Genetics, July 20, 2014. “Thanks to the boost in statistical power that comes with ample sample size, autism geneticists can now detect common as well as rare genetic variation associated with risk,” said Thomas R. Insel, M.D., director of the NIH’s National Institute of Mental Health (NIMH). “Knowing the nature of the genetic risk will reveal clues to the molecular roots of the disorder. Common variation may be more important than we thought.”

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19863 - Posted: 07.22.2014

|By Nidhi Subbaraman and SFARI.org A team at Duke University in Durham, North Carolina, is set to launch a $40 million clinical trial to explore stem cells from umbilical cord blood as a treatment for autism. But experts caution that the trial is premature. A $15 million grant from the Marcus Foundation, a philanthropic funding organization based in Atlanta, will bankroll the first two years of the five-year trial, which also plans to test stem cell therapy for stroke and cerebral palsy. The autism arm of the trial aims to enroll 390 children and adults. Joanne Kurtzberg, the trial’s lead investigator, has extensive experience studying the effectiveness of cord blood transplants for treating various disorders, such as leukemia and sickle cell anemia. Most recently, she showed that cord blood transplants can improve the odds of survival for babies deprived of oxygen at birth. A randomized trial of the approach for this condition is underway. “To really sort out if [stem] cells can treat these children, we need to do randomized, controlled trials that are well designed and well controlled, and that’s what we intend to do,” says Kurtzberg, professor of pediatrics and pathology at Duke. “We firmly believe we should be moving ahead in the clinic.” Early animal studies have shown that stem cells isolated from umbilical cord blood can stimulate cells in the spinal cord to regrow their myelin layers, and in doing so help restore connections with surrounding cells. Autism is thought to result from impaired connectivity in the brain. Because of this, some groups of children with the disorder may benefit from a stem cell transplant, Kurtzberg says. © 2014 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19840 - Posted: 07.16.2014

|By Jessica Wright and SFARI.org CHD8, a gene that regulates the structure of DNA, is the closest thing so far to an ‘autism gene,’ suggests a study published today in Cell. People with mutations in this gene all have the same cluster of symptoms, including a large head, constipation and characteristic facial features; nearly all also have have autism. Autism is notoriously heterogeneous, perhaps involving mutations in any of hundreds of genes. Typically, researchers begin by studying people with similar symptoms and working backward to identify what causes those symptoms. But that approach has not been particularly productive. “We’ve tried for so long to identify subtypes of autism based on behavior alone and we’ve done abysmally at that,” says lead researcher Raphael Bernier, associate professor of psychiatry at the University of Washington in Seattle. The reverse approach — that is, beginning with people who all have mutations in the same gene and characterizing their symptoms — may prove to be more useful for simplifying autism’s complexity. For example, identifying subtypes of autism may help researchers develop drugs tailored to that particular cause, says Evan Eichler, professor of genome sciences at the University of Washington, who spearheaded the genetics side of the study. “I think the most important realization is that not all autisms are created equal,” he says. © 2014 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19795 - Posted: 07.04.2014

By Gary Stix Tony Zador: The human brain has 100 billion neurons, a mouse brain has maybe 100 million. What we’d really like to understand is how we go from a bunch of neurons to thought, feelings, behavior. We think that the key is to understand how the different neurons are connected to one another. So traditionally there have been a lot of techniques for studying connectivity but at a fairly crude level. We can, for instance, tell that a bunch of neurons here tend to be connected to a bunch of neurons there. There are also techniques for looking at how single neurons are connected but only for individual links between those neurons. What we would love to be able to do is to tell how every single neuron in the brain is connected to every single other neuron in the brain. So if you wanted to navigate through the United States, one of the most useful things you could have is a roadmap. It wouldn’t tell you everything about the United States, but it would be very hard to get around without a complete roadmap of the country. We need something like that for the brain. Zador: Traditionally the way people study connectivity is as a branch of microscopy. Typically what people do is they use one method or another to label a neuron and then they observe that neuron at some level of resolution. But the challenge that’s at the core of all the microscopy techniques is that neurons can extend long distances. That might be millimeters in a mouse brain or, in fact, in a giraffe brain, there are neurons that go all the way from the brain to its foot, which can be over 15 feet. Brain cells are connected with one another at structures called synapses, which are below the resolution of light microscopy. That means that if you really want to understand how one neuron is connected to another, you need to resolve the synapse, which requires electron microscopy. You have to take incredibly thin sections of brain and then image them. © 2014 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 19769 - Posted: 06.25.2014

|By Lindsey Konkel and Environmental Health News Babies whose moms lived within a mile of crops treated with widely used pesticides were more likely to develop autism, according to new research. The study of 970 children, born in farm-rich areas of Northern California, is part of the largest project to date that is exploring links between autism and environmental exposures. The University of California, Davis research – which used women’s addresses to determine their proximity to insecticide-treated fields – is the third project to link prenatal pesticide exposures to autism and related disorders. “The weight of evidence is beginning to suggest that mothers’ exposures during pregnancy may play a role in the development of autism spectrum disorders,” said Kim Harley, an environmental health researcher at the University of California, Berkeley who was not involved in the new study. One in every 68 U.S. children has been identified with an autism spectrum disorder—a group of neurodevelopmental disorders characterized by difficulties with social interactions, according to the Centers for Disease Control and Prevention. “This study does not show that pesticides are likely to cause autism, though it suggests that exposure to farming chemicals during pregnancy is probably not a good thing,” said Dr. Bennett Leventhal, a child psychiatrist at University of California, San Francisco who studies autistic children. He did not participate in the new study. The biggest known contributor to autism risk is having a family member with it. Siblings of a child with autism are 35 times more likely to develop it than those without an autistic brother or sister, according to the National Institutes of Health. © 2014 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19764 - Posted: 06.24.2014

By Elizabeth Norton A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood. That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. "Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn't seem to be there before, if only for a short time during a fever or other stress" says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders. Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child. As a specialist in the cell's life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay "higher up" in the cell's metabolism. © 2014 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19749 - Posted: 06.19.2014

Ian Sample, science correspondent Research on children in Denmark has found that boys with autism were more likely to have been exposed to higher levels of hormones in their mother's wombs than those who developed normally. Boys diagnosed with autism and related disorders had, on average, raised levels of testosterone, cortisol and other hormones in the womb, according to analyses of amniotic fluid that was stored after their mothers had medical tests during pregnancy. The findings add to a growing body of evidence that the biological foundations of autism are laid down well before birth and involve factors that go beyond the child's genetic make-up. The results may help scientists to unravel some of the underlying causes of autism and explain why boys are four to five times more likely to be diagnosed with the condition, which affects around one percent of the population. Amniotic fluid surrounds babies in the womb and contains hormones and other substances that they have passed through their urine. The liquid is collected for testing when some women have an amniocentesis around four months into their pregnancy. Scientists in Cambridge and Copenhagen drew on Danish medical records and biobank material to find amniotic fluid samples from 128 boys who were later diagnosed with autism. Compared to a control group, the boys with autism and related conditions had higher levels of four "sex steroid" hormones that form a biological production line in the body that starts with progesterone and ends with testosterone. "In the womb, boys produce about twice as much testosterone as girls, but compared with typical boys, the autism group has even higher levels. It's a significant difference and may have a large effect on brain development," said Simon Baron-Cohen, director of the Autism Research Centre at Cambridge University. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 19687 - Posted: 06.03.2014

By By Tanya Lewis, It's not every day you see a mouse with a mohawk. But that's what researchers saw while studying mice that had a genetic mutation linked to autism. The mohawks that the mice were sporting actually resulted from their "over-grooming" behavior, repeatedly licking each other's hair in the same direction. The behavior resembles the repetitive motions displayed by some people with autism, and the researchers say their experiments reveal a link between the genetic causes of autism and their effects on the brain, suggesting potential avenues for treating the disorder. "Our study tells us that to design better tools for treating a disease like autism, you have to get to the underlying genetic roots of its dysfunctional behaviors, whether it is over-grooming in mice or repetitive motor behaviors in humans," study researcher Gordon Fishell, a neuroscientist at NYU Langone Medical Center, said in a statement. Autism is a spectrum of developmental disorders that involve social impairments and communication deficits. People with autism may also engage in repetitive behaviors, such as rocking or hand flapping. In the study, detailed today (May 25) in the journal Nature, the researchers bred mice that lacked a gene for a protein called Cntnap4, which is found in brain cells called interneurons. Having low levels of this protein leads to the abnormal release of two brain-signaling molecules, known as dopamine and GABA. Dopamine is involved in sensations of pleasure; GABA (which stands for gamma-aminobutyric acid) dampens neural activity and regulates muscle tone. Mice that lacked the gene for this critical brain protein were found to obsessively groom their fellow animals' fur into mohawk-like styles, suggesting a link between genetics, brain function and autistic behaviors.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19661 - Posted: 05.26.2014

By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 19607 - Posted: 05.13.2014

Autism was formally described for the first time 71 years ago. The medical notes for "Case one", a 10-year-old from Mississippi, US, referred to as Donald T, describe a perplexing condition that was different from "anything reported so far". In 1943, when Donald Triplett was diagnosed, autism was considered extremely rare and treatment consisted of institutionalisation and – all too often – isolation. Today we know "autism disorder" as one of a number of autism spectrum disorders alongside Asperger's syndrome, pervasive developmental disorder and single gene disorders such as Rett syndrome. But of all neuropsychiatric conditions, autism remains one of the least understood. We now know that genetics almost certainly plays a key role, with researchers finding that if a family has one child with autism, then the likelihood of a future child having the condition is as high as 25%. But to what extent autism is defined by genes remains a mystery. "Everyone recognises that genes are part of the story but autism isn't 100% genetic," says Professor Simon Baron-Cohen of the Autism Research Centre at the University of Cambridge. "Even if you have identical twins who share all their genes, you can find that one has autism and one doesn't. That means that there must be some non-genetic factors." One of the most controversial theories about how autism develops is neuroinflammation. MRI scans of autistic patients have revealed abnormalities in the white matter – the wiring tissue responsible for connecting brains areas. Some scientists have drawn comparisons with multiple sclerosis, in which inflammatory processes attack the myelin sheath around the axons of brain cells, slowing down signalling and making it less efficient. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19573 - Posted: 05.05.2014

by Simon Makin Could drama workshops help children with autism-spectrum disorders? Results from a pilot study called Imagining Autism suggests this might be the case. The research involved 22 children aged between 7 and 12 and consisted of one 45-minute session every week for 10 weeks. During this time, groups of four children entered an enclosed themed environment, such as a forest or outer space. These environments were designed to engage all senses simultaneously, using lights, sounds, puppetry and interactive digital elements. Trained performers used improvisation techniques to encourage the children to engage creatively with the environment and each other, both physically and verbally. The hope was that the sessions would help develop the children's communication, social interaction, and imagination skills – the "triad of impairments" seen in autism. Children were assessed before the intervention, and again between two and six weeks after the sessions ended. As well as looking at whether behaviours used to diagnose autism changed after the drama sessions, the researchers also assessed emotion recognition, imitation, IQ and theory of mind – the ability to infer what others are thinking and feeling. Subjective ratings were also gathered from parents and teachers and follow-up assessments were conducted up to a year later. At the early assessments, all children showed some improvement. The most significant change was in the number of facial expressions recognised, a key communication skill. Nine children improved on this. Six children improved on their level of social interaction. The majority of these changes were also seen at the follow-up assessments. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19494 - Posted: 04.16.2014

Simon Baron-Cohen, professor of developmental psychopathology at the University of Cambridge and director of the Autism Research Center, replies: Your mother is correct that the scientific evidence points to the brain of people with autism and Asperger's syndrome as being different but not necessarily “disordered.” Studies have shown that the brain in autism develops differently, in terms of both structure and function, compared with more typical patterns of development, and that certain parts of the brain are larger or smaller in people who have autism compared with those who have a more typical brain. One structural difference resides in the brain's corpus callosum, which connects the right and left hemispheres. Most studies show that the corpus callosum is smaller in certain sections in people with autism, which can limit connectivity among brain regions and help explain why people with autism have difficulty integrating complex ideas. An example of a functional difference is in the activity of the ventromedial prefrontal cortex, which is typically active in tasks involving theory of mind—the ability to imagine other people's thoughts and feelings—but is underactive when people with autism perform such tasks. The brain of those with autism also shows advantages. When some people with this condition are asked to complete detail-oriented tasks, such as finding a target shape in a design, they are quicker and more accurate. Additionally, those with autism generally exhibit less activity in the posterior parietal cortex, involved in visual and spatial perception, which suggests that their brain is performing the task more efficiently. © 2014 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 19489 - Posted: 04.15.2014

By Dominic Basulto The latest numbers from the Center for Disease Control showing a steep rise in the number of children with autism are so off the charts that it’s hard not to come to one of two conclusions: There’s something wrong in the way that we measure the data or there’s something extraordinary going on. 1 in 68 American children now has autism, up from 1 in 88 children just two years ago, an increase of 30 percent. A decade ago, one in 166 children were diagnosed as having autism. In 1975, it was 1 in 5000. Plot this as a graph using CDC data and you get a hockey stick curve showing exponential growth in autism over just the past decade. If you accept the first conclusion – that we’re simply not measuring autism correctly – there’s actually a fair amount of evidence to suggest that as much as 53 percent of the variation in data can be explained away by factors such as better diagnosis, better detection and better awareness. And it’s true that the very definition of “autism” continues to change to include a much wider description of symptoms along a spectrum, so it’s only natural to expect an increase in the number of cases if we’re making it easier to define people as having autism. There’s even a growing consensus in the scientific community that the current numbers are “no cause for alarm” and may actually underestimate the incidence of autism in the population, due to problems in collecting information in more rural areas and among some demographic groups. That still leaves approximately 50 percent of the rise in autism cases to explain through science. It won’t be easy. There may be as many as 60 different disorders that are associated with autism, and a multitude of factors at work, with most of them thought to be linked to changes in our environment or genetic factors resulting from increasing parental age. As a result, even the Chief Science Officer at Autism Speaks concedes that what causes autism remains a mystery. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19474 - Posted: 04.12.2014

By BENEDICT CAREY Therapists who specialize in autism often use a child’s own interests, toys or obsessions as a way to connect, and sometimes to reward effort and progress on social skills. The more eye contact a child makes, for example, the more play time he or she gets with those precious maps or stuffed animals. But now a group of scientists and the author of a new book are suggesting that those favorite activities could be harnessed in a deeper, more organic way. If a child is fascinated with animated characters like Thomas the Tank Engine, why not use those characters to prompt and reinforce social development? Millions of parents do this routinely, if not systematically, flopping down on the floor with a socially distant child to playact the characters themselves. “We individualize therapy to each child already, so if the child has an affinity for certain animated characters, it’s absolutely worth studying a therapy that incorporates those characters meaningfully,” said Kevin Pelphrey, director of the child neuroscience laboratory at Yale. He and several other researchers, including John D. E. Gabrieli of M.I.T., Simon Baron-Cohen of the University of Cambridge and Pamela Ventola of Yale, are proposing a study to test the approach. The idea came from Ron Suskind, a former Wall Street Journal reporter whose new book “Life, Animated” describes his family’s experience reaching their autistic son, Owen, through his fascination with Disney movies like “The Little Mermaid” and “Beauty and the Beast.” It was Mr. Suskind’s story that first referred to ‘“affinity therapy.” He approached the researchers to put together a clinical trial based on the idea that some children can develop social and emotional instincts through the characters they love. Experts familiar with his story say the theory behind the therapy is plausible, given what’s known from years of studying the effects of other approaches. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19459 - Posted: 04.08.2014

By SAM WANG A STUDY published last week found that the brains of autistic children show abnormalities that are likely to have arisen before birth, which is consistent with a large body of previous evidence. Yet most media coverage focuses on vaccines, which do not cause autism and are given after birth. How can we help people separate real risks from false rumors? Over the last few years, we’ve seen an explosion of studies linking autism to a wide variety of genetic and environmental factors. Putting these studies in perspective is an enormous challenge. In a database search of more than 34,000 scientific publications mentioning autism since its first description in 1943, over half have come since 2008. As a statistically minded neuroscientist, I suggest a different approach that relies on a concept we are familiar with: relative odds. As a single common measuring stick to compare odds, I have chosen the “risk ratio,” a measure that allows the bigger picture to come into focus. For a variety of studies I asked the same question: How large is the increased risk for autism? My standard for comparison was the likelihood in the general population of autism spectrum disorder. Here’s an example. Start from the fact that the recorded rate of autism is now 1 in 68, according to a report released last week by the Centers for Disease Control and Prevention. If babies born in purple farmhouses have a rate of autism of 2 in 68, this doubling means that the purple farmhouse carries a risk ratio of 2. However, correlation is not causation, and there is no need to repaint that farmhouse just yet. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19429 - Posted: 03.31.2014

by Laura Sanders Ever-increasing numbers of autism diagnoses have parents worried about a skyrocketing epidemic, and this week’s news may only drive alarm higher. Perhaps it shouldn’t. In 2010, 1 in 68 (or 14.7 per 1,000) 8-year-olds had an autism spectrum disorder, the Centers for Disease Control and Prevention now estimates. That number is a substantial increase from 2008, which had an estimate of 1 in 88 (or 11.3 per 1,000). But the numbers might not reflect a spike in actual cases. Instead, the rise might be driven, at least in part, by an increase in diagnoses. The estimates are drawn from a collection of organizations that provide services to children with autism, including doctors, schools and social service agencies. As awareness builds and more people look for signs of autism, these numbers will keep going up. Regional spottiness suggests that better autism detection is feeding the increase. The autism rate in Alabama is just one in 175, while the rate in New Jersey is one in 45, the CDC reports. It would be surprising, and scientifically really important, if children in Alabama were truly much more protected from the disorder. Instead, differences in diagnosis rates are probably at play. If these alarmingly high numbers are driven by professionals and parents better spotting autism, that’s nothing to be alarmed at. On the contrary: This is good news. The earlier therapies begin, the better kids with autism do. That’s the idea behind CDC’s “Learn the Signs: Act Early” program to educate people about signs that something might be amiss with a child. So our best move is to find the kids who need help, and find them when they’re young. Most kids, including the ones in the new CDC survey, aren’t diagnosed with autism until about age 4 1/2. But whatever goes wrong happens long before then. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19424 - Posted: 03.29.2014

By Greg Miller Nobody knows what causes autism, a condition that varies so widely in severity that some people on the spectrum achieve enviable fame and success while others require lifelong assistance due to severe problems with communication, cognition, and behavior. Scientists have found countless clues, but so far they don’t quite add up. The genetics is complicated. The neuroscience is conflicted. Now, a new study adds an intriguing, unexpected, and sure-to-be controversial finding to the mix: It suggests the brains of children with autism contain small patches where the normally ordered arrangement of neurons in the cerebral cortex is disrupted. “We’ve found locations where there appears to be a failure of normal development,” said Eric Courchesne, a neuroscientist at the University of California, San Diego and an author of the study, which appears today in the New England Journal of Medicine. “It’s been really difficult to identify a lesion or anything in the brain that’s specific and diagnostic of autism,” said Thomas Insel, director of the National Institute of Mental Health, one of several agencies that funded the project. The new study is notable because it applies sophisticated molecular labeling methods to postmortem tissue from people with autism who died as children, which is incredibly hard to come by, Insel says. “If it’s real, if it’s replicated and it’s a consistent finding, it’s more evidence that autism starts prenatally and only manifests itself when kids start to have trouble with language or social behavior around age two or three,” Insel said. “These kinds of changes in cellular architecture would happen during brain development, probably around the first part of the second trimester.” © 2014 Condé Nast

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19416 - Posted: 03.27.2014

By Jennifer Richler A few days ago, an old friend sent me a panicked email. She had just finished reading Ron Suskind’s beautiful essay in the New York Times Magazine about raising a son with autism: “Reaching My Autistic Son Through Disney.” Suskind describes how, at almost 3 years of age, his son Owen “disappeared.” The child was once “engaged, chatty, full of typical speech,” but then he stopped talking, lost eye contact, even struggled to use a sippy cup. Owen was eventually diagnosed with a regressive form of autism, which Suskind says affects about a third of children with the disorder. “Unlike the kids born with it,” he continues, “this group seems typical until somewhere between 18 and 36 months—then they vanish.” That was the line that alarmed my friend, whose son is nearing his third birthday. “What is this ‘regressive autism?’ ” she asked me, the resident autism expert in her peer group. (I conducted research on autism and regression in autism before becoming a freelance writer.) “I thought we were out of the woods!” I’m sure many parents of young children who read the piece had the same reaction, and it’s completely understandable. It’s also unwarranted. The claim that many kids with autism develop typically for almost three years and then experience a near-complete loss of language, social skills, and motor ability—a claim I’ve read many times before—simply isn’t true. It’s time to set the record straight. © 2014 The Slate Group LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19409 - Posted: 03.26.2014

Claudia Dreifus The biochemist Ricardo E. Dolmetsch has pioneered a major shift in autism research, largely putting aside behavioral questions to focus on cell biology and biochemistry. Dr. Dolmetsch, 45, has done most of his work at Stanford. Since our interviews — a condensed and edited version of which follows — he has taken a leave to join Novartis, where his mission is to organize an international team to develop autism therapies. “Pharmaceutical companies have financial and organizational resources permitting you to do things you might not be able to do as an academic,” he said. “I really want to find a drug.” Q. Did you start out your professional life studying the biochemistry of autism? A. No. In graduate school and as a postdoc, I’d done basic research on the ion channels on the membranes of cells. By my mid-20s, I had my name on some high-profile papers. Then, around 2006, my son who was then 4 was diagnosed with autism. We had suspected it. He didn’t talk much, was hyperactive, very moody. He assembled huge towers based on the color spectrum. He did all sorts of things that were very unusual. Given the signs, why did you wait that long to seek a diagnosis? I’m from Latin America [Cali, Colombia], and my Latin thing was, “This is the way boys are.” But he would just scream for hours and hours, uncontrollable. He didn’t sleep. We didn’t understand it. After a while, his teachers said, “You probably ought to have him seen.” So we went to a psychiatrist and neurologist and ultimately we got differing diagnoses. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19404 - Posted: 03.25.2014

by Simon Makin How much can environmental factors explain the apparent rise in autism spectrum disorders? Roughly 1 per cent of children in the US population are affected by autism spectrum disorder (ASD). Rates in many countries, including the US, have risen sharply in recent years but no one is sure why. It is still not clear whether this is prompted by something in the environment, increased awareness of the condition and changes in diagnoses, or a result of people having children later. The environmental case is hotly debated. There is some evidence that maternal infections during pregnancy can increase the risk. Other studies have pointed to a possible link with antidepressants while others have looked at elevated levels of mercury. But determining prenatal exposure to any substance is difficult because it is hard to know what substances people have been exposed to and when. To get around this, Andrey Rzhetsky and colleagues at the University of Chicago analysed US health insurance claims containing over 100 million patient records – a third of the population – dating from 2003 to 2010. They used rates of genital malformations in newborn boys as a proxy of parents' exposure to environmental risk factors. This is based on research linking a proportion of these malformations to toxins in the environment, including pesticides, lead and medicines. Toxic environment? The team compared the rates of these malformations to rates of ASD county by county. After adjusting for gender, income, ethnicity and socio-economic status, they found that a 1 per cent increase in birth defects – their measure for environmental effects - was associated with an average increase of 283 per cent in cases of ASD. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
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Link ID: 19393 - Posted: 03.21.2014