Links for Keyword: Autism

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By Catherine Saint Louis KATY, Tex. — Like many parents of children with autism, Nicole Brown feared she might never find a dentist willing and able to care for her daughter, Camryn Cunningham, now a lanky 13-year-old who uses words sparingly. Finishing a basic cleaning was a colossal challenge, because Camryn was bewildered by the lights in her face and the odd noises from instruments like the saliva suctioner — not to mention how utterly unfamiliar everything was to a girl accustomed to routine. Sometimes she’d panic and bolt from the office. Then in May, Ms. Brown, 45, a juvenile supervision officer, found Dr. Amy Luedemann-Lazar, a pediatric dentist in this suburb of Houston. Unlike previous dentists, Dr. Luedemann-Lazar didn’t suggest that Camryn would need to be sedated or immobilized. Instead, she suggested weekly visits to help her learn to be cooperative, step by step, with lots of breaks so she wouldn’t be overwhelmed. Bribery helped. If she sat calmly for 10 seconds, her reward was listening to a snippet of a Beyoncé song on her sister’s iPod. This month, Camryn sat still in the chair, hands crossed on her lap, for no less than 25 minutes through an entire cleaning — her second ever — even as purple-gloved hands hovered near her face, holding a noisy tooth polisher. At the end, Dr. Luedemann-Lazar examined Camryn’s teeth and declared her cavity-free and ready to see an orthodontist. “It was like a breakthrough,” Ms. Brown said, adding, “Dr. Amy didn’t just turn her away.” Parents of children with special needs have long struggled to find dentists who will treat them. In a 2005 study, nearly three-fifths of 208 randomly chosen general dentists in Michigan said they would not provide care for children on the autism spectrum; two-thirds said the same for adults. But as more and more children receive diagnoses of autism spectrum disorder, more dentists and dental hygienists are recognizing that with accommodations, many of them can become cooperative patients. © 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: 20222 - Posted: 10.21.2014

|By Jenni Laidman During the second and third trimester of pregnancy, the outer layer of the embryo's brain, the cortex, assembles itself into six distinct layers. But in autism, according to new research, this organization goes awry—marring parts of the brain associated with the abilities often impaired in the disorder, such as social skills and language development. Eric Courchesne, director of the Autism Center of Excellence at the University of California, San Diego, and his colleagues uncovered this developmental misstep in a small study that compared 11 brains of children with autism who died at ages two through 15 with 11 brains of kids who died without the diagnosis. The study employed a sophisticated genetic technique that looked for signatures of the activity of 25 genes in brain slices taken from the front of the brain—an area called the prefrontal cortex—as well as from the occipital cortex at the back of the brain and the temporal cortex near the temple. The researchers found disorganized patches, roughly a quarter of an inch across, in which gene expression indicated cells were not where they were supposed to be, amid the folds of tissue in the prefrontal cortex in 10 of 11 brains from children with autism. That part of the brain is associated with higher-order communication and social interactions. The team also found messy patches in the temporal cortices of autistic brains but no disorder at the back of the brain, which also matches typical symptom profiles. The patches appeared at seemingly random locations within the frontal and temporal cortices, which may help explain why symptoms can differ dramatically among individuals, says Rich Stoner, then at U.C. San Diego and the first author of the study, which appeared in the New England Journal of Medicine. © 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: 20205 - Posted: 10.14.2014

|By Melinda Wenner Moyer Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder's behavioral symptoms. At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health. One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. © 2014 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 20104 - Posted: 09.23.2014

By Filipa Ioannou Per the Associated Press, the Food and Drug Administration is considering a ban on electric-shock devices that are used to punish unwanted behavior by patients with autism and other developmental disabilities. If it comes as a surprise to you that any involuntary electric shocks are administered to autism patients in the United States, that's because the devices are only used at one facility in the country—the Judge Rotenberg Educational Center in Canton, Mass. The school has been a target of media attention in the past; in 2012, video leaked of 18-year-old patient Andre McCollins being restrained face-down and shocked 31 times. McCollins’ mother sued the center, and the lawsuit was settled outside of court. Rotenberg must get a court’s approval to begin administering skin shocks to a student. The center uses a graduated electronic decelerator, or GED, that is attached to the arms or legs. If the student acts aggressively – head-banging, throwing furniture, attacking someone – then a center worker can press a button to activate the electrode, delivering a two-second shock to the skin. The amount of pain generated by the device is a contentious subject. The Rotenberg Center's Glenda Crookes compared the sensation to “a bee sting” in comments to CBS News, and some Rotenberg parents are strong proponents of the device. But a U.N. official in 2010 said the shocks constituted “torture." An FDA report also addresses the widely held belief that autistic individuals have a high pain threshold, pointing out the possibility that “not all children with ASD express their pain in the same way as a ‘neurotypical child’ would (e.g., cry, moan, seek comfort, etc.), which may lead to misinterpretation by caregivers and medical professionals that patients are insensitive or to an incorrect belief that the child is not in pain.” © 2014 The Slate Group LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 20090 - Posted: 09.18.2014

By Maggie Fox, Erika Edwards and Judy Silverman Here’s how you might be able to turn autism around in a baby: Carefully watch her cues, and push just a little harder with that game of peek-a-boo or “This little piggy.” But don’t push too hard — kids with autism are super-sensitive. That’s what Sally Rogers of the University of California, Davis has found in an intense experiment with the parents of infants who showed clear signs of autism. It’s one of the most hopeful signs yet that if you diagnose autism very early, you can help children rewire their brains and reverse the symptoms. It was a small study, and it’s very hard to find infants who are likely to have autism, which is usually diagnosed in the toddler years. But the findings, published in the Journal of Autism and Developmental Disorders, offer some hope to parents worried about their babies. “With only seven infants in the treatment group, no conclusions can be drawn,” they wrote. However, the effects were striking. Six out of the seven children in the study had normal learning and language skills by the time they were 2 to 3. Isobel was one of them. “She is 3 years old now and she is a 100 percent typical, normally developing child,” her mother, Megan, told NBC News. The family doesn’t want their last name used for privacy reasons. “We don’t have to do the therapy any more. It literally rewired her brain.” Autism is a very common diagnosis for children in the U.S. The latest survey by the Centers for Disease Control and Prevention shows a startling 30 percent jump among 8-year-olds diagnosed with the disorder in a two-year period, to one in every 68 children.

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: 20047 - Posted: 09.09.2014

Moheb Costandi Autism can be baffling, appearing in various forms and guises and thwarting our best attempts to understand the minds of people affected by it. Anything we know for sure about the disorder can probably be traced back to the pioneering research of the developmental psychologist Uta Frith. Frith was the first to propose that people with autism lack theory of mind, the ability to attribute beliefs, intentions and desires to others. She also recognized the superior perceptual abilities of many with the disorder — and their tendency to be unable to see the forest for the trees. Frith, now affiliated with the Institute of Cognitive Neuroscience at University College London (UCL), has shaped autism research for an entire generation of investigators. Meanwhile, her husband Chris Frith formulated a new view of schizophrenia, a mental illness marked by hallucinations, disordered thinking and apathy. His work explored how the disorder affects the experience of agency, the sense that we are in control of our bodies and responsible for our actions. And his innovations in brain imaging helped researchers examine the relationship between brain and mind. Independently, husband and wife explored the social and cognitive aspects of these psychiatric disorders. Together, they helped lay the foundations of cognitive neuroscience, the discipline that seeks to understand the biological basis of thought processes. Trevor Robbins, a cognitive neuroscientist at the University of Cambridge in the U.K., calls them “tremendously influential pioneers,” in particular because both brought a social perspective to cognitive neuroscience. © Copyright 2014 Simons Foundation

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: 20019 - Posted: 09.02.2014

|By Michael Leon I had been working quite happily on the basic biology of the brain when a good friend of mine called for advice about his daughter, who had just been diagnosed with autism. I could hear the anguish and fear in his voice when he asked me whether there was anything that could be done to make her better. I told him about the standard-care therapies, including Intensive Behavioral Intervention, Early Intensive Behavioral Intervention, Applied Behavior Analysis, and the Early Start Denver Model (ESDM). These therapies also are expensive, time-consuming and have variable outcomes, with the best outcomes seen for ESDM. There are, however, few ESDM therapists, and the cost of such intensive therapy can be quite high. Moreover, my friend’s daughter was already past the age of the oldest children in the study that demonstrated the efficacy of ESDM. My feeling was that there was a good chance that there was an effective therapy for her using a simple, inexpensive at-home approach involving daily exposure to a wide variety of sensory stimulation. This is a partial list of the disorders whose symptoms can be greatly reduced, or even completely reversed, with what is known as “environmental enrichment”: Autism Stroke Seizures Brain damage Neuronal death during aging ADHD Prenatal alcohol syndrome Lead exposure Multiple sclerosis Addiction Schizophrenia Memory loss Huntington’s disease Parkinson’s disease Alzheimer’s disease Down syndrome Depression But why haven’t you heard about this? The reason is that all of these disorders that have been successfully treated only in animal models of these neurological problems. However, the effects seen in lab animals can be dramatic. © 2014 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 20003 - Posted: 08.27.2014

By PAM BELLUCK As a baby’s brain develops, there is an explosion of synapses, the connections that allow neurons to send and receive signals. But during childhood and adolescence, the brain needs to start pruning those synapses, limiting their number so different brain areas can develop specific functions and are not overloaded with stimuli. Now a new study suggests that in children with autism, something in the process goes awry, leaving an oversupply of synapses in at least some parts of the brain. The finding provides clues to how autism develops from childhood on, and may help explain some symptoms like oversensitivity to noise or social experiences, as well as why many people with autism also have epileptic seizures. It could also help scientists in the search for treatments, if they can develop safe therapies to fix the system the brain uses to clear extra synapses. The study, published Thursday in the journal Neuron, involved tissue from the brains of children and adolescents who had died from ages 2 to 20. About half had autism; the others did not. The researchers, from Columbia University Medical Center, looked closely at an area of the brain’s temporal lobe involved in social behavior and communication. Analyzing tissue from 20 of the brains, they counted spines — the tiny neuron protrusions that receive signals via synapses — and found more spines in children with autism. The scientists found that at younger ages, the number of spines did not differ tremendously between the two groups of children, but adolescents with autism had significantly more than those without autism. Typical 19-year-olds had 41 percent fewer synapses than toddlers, but those in their late teenage years with autism had only 16 percent fewer than young children with autism. © 2014 The New York Times Company

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: 19988 - Posted: 08.22.2014

By Rachel Feltman At every waking moment, your brain is juggling two very different sets of information. Input from the world around you, like sights and smells, has to be processed. But so does internal information — your memories and thoughts. Right now, for example, I’m looking at a peach: It’s yellow and pink, and has a lot of fuzz. But I also know that it smells nice (a personal assessment) and I’m imagining how good it will taste, based on my previous experience with fragrant pink fruits. The brain’s ability to handle these different signals is key to cognitive function. In some disorders, particularly autism and schizophrenia, this ability is disrupted. The brain has difficulty keeping internal and external input straight. In a new study published Thursday in Cell, researchers observe the switching method in action for the first time. While the research used mice, not humans, principal investigator and NYU Langone Medical Center assistant professor Michael Halassa sees this as a huge step toward understanding and manipulating the same functions in humans. “This is one of the few moments in my life where I’d actually say yes, absolutely this is going to translate to humans,” Halassa said. “This isn’t something based on genes or molecules that are specific to one organism. The underlying principles of how the brain circuitry works are likely to be very similar in humans and mice.” That circuitry has been hypothesized for decades. Neurologists know that the cortex of the brain is responsible for higher cognitive functions, like music and language. And the thalamus, which is an egg-like structure in the center of the brain, works to direct the flow of internal and external information before it gets to the cortex.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 19964 - Posted: 08.16.2014

Claudia M. Gold In the course of working on my new book about listening to parents and children, I have had the pleasure of immersing myself in the writing of D.W. Winnicott, pediatrician turned psychoanalyst. Winnicott's professional life included both caring for countless young children and families as a pediatrician, and psychoanalytic practice, where his adult patients "regressed to dependence," giving him an opportunity to interact with their infantile qualities, but with adult capacities for communication. This combination of experiences gave him a unique vantage point from which to make his many brilliant observations about children and the nature of the parent-child relationship. A recent New York Times Magazine article on autism prompted me to share his words of wisdom on the subject, which, though written in 1966, still have relevance today. The following is from a collection of papers, Thinking About Children: From my point of view the invention of the term autism was a mixed blessing...I would like to say that once this term has been invented and applied, the stage was set for something which is slightly false, i.e. the discovery of a disease…Pediatricians and physically minded doctors as a whole like to think in terms of diseases which gives a tidy look to the textbooks... The unfortunate thing is that in matters psychological things are not like that. Winnicott implores the reader to instead understand the child in relational and developmental context. He writes: The subject quickly becomes one not of autism and not of the early roots of a disorder that might develop in to autism, but rather one of the whole story of human emotional development and the relationship of the process in the individual child to the environmental provision which may or may not in any one particular case facilitate the maturational process. ©2014 Boston Globe Media Partners, 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: 19915 - Posted: 08.05.2014

By RUTH PADAWER At first, everything about L.'s baby boy seemed normal. He met every developmental milestone and delighted in every discovery. But at around 12 months, B. seemed to regress, and by age 2, he had fully retreated into his own world. He no longer made eye contact, no longer seemed to hear, no longer seemed to understand the random words he sometimes spoke. His easygoing manner gave way to tantrums and head-banging. “He had been this happy, happy little guy,” L. said. “All of a sudden, he was just fading away, falling apart. I can’t even describe my sadness. It was unbearable.” More than anything in the world, L. wanted her warm and exuberant boy back. A few months later, B. received a diagnosis of autism. His parents were devastated. Soon after, L. attended a conference in Newport, R.I., filled with autism clinicians, researchers and a few desperate parents. At lunch, L. (who asked me to use initials to protect her son’s privacy) sat across from a woman named Jackie, who recounted the disappearance of her own boy. She said the speech therapist had waved it off, blaming ear infections and predicting that Jackie’s son, Matthew, would be fine. She was wrong. Within months, Matthew acknowledged no one, not even his parents. The last word he had was “Mama,” and by the time Jackie met L., even that was gone. In the months and years that followed, the two women spent hours on the phone and at each other’s homes on the East Coast, sharing their fears and frustrations and swapping treatment ideas, comforted to be going through each step with someone who experienced the same terror and confusion. When I met with them in February, they told me about all the treatments they had tried in the 1990s: sensory integration, megadose vitamins, therapeutic horseback riding, a vile-tasting powder from a psychologist who claimed that supplements treated autism. None of it helped either boy. Together the women considered applied behavior analysis, or A.B.A. — a therapy, much debated at the time, that broke down every quotidian action into tiny, learnable steps, acquired through memorization and endless repetition; they rejected it, afraid it would turn their sons into robots. But just before B. turned 3, L. and her husband read a new book by a mother claiming that she used A.B.A. on her two children and that they “recovered” from autism. © 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: 19913 - Posted: 08.02.2014

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