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by Greg Miller On Saturday, the board of trustees of the American Psychiatric Association (APA) voted to approve the final text of the DSM-5, the next revision to the leading manual for diagnosing mental illness. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, which originated in 1952, will be released next May at the APA's annual meeting in San Francisco. The revision process leading to DSM-5 began in 1999, and APA says it consulted more than 1500 experts in 39 countries in updating the criteria for diagnosing hundreds of psychiatric conditions. It has been a bumpy ride. Controversy has dogged the revision process for years. Even before the first draft of proposed changes was released in 2010, critics alleged that too much of the deliberation was conducted in secret and that too many of those involved had ties to drug companies that stood to benefit from changes to diagnostic criteria—APA has repeatedly rejected these charges. And many of the diagnostic proposals have elicited a strong reaction. A proposal to combine several autism-related disorders into a single diagnosis raised concerns among some critics that it would radically alter who gets diagnosed with those disorders and angered advocates for Asperger syndrome, a milder form of autism that would be eliminated in the new scheme. A new childhood condition called disruptive mood dysregulation disorder, characterized by irritability and violent outbursts, was intended to stem the perceived overdiagnosis of childhood bipolar disorder, but critics have argued that the diagnosis lacks scientific validity. Yet another controversial proposal, to remove language that excludes people who've recently experienced the loss of a loved one from being diagnosed with major depression, elicited complaints that it would lead to the medicalization of normal grief. These changes will stand, APA said in a press release. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17569 - Posted: 12.04.2012

By Lindsey Tanner, The Associated Press CHICAGO -- The now familiar term "Asperger's disorder" is being dropped. And abnormally bad and frequent temper tantrums will be given a scientific-sounding diagnosis called DMDD. But "dyslexia" and other learning disorders remain. The revisions come in the first major rewrite in nearly 20 years of the diagnostic guide used by the nation's psychiatrists. Changes were approved Saturday. Full details of all the revisions will come next May when the American Psychiatric Association's new diagnostic manual is published, but the impact will be huge, affecting millions of children and adults worldwide. The manual also is important for the insurance industry in deciding what treatment to pay for, and it helps schools decide how to allot special education. This diagnostic guide "defines what constellations of symptoms" doctors recognize as mental disorders, said Dr. Mark Olfson, a Columbia University psychiatry professor. More important, he said, it "shapes who will receive what treatment. Even seemingly subtle changes to the criteria can have substantial effects on patterns of care." Olfson was not involved in the revision process. The changes were approved Saturday in suburban Washington, D.C., by the psychiatric association's board of trustees. The aim is not to expand the number of people diagnosed with mental illness, but to ensure that affected children and adults are more accurately diagnosed so they can get the most appropriate treatment, said Dr. David Kupfer. He chaired the task force in charge of revising the manual and is a psychiatry professor at the University of Pittsburgh. © 2012 NBCNews.com

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: 17561 - Posted: 12.03.2012

By James Gallagher Health and science reporter, BBC News The possibility that autism is linked to traffic pollution has been raised by researchers in California. Their study of more than 500 children said those exposed to high levels of pollution were three times more likely to have autism than children who grew up with cleaner air. However, other researchers said traffic was a "very unlikely" and unconvincing explanation for autism. The findings were presented in the Archives of General Psychiatry journal. Data from the US Environmental Protection Agency were used to work out levels of pollution for addresses in California. This was used to compare exposure to pollution, in the womb and during the first year of life, in 279 children with autism and 245 without. The researchers from the University of Southern California said children in homes exposed to the most pollution "were three times as likely to have autism compared with children residing in homes with the lowest levels of exposure". BBC © 2012

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: 17545 - Posted: 11.27.2012

Dan Jones As diagnoses of autism spectrum disorder rise, the need for effective therapies has increased in urgency. Today, a paper in Nature describes two ways of reversing autism-like symptoms in a new mouse model of the condition1. Autism spectrum disorder (ASD) affects up to 1 in 110 people. Although a few drugs have shown promise in mouse models, none is able to treat the core social deficits common to ASD in humans. A team of researchers led by Nahum Sonenberg of McGill University in Montreal, Quebec, created a new model of mouse autism, and then reversed its symptoms. They began by genetically engineering mice so that they lacked the gene Eif4ebp2. The 4E-BP2 protein that this produces suppresses the translation of certain messenger RNAs, so knocking out Eif4ebp2 allows the proteins that these mRNAs produce to be synthesized at above normal levels. Mice lacking Eif4ebp2 exhibit many autism-like symptoms, including poor social interaction, altered communication and repetitive behaviours. Sonenberg and his co-workers found that one group of proteins that proliferates in the absence of Eif4ebp2 is the neuroligins (NLGNs), which sit in the membrane of neurons and help to create and maintain the connections, or synapses, between nerve cells. When the authors examined mouse brain slices, they discovered that overproduction of NLGNs results in synapses that are prone to overstimulation, establishing a ‘hyperconnectivity’ that many researchers believe underlies the symptoms of ASD. © 2012 Nature Publishing Group

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: 17526 - Posted: 11.24.2012

Flora Graham, deputy editor, newscientist.com These glowing shapes aren't the ears of a rave-happy Vulcan - they're slices from a mouse's brain. The slice on the right is from a mouse that lacks a gene called Arl13b - the same gene whose mutation causes Joubert syndrome in humans. This is a rare neurological condition that is linked with autism-spectrum disorders and brain structure malformations. Without Arl13b, the nerve cells known as interneurons can't find the right destination in the cerebral cortex during the brain's development. Since the interneurons don't end up in the right places, they can't be wired up properly later on. This causes the disrupted brain development, typical of Joubert syndrome, visible in the image on the right. The researchers hope that their findings will lead to better treatments for people who have the syndrome. "Ultimately, if you're going to come up with therapeutic solutions, it's important to understand the biology of the disease," says Eva Anton of the University of North Carolina in Chapel Hill, who worked on the research, which was published in Developmental Cell last week. Journal reference: Developmental cell doi:10.1016/j.devcel.2012.09.019 © 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: 17525 - Posted: 11.24.2012

By Maggie Fox, NBC News Doctors trying to find some of the causes of autism put another piece into the puzzle on Monday: They found women who had flu while they were pregnant were twice as likely to have a child later diagnosed with autism. Those who had a fever lasting a week or longer -- perhaps caused by flu or maybe by something else -- were three times as likely to have an autistic child. The study of 96,000 children in Denmark raises as many questions as it answers. But it fits in with a growing body of evidence that suggests that, in at least some cases, something is going on with a mother’s immune system during pregnancy that affects the developing child’s brain. Autism seems to be a growing problem in the United States. According to the U.S. Centers for Disease Control and Prevention, autism spectrum disorder affects one in 88 children, including about one in 54 boys. The autism spectrum refers to a broad range of symptoms, from the relatively mild social awkwardness of Asperger’s syndrome to profound mental retardation, debilitating repetitive behaviors and an inability to communicate. Scientists agree that it’s not just a matter of better diagnosis; the numbers seem to be growing because more children are indeed developing autism. But no one is sure why. Genetics are a large factor -- if one twin has autism the other twin is very likely to -- but genes don’t explain it all. © 2012 NBCNews.com

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: 17478 - Posted: 11.12.2012

By Gary Stix Oliver Sacks, HBO and others have chronicled the life of autistic savant Temple Grandin. The unique patterns of thought produced by Grandin’s brain enabled her to design now-ubiquitous methods to treat cattle more humanely, and she has served as inspiration to others diagnosed with the condition. Until now, no one has tried to assess the actual brain physiology of the professor of animal sciences at Colorado State University. Grandin herself wanted to know more about the biological basis of her cognitive strengths and deficits. So she entered into a collaboration with the University of Utah, which performed a battery of imaging tests—MRI, DTI and fMRI—to determine brain volume, cortical thickness and the structure of the insulating white matter that surrounds the long, wire-like axons that connect one brain cell with another. Supplemented with neuropsychological testing, researchers compared these results with those from three other “neurotypical” female subjects of about the same age. It turns out that Grandin’s brain appears to be similar to that of other autistic savants. She has greater volume in the right hemisphere, which might account for her superior visuospatial abilities. She also has increased thickness of the entorhinal cortex, an area involved with memory As with others with autism, she has an overall larger brain size. And the enlarged amygdala and the smaller cortical thickness in the fusiform gyrus may relate to the deficits autistic individuals experience in dealing with emotion and reading faces. “There’s this idea in the savant literature that left hemisphere damage occurs during development and the right hemisphere compensates in some way,” says Jason Cooperrider, a graduate student at the University of Utah who presented the findings at the conference. “All of the savant skills are right hemisphere-dominant abilities, which would include Dr. Grandin’s exceptional visual and spatial ability which would be considered savant level.” © 2012 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 17399 - Posted: 10.22.2012

By RONI CARYN RABIN When Patrick Murphy was 6, he became obsessed with vacuum cleaners. The boy, who has autism, used to slip out of his house near Buffalo without telling his parents, running to a nearby appliance store or into strangers’ homes to marvel at vacuum cleaners. Patrick is now 14, and his parents have double bolts on the doors in their home and brackets on their windows. Still, Patrick — who is now focused on dogs — manages to sneak out. Two weeks ago, he crept from the house after his mother went to bed. When his father came home, he alerted the police. They found Patrick running barefoot in his pajamas at 2 a.m., three miles from his home. “That was very scary,” said Patrick’s father, Brian Murphy, who has now added an alarm system to the house to keep his son safe. “He has broken through brackets, windows, picked locks, you name it. It’s absolutely the most stressful part of parenting a child with autism.” The behavior, called wandering or elopement, has led to numerous deaths in autistic children by drowning and in traffic accidents. Now a new study of more than 1,200 families with autistic children suggests wandering is alarmingly common. Nearly half of parents with an autistic child age 4 or older said their children had tried to leave a safe place at least once, the study reported. One in four said their children had disappeared long enough to cause concern. Many parents said their wandering children had narrowly escaped traffic accidents or had been in danger of drowning. © 2012 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: 17341 - Posted: 10.08.2012

By BENEDICT CAREY Proposed changes to the official diagnosis of autism will not reduce the proportion of children found to have it as steeply as many have feared, scientists reported on Tuesday, in an analysis that contradicts several previous studies. Earlier research had estimated that 45 percent or more of children currently on the “autism spectrum” would not qualify under a new definition now being refined by psychiatric researchers — a finding that generated widespread anxiety among parents who rely on state-financed services for their children. The new report, posted online Tuesday by The American Journal of Psychiatry, concluded that the number who would be excluded is closer to 10 percent. The finding may soothe the anxieties of some parents, but will not likely settle the debate over the effect of the new diagnosis. All sides agree that the proposed criteria are narrower and will likely result in fewer diagnoses of autism, but until doctors begin using the new definition widely, the predictions of its effect are just that: predictions. The debate has simmered over the past year as an expert panel appointed by the American Psychiatric Association has updated its proposals for the association’s Diagnostic and Statistical Manual of Mental Disorders, scheduled to take effect in May 2013. The manual is the field’s standard reference, and several recent studies suggested that the amended autism definition was far narrower than intended. © 2012 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior
Link ID: 17319 - Posted: 10.02.2012

By Ranit Mishori, One of the least fun moments I recall from my years of growing up with an autistic brother was when he bit me on the cheek — just in time for my class photo. I was 12 and he was 11. I went into school with visible bite marks, and when they sat me in the chair for my solo shot, I told them that the cat had done it. That’s one of the bad stories. As for a good one . . . um, to be honest, I have a hard time coming up with much. I know that people are warmed by stories of siblings who selflessly shower the disabled child with love, attention and support. I think that’s great, too. And it’s for real for some siblings. But for many of us, relating to a sibling who is on the autism spectrum can be complicated. The challenges to a warm, close relationship are many. Normal sibling rivalry doesn’t work, because it can never be a fair fight. These are all fertile ground for building resentment. And then feeling guilty about feeling resentment. Because, after all, even as youngsters, we do understand that our disabled sibling cannot help being disabled. The feeling that our needs come second is echoed in the small volume of research on how autism affects siblings. Understandably, most of the scientific focus goes to the child who has the condition. (One in 88 children in the United States has some form of autism, according to the Centers for Disease Control and Prevention.) © 1996-2012 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: 17225 - Posted: 09.07.2012

Ewen Callaway A rare, hereditary form of autism has been found — and it may be treatable with protein supplements. Genome sequencing of six children with autism has revealed mutations in a gene that stops several essential amino acids being depleted. Mice lacking this gene developed neurological problems related to autism that were reversed by dietary changes, a paper published today in Science shows1. “This might represent the first treatable form of autism,” says Joseph Gleeson, a child neurologist at the University of California, San Diego, who led the study. “That is both heartening to families with autism, and also I think revealing of the underlying mechanisms of autism.” He emphasizes, however, that the mutations are likely to account for only a very small proportion of autism cases. “We don’t anticipate this is going to have implications for patients in general with autism,” says Gleeson. And there is as yet no proof that dietary supplements will help the six children, whose mutations the researchers identified by sequencing the exome — the part of the genome that codes for proteins. The children came from three families with Middle Eastern ancestry; in each case the parents were first cousins. Studying such families makes the hunt for the rare recessive mutations underlying some forms of autism simpler than it would be among the general population, Gleeson says, because the odds are higher that children will be born with two copies of the recessive mutation. © 2012 Nature Publishing Group,

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: 17224 - Posted: 09.07.2012

Steve Connor Babies of older fathers are more likely to carry genetic mutations than those of younger fathers. And the mutations could lead to illnesses such as autism and schizophrenia in later life, a landmark study has shown. Scientists have, for the first time, counted the number of new mutations linked with a father's age at the time of conception and have concluded that older men are significantly more likely to have children with potentially harmful genetic changes. The results could explain previous studies showing that certain mental and developmental illnesses with strong genetic components tend to be more common among people whose fathers were older at the time of conception. Although the age of a child's mother has been linked with problems associated with chromosomal defects, such as Down's syndrome, there has been scant information about the contribution made by older fathers to the future health of their offspring. "These observations shed light on the importance of the father's age on the risk of diseases such as schizophrenia and autism," the researchers say in their study published in the journal Nature. The scientists found that a new-born baby's genome contains around 60 new small-scale mutations compared with its parents and that the actual number of new mutations carried by each child was strongly dependent on the age of the father, rather than the mother, at the time of conception. The researchers, led by Augustine Kong and Kari Stefansson of deCode Genetics in Reykjavik, calculated that a 20-year-old father transmits about 25 new mutations to his child while a 40-year-old man will pass on 65. © independent.co.uk

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: 17196 - Posted: 08.25.2012

Posted by Kathleen Raven Families with autistic children must navigate a condition where questions outnumber the answers, and therapies remain sparse and largely ineffective. A clinical trial being conducted by the Sutter Neuroscience Institute in Sacramento, California to address this situation began recruiting participants today for a highly experimental stem cell therapy for autism. The institute plans to find 30 autistic children between ages 2 and 7 with cord blood banked at the privately-run Cord Blood Registry, located about 100 miles west of the institute. Already one other clinical trial, with 37 total participants between ages 3 and 12 years old, has been completed in China. The researchers affiliated with Beike Biotechnology in Shenzhen, the firm that sponsored the study, have not yet published any papers from that the trial, which used stem cells from donated cord blood. Mexican researchers are currently recruiting kids for yet another type of autism stem cell trial that will harvest cells from the participant’s fat tissue. But for each of these officially registered trials, many more undocumented stem cell therapy treatments take place for clients who are willing to pay enough. “Our research is important because many people are going to foreign countries and spending a lot of money on therapy that may not be valid,” says Michael Chez, a pediatric neurologist and lead investigator of the study at Sutter. © 2012 Nature Publishing Group,

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: 17185 - Posted: 08.22.2012

by Michael Slezak A lack of anti-Müllerian hormone in boys with autistic spectrum disorder (ASD) may lead to a greater number of symptoms. Michael Pankhurst and Ian McLennan from the University of Otago in New Zealand say hormones like anti-Müllerian hormone (AMH) that control the speed at which the body and brain develop might play a central role in the way that ASD progresses through childhood. The pair analysed the level of AMH in 82 boys with ASD. The lower the level of AMH in their blood, the greater the number of autistic traits they displayed. In an earlier study, McLennan and his colleagues found that an increased level of AMH was associated with slower overall growth and development in boys. Together, he thinks the two studies suggest that a lack of AMH could cause the brain to develop too quickly, leading to an increased number of symptoms in boys with ASD. "Rapid development is associated with a greater frequency of developmental disorders," says McLennan. A complex system that develops quickly is more likely to contain errors than one that develops more slowly, he explains. Surprisingly, there was no difference between the average level of anti-Müllerian hormone in the children with ASD and 16 boys without autism. McLennan says this shows that the hormone doesn't cause ASD, but may increase the number of symptoms in people who have the condition. © Copyright Reed Business Information Ltd.

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: 17167 - Posted: 08.15.2012

By Marissa Fessenden Autistic children struggle with many obstacles, including learning to speak. And, experts have noted, if these children learn verbal skills by age five, they tend to become happier and higher-functioning adults than do their nonverbal peers. Thirty years ago, psychiatrists expected only half of all autistic children would gain speaking abilities. Recent studies, however, indicate that as many as 80 percent of children with autism can learn to talk. One such study in 2006 showed that toddlers who received intensive therapy aimed at developing foundational oral language skills made significant gains in their ability to communicate verbally. Now researchers have followed up with a number of those kids and found that most of them continued to reap the benefits of that therapy years after it had ended. Several early behaviors build a foundation for language. These abilities have also been linked to whether a child can anticipate another person's mental state and use that understanding to explain and predict behavior. Developing this "theory of mind" may be a central difficulty for children with autism. Kasari's team targeted two of the early behaviors in their work: The first is the ability to engage in symbolic play, in which one object represents another—a child pretending a doll is his parent, for instance. The second is joint attention, wherein a child divides focus between an object and another person. This behavior can be thought of as "sharing looks." For example, when a child points to show a playmate a toy train, she looks at the moving train and checks to see if her playmate is engaged. In the initial study, Connie Kasari of the University of California, Los Angeles, and her colleagues evaluated 58 children between three and four years old in a randomized controlled study. © 2012 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Language and Our Divided Brain
Link ID: 17057 - Posted: 07.18.2012

By BENEDICT CAREY Clare True had autism and periodic seizures, but nothing prepared her family for Christmas Eve in 2006, when the 26-year-old went to bed after watching a movie and stopped breathing. “I got home from a party, went to check on her just after midnight, and she was — she was gone,” said her mother, Jane True. Paramedics tried to revive the young woman, then rushed her to the hospital, and somewhere in that firestorm of activity and grief, the Trues, Jane and her husband, Jim, considered donation. “I thought of it as a gift, her brain,” she said. “To my mind, the idea that scientists would be learning from her for years to come — how can you put a price on that?” Clare True’s was one of 150 specimens stored in a Harvard brain bank that was ruined because of a freezer failure, doctors acknowledged this month. The loss, while a setback for scientists studying disorders like Huntington’s disease, Alzheimer’s and schizophrenia, especially mortified those working on autism, for it exposed what is emerging as the largest obstacle to progress: the shortage of high-quality autopsied brains from young people with a well-documented medical history. The malfunction reduced by a third Harvard’s frozen autism collection, the world’s largest. A bank maintained by the University of Maryland has 52, and there are smaller collections elsewhere. Altogether there are precious few, given escalating research demands. The loss at the Harvard Brain Tissue Resource Center makes donations from parents like the Trues only more urgent. © 2012 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: 16965 - Posted: 06.26.2012

By Michelle Roberts Health editor, BBC News online A simple brain trace can identify autism in children as young as two years old, scientists believe. A US team at Boston Children's Hospital say EEG traces, which record electrical brain activity using scalp electrodes, could offer a diagnostic test for this complex condition. EEG clearly distinguished children with autism from other peers in a trial involving nearly 1,000 children. Experts say more work is needed to confirm the BMC Medicine study results. Early detection There are more than 500,000 people with autism in the UK. Autism is a spectrum disorder, which means that it is not a single condition and will affect individuals in different ways. Commonly, people with autism have trouble with social interaction and can appear locked in their own worlds. It can be a difficult condition to diagnose and can go undetected for years. The latest study found 33 specific EEG patterns that appeared to be linked to autism. BBC © 2012

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: 16964 - Posted: 06.26.2012

An intervention in which adults actively engaged the attention of preschool children with autism by pointing to toys and using other gestures to focus their attention results in a long term increase in language skills, according to researchers supported by the National Institutes of Health. At age 8, children with autism who received therapy centered on sharing attention and play when they were 3 or 4 years old had stronger vocabularies and more advanced language skills than did children who received standard therapy. All of the children in the study attended preschool for 30 hours each week. “Some studies have indicated that such pre-verbal interactions provide the foundation for building later language skills,” said Alice Kau, Ph.D., of the Intellectual and Developmental Disabilities Branch of the Eunice Kennedy Shriver NICHD.“This study confirms that intensive therapy to engage the attention of young children with autism helps them acquire language faster and build lasting language skills.” The study findings appear in the Journal of the American Academy of Child and Adolescent Psychiatry. The 40 children who participated in the study were 8 and 9 years old. Five years earlier, they had been diagnosed with an autism spectrum disorder and received the intensive therapy program or standard intervention, as part of a separate study.

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: 16956 - Posted: 06.23.2012

By ANDREW POLLACK Two of the front-runners in the race to develop drugs to treat mental retardation and autism are joining forces, hoping to save money and get to the market sooner. A deal, expected to be announced on Tuesday, will pool the resources of Roche, the Swiss pharmaceutical giant, and Seaside Therapeutics, a private 30-employee company based in Cambridge, Mass. “This deal will establish the biggest effort to date” in autism drugs, Luca Santarelli, head of neuroscience for Roche, said before the announcement. Financial terms are not being disclosed. There is rising excitement that drugs might be able to relieve some of the behavioral problems associated with autism and in particular a cause of autism and mental retardation known as fragile X syndrome. About 100,000 Americans have fragile X syndrome. Some parents of children being treated with new drugs in clinical trials have said they see positive changes in behavior. Becky Zorovic of Sharon, Mass., said that when she used to take her son Anders, who has fragile X, to the dentist, she would have to lie in the chair and hold him on top of her as he screamed. But after Anders starting taking Seaside’s drug, arbaclofen, in a clinical trial, she said, “He sat in the chair by himself and he opened his mouth and let the dentist polish his teeth and even scrape his teeth.” Anders has also has gone to birthday parties, which he once refused to do, she said. © 2012 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: 16929 - Posted: 06.19.2012

By Karen Weintraub A freezer malfunction at Harvard-affiliated McLean Hospital has severely damaged one-third of the world’s largest collection of autism brain samples, potentially setting back research on the disorder by years, scientists say. An official at the renowned brain bank in Belmont discovered that the freezer had shut down in late May, without triggering two alarms. Inside, they found 150 thawed brains that had turned dark from decay; about a third of them were part of a collection of autism brains. “This was a priceless collection,’’ said Dr. Francine Benes, director of the Harvard Brain Tissue Resource Center, where the brains were housed. “You can’t express its value in dollar amounts,’’ said Benes, who is leading one of two internal investigations into the freezer failure. The damage to these brains could slow autism research by a decade as the collection is restored, said Carlos Pardo, a neuropathologist and associate professor of neurology at Johns Hopkins University. The collection, owned by the advocacy and research organization Autism Speaks, “yields very, very important information that allows us to have a better understanding of what autism is, as well as the contribution of environmental and immune factors,’’ said Pardo, whose 2004 study of brains stored in the bank was the first to find that autism involves the immune system. “The benefit has been great.’’ © 2012 NY Times Co.

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: 16894 - Posted: 06.11.2012