Tag Archives: Neurodevelopmental Disorders

Question?: Pdd Nos Symptoms

George asks…

Poll: Do you think vaccines cause or contribute to autism?

I’m curious to see what people really think.

admin answers:

No i dont believe they do whatsoever! I think parents are just being over cautious and flipping out for no reason. Vaccines have been around for ages, and now they are trying to say that it causes autisim? I dont think so. Dont you think there would have been more causes of that if it was actually linked to the vaccines. Its the same vaccine schedule, its not like the vaccines have changed much in the last 50 years.

Autism and autism spectrum disorders are complex neurodevelopmental disorders.Heritability contributes about 90% of the risk of a child developing autism, but the genetics of autism are complex and typically it is unclear which genes are responsible.Many other causes have been proposed, such as exposure of children to vaccines; these proposals are controversial and the vaccine hypotheses have no convincing scientific evidence.

Autism is a condition involving abnormalities of brain development and behavior which manifests itself before a child is three years old and has a steady course with no remission. It is characterized by impairments in social interaction and communication, as well as restricted and repetitive behavior. It is part of a larger family called the autism spectrum disorders (ASD) or pervasive developmental disorders (PDD), which include closely related syndromes such as Asperger syndrome and PDD-NOS. This article uses autism to denote the classic autistic disorder and ASD to denote the wider family.

Autism’s theory of causation is still incomplete. It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism’s characteristic triad of symptoms. However,here is increasing suspicion among researchers that autism does not have a single cause, but is instead a complex disorder with a set of core aspects that have distinct causes. Although these distinct causes have been hypothesized to often co-occur, it has also been suggested that the correlation between the causes has been exaggerated.The number of people known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; it is unknown whether prevalence has increased as well. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.

The consensus among mainstream autism researchers is that genetic factors predominate, but some are concerned, as one anonymous researcher put it, that “geneticists are running the show, and ignoring the environmental aspects.”Environmental factors that have been claimed to contribute to autism or exacerbate its symptoms, or may be important to consider in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, and vaccines. Among these factors, vaccines have attracted much attention, as parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and parental concern about vaccines has led to a decreasing uptake of childhood immunizations and an increasing likelihood of measles outbreaks. However, as described in Mercury and MMR vaccine below, there is overwhelming scientific evidence showing no causal association between the measles-mumps-rubella vaccine and autism, and there is no scientific evidence that the vaccine preservative thiomersal helps cause autism.

In 2007 the National Institutes of Health announced an Autism Centers of Excellence (ACE) research program to find the causes of autism and identify new treatments for the disorder. Initial recipients are focusing on genetic factors, brain imaging, brain chemicals and functions including mirror neurons, effect on early parent-child behavior on autism, and learning in autistic children.
Http://en.wikipedia.org/wiki/Causes_of_autism

I am a mother of a 12 month old boy… Who is up to date on all his vaccines so far. And he will continue to get all his vaccinations. As so will any other children i should have. Im sorry but i wouldnt take the risk of my child actually contracting one of those disease just because some parents believe that it may be linked to autisim. Sorry, i would rather have my child vaccinated.

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Can Videogaming Benefit Young People With Autism Spectrum Disorder?

Main Category: Autism
Also Included In: IT / Internet / E-mail
Article Date: 08 Sep 2012 – 0:00 PDT Current ratings for:
Can Videogaming Benefit Young People With Autism Spectrum Disorder?
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According to the Centers for Disease Control and Prevention (CDC), 1 in 88 children in the U.S. has autism spectrum disorder (ASD), a broad group of neurodevelopmental disorders. Children and adolescents with ASD are typically fascinated by screen-based technology such as videogames and these can be used for educational and treatment purposes as described in an insightful Roundtable Discussion published in Games for Health Journal: Research Development, and Clinical Applications, a peer-reviewed publication from Mary Ann Liebert, Inc.. The article is available free on the Games for Health Journal website.

Individuals with ASD have difficulty with communication and social interaction, but they often have particularly good visual perceptual skills and respond well to visual stimuli. Videogames offer opportunities for successful learning, motivation to improve skills such as planning, organization, and self-monitoring, and reinforcement of desired behaviors without the need for direct human-to-human interaction.

Autism is a growing area of interest for the gamification community, and Games for Health Journal continues to explore various aspects of how videogame technology can be beneficial in treating this complex spectrum of disorders. In a previous issue of the Journal, the article “Comparing Energy Expenditure in Adolescents with and without Autism while Playing Nintendo® Wii™ Games” described how gaming might help individuals with ASD increase their daily physical activity to prevent obesity.

“Children and young adults with ASD have unique opportunities to capitalize on their interest and aptitude in videogames as a resource to develop desired social behaviors and life skills and to increase their physical activity,” says Games for Health Journal Editor-in-Chief Bill Ferguson, PhD, who moderated the Roundtable.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
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Autism In The News, 2012, Week 35

Evidence weak that vocational programs help young adults with autism – CNN (blog)

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Google “vocational interventions for young adults with autism” and you’ll get more than 200,000 results. But a new study finds there’s little science to backup the efficacy of current methods used to help young adults with these neurodevelopmental disorders segue into the workforce.

“There’s startlingly little information on the best ways to help adolescents and adults with autism achieve their maximum potential in the workplace and across the board,” says lead study author Julie Lounds Taylor.

Developmental Delays, Autism Often Missed in Hispanic Children – PsychCentral.com

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Developmental Delays, Autism Often Missed in Hispanic Children

Hispanic children often have undiagnosed developmental delays, according to new research that also found that large numbers of all children who were first thought to have developmental delays actually had autism.

“Our study raises concerns about access to accurate, culturally relevant information regarding developmental milestones and the importance of early detection and treatment,” said Virginia Chaidez, Ph.D., the lead author and a postdoctoral researcher in the University of California Davis when the study was conducted.

Father of autistic boy creates an innovative approach to therapy that’s … – Sacramento Bee

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Father of autistic boy creates an innovative approach to therapy that’s bringing children to the table – literally.
Delightful online puppet videos make learning a ‘preferred activity’

“We wanted to create an educational program that children with autism and similar challenges would enjoy watching, and a title character that was smart and silly – and autistic!” says series creator Dan Kalinowski. “Making it fun removes barriers to therapy, encourages imitation, and increases memorization. We also hope the fact that Buddy has autism makes him familiar and shows that using visual schedules and reward systems is a perfectly acceptable part of life that deserve screen time, too.”

Autism’s ‘punch in the gut’ – Examiner.com

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As controversy flares over a recently published column suggesting a link between autism and a reduction in parasitic organism in the bodies of people from developed worlds, a new theory seeks to establish credibility with scientific research on autism.

On Monday, TIME Magazine released research examining a potential microbiological link between gut bacteria and autism.

Scientifically known as microbiomes, these non-human cells primarily occupy the intestines and other organs in the digestive system. The cells are much smaller than human cells, but an average person has 10 times the amount of gut bacterial cells compared to the human variety.

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Evidence Of Link Discovered Between Immune Irregularities And Autism

Main Category: Autism
Also Included In: Immune System / Vaccines
Article Date: 19 Jul 2012 – 1:00 PDT Current ratings for:
Evidence Of Link Discovered Between Immune Irregularities And Autism
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Scientists at the California Institute of Technology (Caltech) pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder.

What has remained unanswered, however, is whether the immune changes play a causative role in the development of the disease or are merely a side effect. Now a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.

The results appear in a paper this week in the Proceedings of the National Academy of Sciences (PNAS).

“We have long suspected that the immune system plays a role in the development of autism spectrum disorder,” says Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, who led the work. “In our studies of a mouse model based on an environmental risk factor for autism, we find that the immune system of the mother is a key factor in the eventual abnormal behaviors in the offspring.”

The first step in the work was establishing a mouse model that tied the autism-related behaviors together with immune changes. Several large epidemiological studies – including one that involved tracking the medical history of every person born in Denmark between 1980 and 2005 – have found a correlation between viral infection during the first trimester of a mother’s pregnancy and a higher risk for autism spectrum disorder in her child. To model this in mice, the researchers injected pregnant mothers with a viral mimic that triggered the same type of immune response a viral infection would.

“In mice, this single insult to the mother translates into autism-related behavioral abnormalities and neuropathologies in the offspring,” says Elaine Hsiao, a graduate student in Patterson’s lab and lead author of the PNAS paper.

The team found that the offspring exhibit the core behavioral symptoms associated with autism spectrum disorder – repetitive or stereotyped behaviors, decreased social interactions, and impaired communication. In mice, this translates to such behaviors as compulsively burying marbles placed in their cage, excessively self grooming, choosing to spend time alone or with a toy rather than interacting with a new mouse, or vocalizing ultrasonically less often or in an altered way compared to typical mice.

Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive – one that promotes inflammation.

“Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers,” Hsiao says. “This tells us that a prenatal challenge can result in long-term consequences for health and development.”

With the mouse model established, the group was then able to test whether the offspring’s immune problems contribute to their autism-related behaviors. In a revealing test of this hypothesis, the researchers were able to correct many of the autism-like behaviors in the offspring of immune-activated mothers by giving the offspring a bone-marrow transplant from typical mice. The normal stem cells in the transplanted bone marrow not only replenished the immune system of the host animals but altered their autism-like behavioral impairments.

The researchers emphasize that because the work was conducted in mice, the results cannot be readily extrapolated to humans, and they certainly do not suggest that bone-marrow transplants should be considered as a treatment for autism. They also have yet to establish whether it was the infusion of stem cells or the bone-marrow transplant procedure itself – complete with irradiation – that corrected the behaviors.

However, Patterson says, the results do suggest that immune irregularities in children could be an important target for innovative immune manipulations in addressing the behaviors associated with autism spectrum disorder. By correcting these immune problems, he says, it might be possible to ameliorate some of the classic developmental delays seen in autism.

In future studies, the researchers plan to examine the effects of highly targeted anti-inflammatory treatments on mice that display autism-related behaviors and immune changes. They are also interested in considering the gastrointestinal (GI) bacteria, or microbiota, of such mice. Coauthor Sarkis Mazmanian, a professor of biology at Caltech, has shown that gut bacteria are intimately tied to the function of the immune system. He and Patterson are investigating whether changes to the microbiota of these mice might also influence their autism-related behaviors.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Along with Patterson, Hsiao, and Mazmanian, additional Caltech coauthors on the PNAS paper, “Modeling an autism risk factor in mice leads to permanent immune dysregulation,” are Mazmanian lab manager Sara McBride and former graduate student Janet Chow. The work was supported by an Autism Speaks Weatherstone Fellowship, National Institutes of Health Graduate Training Grants, a Weston Havens Foundation grant, a Gregory O. and Jennifer W. Johnson Caltech Innovation Fellowship, a Caltech Innovation grant, and a Congressionally Directed Medical Research Program Idea Development Award.
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Seizure Susceptibility In Angelman Syndrome May Be Due To Brain Cell Activity Imbalance

Main Category: Epilepsy
Also Included In: Autism;  Genetics
Article Date: 08 Jun 2012 – 0:00 PDT Current ratings for:
‘Seizure Susceptibility In Angelman Syndrome May Be Due To Brain Cell Activity Imbalance’
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New research by scientists at the University of North Carolina School of Medicine may have pinpointed an underlying cause of the seizures that affect 90 percent of people with Angelman syndrome (AS), a neurodevelopmental disorder.

Published online in the journal Neuron, researchers led by Benjamin D. Philpot, PhD, professor of cell and molecular physiology at UNC, describe how seizures in individuals with AS could be linked to an imbalance in the activity of specific types of brain cells.

“Our study indicates that a common abnormality that may apply to many neurodevelopmental disorders is an imbalance between neuronal excitation and inhibition,” Philpot said. This imbalance has been observed in several genetic disorders including Fragile X and Rett syndromes, both of these, like AS, can be associated with autism.

Angelman syndrome occurs in one in 15,000 live births. The syndrome often is misdiagnosed as cerebral palsy or autism. Its characteristics, along with seizures, include cognitive delay, severe intellectual disability, lack of speech (minimal or no use of words), sleep disturbance, hand flapping and motor and balance disorders.

The most common genetic defect of the syndrome is the lack of expression of the maternally inherited allele of gene UBE3A on chromosome 15.

This loss of gene function in AS animal models has been linked to decreased release of an excitatory neurotransmitter which increases the activity of other neurons. But that seems at odds with the high seizure activity observed in AS patients. The new study may clarify this issue.

In his lab in UNC’s Neuroscience Research Center, Philpot and graduate student Michael L. Wallace, the study’s first author, explored the neurocircuitry of an Angelman syndrome mouse model. These mice show behavioral features similar to humans with AS, including seizures.

The researchers used electrophysiological methods to record excitatory and inhibitory activity from individual neurons. These involved highly precise recording electrodes, microscopic tips attached to individual neurons. “In this way you can record from precise neuron types and tell which neuron you’re recording from and what its activity is,” explained Philpot.

“You can stimulate it to drive other neurons and also record the activity on other neurons onto it.”

The researchers found that neurotransmitters sent from inhibitory neurons and carrying chemical messages meant to stop excitatory neurons from increasing their activity were defective.

In addition, they found that AS model mice have a defect in their inhibitory neurons which decreases their ability to recover from high levels of activity. “One of the reasons why inhibition is so important is that it’s needed to ensure that brain activity is regulated,” Philpot said. “Inhibition plays an important role in timing of information transfer between neurons, and if the timing is messed up, as you might observe if you had a decrease in inhibition, then a lot of information is lost in that transfer.”

“We found a disproportionately large decrease in inhibition to excitation,” Wallace said. “We think that the circuit we investigated is in a hyperexcitable state and may be underlying some of the epileptic problems observed in the AS animal model. This improperly regulated brain activity might also underlie cognitive impairments in AS.”

Philpot says one of their goals is to understand exactly how these changes in the connections between neurons underlie seizures in AS. “A very long term goal is to try to get better treatments for these individuals because their epilepsy is very hard to treat.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our epilepsy section for the latest news on this subject. Along with Wallace and Philpot, other UNC co-authors are Alain C. Burette and Richard J. Weinberg from the department of cell and developmental biology.
Support for the research came from a National Institute of Neurological Disorders and Stroke, the Angelman Syndrome Foundation, the Simons Foundation, the National Eye Institute, and the National Institute of Mental Health.
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Learning Mechanism Of The Adult Brain Revealed

Main Category: Epilepsy
Also Included In: Autism;  Schizophrenia
Article Date: 30 Apr 2012 – 0:00 PDT

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They say you can’t teach an old dog new tricks. Fortunately, this is not always true. Researchers at the Netherlands Institute for Neuroscience (NIN-KNAW) have now discovered how the adult brain can adapt to new situations. The Dutch researchers’ findings are published in the prestigious journal Neuron. Their study may be significant in the treatment of neurodevelopmental disorders such as epilepsy, autism and schizophrenia.

Ability to learn

Our brain processes information in complex networks of nerve cells. The cells communicate and excite one another through special connections, called synapses. Young brains are capable of forming many new synapses, and they are consequently better at learning new things. That is why we acquire vital skills – walking, talking, hearing and seeing – early on in life. The adult brain stabilises the synapses so that we can use what we have learned in childhood for the rest of our lives.

Disappearing inhibitors

Earlier research found that approximately one fifth of the synapses in the brain inhibit rather than excite other nerve-cell activity. Neuroscientists have now shown that many of these inhibitory synapses disappear if the adult brain is forced to learn new skills. They reached this conclusion by labelling inhibitory synapses in mouse brains with fluorescent proteins and then tracking them for several weeks using a specialised microscope. They then closed one of the mice’s eyes temporarily to accustom them to seeing through just one eye. After a few days, the area of the brain that processes information from both eyes began to respond more actively to the open eye. At the same time, many of the inhibitory synapses disappeared and were later replaced by new synapses.

Regulating the information network

Inhibitory synapses are vital for the way networks function in the brain. “Think of the excitatory synapses as a road network, with traffic being guided from A to B, and the inhibitory synapses as the matrix signs that regulate the traffic,” explains research leader Christiaan Levelt. “The inhibitory synapses ensure an efficient flow of traffic in the brain. If they don’t, the system becomes overloaded, for example as in epilepsy; if they constantly indicate a speed of 20 kilometres an hour, then everything will grind to a halt, for example when an anaesthetic is administered.

If you can move the signs to different locations, you can bring about major changes in traffic flows without having to entirely reroute the road network.”

Hope

Inhibitory synapses play a hugely influential role on learning in the young brain. People who have neurodevelopmental disorders – for example epilepsy, but also autism and schizophrenia – may have trouble forming inhibitory synapses. The discovery that the adult brain is still capable of pruning or forming these synapses offers hope that pharmacological or genetic intervention can be used to enhance or manage this process. This could lead to important guideposts for treating the above-mentioned neurological disorders, but also repairing damaged brain tissue.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
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PCBs Shown To Promote Dendrite Growth, May Increase Autism Risk

Main Category: Autism
Also Included In: Public Health
Article Date: 27 Apr 2012 – 1:00 PDT

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New research from UC Davis and Washington State University shows that PCBs, or polychlorinated biphenyls, launch a cellular chain of events that leads to an overabundance of dendrites — the filament-like projections that conduct electrochemical signals between neurons — and disrupts normal patterns of neuronal connections in the brain.

“Dendrite growth and branching during early development is a finely orchestrated process, and the presence of certain PCBs confuses the conductor of that process,” said Pamela Lein, a developmental neurobiologist and professor of molecular biosciences in the UC Davis School of Veterinary Medicine. “Impaired neuronal connectivity is a common feature of a number of conditions, including autism spectrum disorders.”

Reported in two related studies in the journal Environmental Health Perspectives, the findings underscore the developing brain’s vulnerability to environmental exposures and demonstrate how PCBs could add to autism risk.

“We don’t think PCB exposure causes autism,” Lein said, “but it may increase the likelihood of autism in children whose genetic makeup already compromises the processes by which neurons form connections.”

The senior authors of the studies were Lein and Isaac Pessah, chair of molecular biosciences in the School of Veterinary Medicine and director of the Center for Children’s Environmental Health at UC Davis. Both are researchers with the UC Davis MIND Institute, which is dedicated to finding answers to autism and other neurodevelopmental disorders. The lead author was Gary Wayman of Washington State University’s Program in Neuroscience, who first described the molecular pathway that controls the calcium signaling in the brain that guides normal dendrite growth.

Wayman found that key cellular players, called calcium and calmodulin kinases, are activated by increased calcium levels. Activated calmodulin kinase then turns on the protein known as CREB that regulates genes that produce Wnt2, a potent molecule and the final arbiter of whether and how dendrites grow. Wnt2 directs structural proteins to construct scaffolding that supports dendrite growth and branching.

“Orderly choreography of the calmodulin kinase-to-Wnt2 pathway translates normal increases in calcium levels into normal levels of dendrite production,” said Wayman. “The wiring of billions of neurons is dependent on the health of this cellular process and is crucial to proper development of virtually all complex behaviors, learning, memories and language.”

For the current studies, the team set out to determine if that pathway was altered by exposure to PCBs, focusing on neurons of the hippocampus — the brain region linked with learning and memory and known to suffer impaired connectivity in many neurodevelopmental disorders.

The scientists also focused on the effects of an understudied PCB subset known as non-dioxin-like PCBs, which have been shown to increase calcium levels in neurons. Both non-dioxin-like PCBs and the more familiar dioxin-like subset were widely used in electrical equipment in the 1950s and 1960s. Banned in the 1970s because of the potential for dioxin-like PCBs to cause cancer, all PCBs are stable compounds that persist throughout the environment today.

One of the current UC Davis studies examined dendrite growth in rat pups born to and nursed by PCB-exposed mothers. Another study analyzed how PCBs affect rat neurons in cell cultures at developmental stages similar to those in the third trimester of pregnancy in humans. In both studies, PCB exposure levels were similar to those found in the human diet and in human tissues, including the placenta and breast milk.

Evaluation of the brains of the rats exposed to PCBs early in life showed significant overproduction of dendrites. The cellular studies showed that PCBs triggered the calcium pathway that led to the aberrant brain architecture, and that dendrite production was normal when that cellular pathway was blocked.

“We are the first to show that non-dioxin-like PCBs alter how the developing brain gets wired by hijacking the calcium signaling pathway and greatly expanding dendrite growth,” said Lein.

The experiments also helped identify for the first time the specific trigger for this cellular chain of events as the ryanodine receptor (RyR) calcium channel. Pessah, a recognized leader in calcium-channel dysfunction and neurodevelopment, previously showed that RyR is selectively activated by non-dioxin-like PCBs. The new studies prove that RyR is a necessary component in the pathway that controls dendritic growth.

“These same calcium pathways are implicated in some forms of autism and, while environmental exposures alone do not cause autism, these new findings provide good evidence that PCBs could add to autism risk in genetically predisposed children,” said Pessah. “Understanding the fundamental mechanisms by which PCBs alter neural networks sets the stage for research on environmental contaminants that are structurally related to PCBs, including flame retardants, and their risks to susceptible populations.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. In addition to Lein, Pessah and Wayman, coauthors on the papers were Dongren Yang, Diptiman Bose and Donald Bruun of UC Davis; Adam Lesiak of Washington State University; and Soren Impey and Veronica Ledoux of the Oregon Health & Science University.
Funding for the studies was provided by the National Institutes of Health (grants R01 ES014901, R01 ES017425, P42 ES04699, R01 MH086032, P01 ES011269 and T32 ES007060), the U.S. Environmental Protection Agency (grants R833292 and R829388), the Hope for Depression Research Foundation and the J.B. Johnson Foundation.
The studies — “PCB 95 Promotes Dendritic Growth via Ryanodine Receptor-Dependent Mechanisms” and “PCB 95 Modulates Calcium-Dependent Signaling Pathway Responsible for Activity-Dependent Dendritic Growth” — will be published in a future print issue of the journal with several other investigations focused on autism and the environment. Copies of the UC Davis-Washington State University studies are available online now at http://dx.doi.org/10.1289/ehp.1104832 and http://dx.doi.org/10.1289/ehp.1104833.
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New Genes Contributing To Autism And Related Neurodevelopmental Disorders Uncovered By Researchers Studying Chromosomal Abnormalities

Main Category: Autism
Also Included In: Genetics
Article Date: 24 Apr 2012 – 0:00 PDT

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When chromosomes replicate, sometimes there is an exchange of genetic material within a chromosome or between two or more chromosomes without a significant loss of genetic material. This exchange, known as a balanced chromosomal abnormality (BCA), can cause rearrangements in the genetic code.

Researchers from 15 institutions in three countries including Brigham and Women’s Hospital (BWH), Massachusetts General Hospital, Harvard Medical School, and the Broad Institute found that due to these rearrangements, BCAs harbor a reservoir of disruptions in the code that could lead to autism and other neurodevelopmental disorders. The researchers also uncovered 22 new genes that may contribute to or increase the risk of autism or abnormal neurodevelopment.

The study will be published in the print issue of Cell on April 27, 2012.

The researchers used a strategy that involved directly sequencing BCAs to reveal genes at the breakpoints and show that these genes are related to autism and other neurodevelopmental disorders.

This study is part of a larger, ongoing collaborative endeavor, the Developmental Genome Anatomy Project (DGAP), to identify genes critical in human development.

The researchers discovered that the genetic code can be disrupted at various distinct sites and still result in autism. The disruptions occur in several different groups of genes, including those already individually suspected to be associated with abnormal neurodevelopment; those which illuminate a single gene as important in large regions previously defined as genomic disorders; as well as those associated with psychiatric disorders that can have much later onset than neurodevelopmental disorders.

“BCAs provide a unique opportunity to pinpoint a gene and validate it in a disorder,” said Cynthia Morton, PhD, BWH director of cytogenetics, and principal investigator of DGAP. “These discoveries can illuminate biological pathways that may be a window to a new therapy. We are all grateful to the individuals and their families who make these fundamental findings possible through their participation as subjects in these studies.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. This research was supported by the Simons Foundation Autism Research Initiative; Autism Speaks; Massachusetts General Hospital ECOR Fund for Medical Discovery Award; and the National Institutes of Health (NIH) and Human Services including the National Institute of General Medical Sciences, the National Institute of Mental Health and the National Human Genome Research Institute. NIH and NIMH grants included P01-GM061354, R21-HD065286 and F32-MH087123.
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Sex differences in cognitive domains and their clinical correlates in higher-functioning autism spectrum disorders

Sex differences in cognitive domains and their clinical correlates in higher-functioning autism spectrum disorders Sign In to gain access to subscriptions and/or My Tools. sign in icon Sign In | My Tools | Contact Us | HELP SJO banner Search all journals Advanced Search Go Search History Go Browse Journals Go Skip to main page content

Home OnlineFirst All Issues Subscribe RSS rss Email Alerts Search this journal Advanced Journal Search » Sex differences in cognitive domains and their clinical correlates in higher-functioning autism spectrum disorders Sven Bölte

Department of Women’s and Children’s Health, Karolinska Institutet Center of Neurodevelopmental Disorders (KIND), Karolinska Institutet, Stockholm, Sweden, sven.bolte{at}ki.se, Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany, Department of Child and Adolescent Psychiatry and Psychotherapy, Goethe-University, Frankfurt am Main, Germany Eftichia Duketis
Department of Child and Adolescent Psychiatry and Psychotherapy, Goethe-University, Frankfurt am Main, Germany Fritz Poustka
Department of Child and Adolescent Psychiatry and Psychotherapy, Goethe-University, Frankfurt am Main, Germany Martin Holtmann
Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany, Department of Child and Adolescent Psychiatry and Psychotherapy, Goethe-University, Frankfurt am Main, Germany, LWL-Hospital for Child and Adolescent Psychiatry, Ruhr-University, Bochum, Germany Abstract Despite the skewed sex ratio, few studies have addressed possible cognitive sex differences in autism spectrum disorders (ASDs). This study compared visual attention to detail (ATTD) and selected executive functions (EF) in 35 males and 21 females with higher-functioning ASD and unaffected sibling controls. Females with ASD outperformed males on EF as assessed by the Trail Making Test B-A. Males with ASD showed superior performance for ATTD as measured by the Block Design Test (BD) when compared with females. EF difficulties in males were correlated with more stereotypic behaviours and interests on the Autism Diagnostic Interview-Revised or the Autism Diagnostic Observation Schedule. The results indicated clinically meaningful cognitive sex differences in ASD, particularly an association between EF and stereotypic behaviours and interests. ATTD as a potential basis for specific cognitive strengths (e.g. scientific/savant skills) might be more pronounced in males with ASD.

PDD neuropsychology gender executive function attention savant © The Author(s), 2011. Add to CiteULikeCiteULike Add to ConnoteaConnotea Add to DeliciousDelicious Add to DiggDigg Add to FacebookFacebook Add to Google+Google+ Add to LinkedInLinkedIn Add to MendeleyMendeley Add to RedditReddit Add to StumbleUponStumbleUpon Add to TechnoratiTechnorati Add to TwitterTwitter What’s this?

« Previous | Next Article » Table of Contents This Article Published online before print March 31, 2011, doi: 10.1177/1362361310391116 Autism July 2011 vol. 15 no. 4 497-511 » Abstract Full Text (PDF) Podcast All Versions of this Article: current version image indicatorVersion of Record – Jul 21, 2011 1362361310391116v1 – Mar 31, 2011 What’s this? References Services Email this article to a colleague Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in PubMed Download to citation manager Request Permissions Request Reprints Load patientINFORMation Citing Articles Load citing article information Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Bölte, S. Articles by Holtmann, M. Search for related content PubMed PubMed citation Articles by Bölte, S. Articles by Holtmann, M. Related Content Load related web page information Share Add to CiteULikeCiteULike Add to ConnoteaConnotea Add to DeliciousDelicious Add to DiggDigg Add to FacebookFacebook Add to Google+Google+ Add to LinkedInLinkedIn Add to MendeleyMendeley Add to RedditReddit Add to StumbleUponStumbleUpon Add to TechnoratiTechnorati Add to TwitterTwitter What’s this?

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Synaptic Mutations Increase The Risk Of Autism Spectrum Disorders

Editor’s Choice
Academic Journal
Main Category: Autism
Also Included In: Neurology / Neuroscience;  Genetics
Article Date: 13 Feb 2012 – 10:00 PST

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A new study published in PLoS Genetics uses a combination of genetic and neurobiological approaches to confirm that synaptic mutations increase the risk of autism spectrum disorders (ASDs) and underlines the effect for modifier genes in these disorders.

ASDs, a heterogeneous group of neurodevelopmental disorders that have a complex inheritance pattern, appears before the age of three years and affects 1 in 100 children, with a higher risk for males than females. The disorder is characterized by impairments in social interaction and communication as well as by restricted and repetitive behavior. Scientists have identified several genes involved in ASD in those who have been diagnosed. However, understanding of their effects on neuronal functions and their interaction with other genetic variations has only recently been learnt.

In their new multi-center international study, Leblond and his collaborators detected mutations altering SHANK2, a gene that encodes a scaffolding protein located at synapses (contacts between neuronal cells). The researchers demonstrated that several of the observed mutations in patients decreased the number of synapses in neuronal cell cultures and a further genomic analysis of three patients with SHANK2 deletions revealed additional rare genomic imbalances that were previously linked to other neuropsychiatric disorders, which could act as modifier genes by modulating the disorder.

These findings highlight the significance of synaptic gene dysfunction in ASD and also underline the role for modifier genes, affirming a “multiple hit model” for ASD. Thomas Bourgeron, one of the study authors, concludes:

“A better knowledge of these genetic interactions will be necessary to understand the complex inheritance pattern of ASD.”

Written by Petra Rattue
Copyright: Medical News Today
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