TAG: "Autism"

Oxytocin shows promise for improving social skills in autistic mice


UCLA study could point way toward therapy for people with autism.

Daniel Geschwind, UCLA

By Mark Wheeler, UCLA

People with autism spectrum disorders have difficulty with social behavior and communication, which can make it challenging to form friendships, engage in routine conversations or pick up on the social cues that are second nature to most people. Similarly, mice with symptoms of autism show little interest in interacting or socializing with other mice.

A drug called risperidone has been shown to treat some symptoms of autism — including repetitive behaviors — in both humans and mice, but so far no medication has been found to help improve the ability to socialize.

In a study published online by the journal Science Translational Medicine, researchers at UCLA found that giving oxytocin to mice with autism-like symptoms restored their normal social behavior. Oxytocin is a neuropeptide, a type of molecule that helps neurons communicate with one another.

But perhaps the study’s biggest surprise was that early postnatal administration of the oxytocin led to longer-lasting positive effects, which continued into the animals’ adolescence and adulthood. “This suggests that there may be critical windows of time for treatment that are better than others,” said Daniel Geschwind, a UCLA professor of psychiatry, neurology and human genetics and senior author of the study.

In 2011, Geschwind and his colleagues developed a mouse model for autism spectrum disorders by knocking out a gene called contactin-associated protein-like 2, or CNTNAP2, which scientists believe plays an important role in the brain circuits responsible for language and speech. Previous research has linked common CNTNAP2 variants to a heightened risk for autism, while rare variants can lead to an inherited form of autism called cortical dysplasia-focal epilepsy syndrome.

“The oxytocin system is a key mediator of social behavior in mammals, including humans, for maternal behavior, mother–infant bonding, and social memory,” said Geschwind, who holds UCLA’s Gordon and Virginia MacDonald Distinguished Chair in Human Genetics and is the director of the Center for Autism Research and Treatment at the Semel Institute for Neuroscience and Human Behavior at UCLA. “So it seemed like a natural target for us to go after.”

The mice that were engineered for autism have fewer oxytocin neurons in the hypothalamus than other mice and lower-than-normal oxytocin levels throughout the brain. But after researchers treated them with oxytocin, the animals spent normal amounts of time interacting with other mice — the measure scientists used to gauge their sociability.

Separately, the researchers gave the mice melanocortin, an agonist that binds to specific receptors on a cell in order to activate it. They found that it caused a natural release of oxytocin from the mice’s brain cells, which also improved the mice’s sociability.

“The study shows that a primary deficit in oxytocin may cause the social problems in these mice, and that correcting this deficit can correct social behavior,” Geschwind said.

The next stage of the research, Geschwind said, will be to determine the lowest dosage of oxytocin that still proves effective. Because the mice in the study displayed symptoms similar to those of people on the autism spectrum, the researchers hope that this therapy may someday be applicable to humans.

The study was funded by the National Institute of Mental Health (R01 MH081754-02R, NIH/NS50220), the NIH Autism Centers of Excellence (HD055784-01 and 5R01-MH081754-04), the Simons Foundation Autism Research Initiative, Autism Speaks (7657), the NIH/National Institute of Neurological Disorders and Stroke (R01 NS049501 and R01 NS074312) and a McKnight Foundation Brain Disorders Award.

The study’s other authors were Olga Peñagarikano, María Lázaro, Xiao-Hong Lu, Hongmei Dong, Hoa Lam, Elior Peles, Nigel Maidment, Niall Murphy and X. William Yang, all of UCLA; Peyman Golshani of UCLA and the West Los Angeles V.A. Medical Center; and Aaron Gordon of Israel’s Weizmann Institute of Science.

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Century-old drug reverses autism-like symptoms


Suramin shows promise in fragile X mouse model.

By Scott LaFee, UC San Diego

Autism spectrum disorders (ASD) affect 1 to 2 percent of children in the United States. Hundreds of genetic and environmental factors have been shown to increase the risk of ASD. Researchers at UC San Diego School of Medicine previously reported that a drug used for almost a century to treat trypanosomiasis, or sleeping sickness, reversed environmental autism-like symptoms in mice.

Now, a new study published in this week’s online issue of Molecular Autism, suggests that a genetic form of autism-like symptoms in mice are also corrected with the drug, even when treatment was started in young adult mice.

The underlying mechanism, according to Robert K. Naviaux, M.D., Ph.D., the new study’s principal investigator and professor of medicine at UC San Diego, is a phenomenon he calls the cellular danger response (CDR). When cells are exposed to danger in the form of a virus, infection, toxin or even certain genetic mutations, they react defensively, shutting down ordinary activities and erecting barriers against the perceived threat. One consequence is that communication between cells is reduced, which the scientists say may interfere with brain development and function, leading to ASD.

Researchers treated a fragile X genetic mouse model, one of the most commonly studied mouse models of ASD, with suramin, a drug long used for sleeping sickness. The approach, called antipurinergic therapy or APT, blocked the CDR signal, allowing cells to restore normal communication and reversing ASD symptoms.

“Our data show that the efficacy of APT cuts across disease models in ASD. Both the environmental and genetic mouse models responded with a complete, or near complete, reversal of ASD symptoms,” Naviaux said. “APT seems to be a common denominator in improving social behavior and brain synaptic abnormalities in these ASD models.”

Weekly treatment with suramin in the fragile X genetic mouse model was started at 9 weeks of age, roughly equivalent to 18 years in humans. Metabolite analysis identified 20 biochemical pathways associated with symptom improvements, 17 of which have been reported in human ASD. The findings of the six-month study also support the hypothesis that disturbances in purinergic signaling – a regulator of cellular functions, and mitochondria (prime regulators of the CDR) – play a significant role in ASD.

Naviaux noted that suramin is not a drug that can be used for more than a few months without a risk of toxicity in humans. However, he said it is the first of its kind in a new class of drugs that may not need to be given chronically to produce beneficial effects. New antipurinergic medicines, he said, might be given once or intermittently to unblock metabolism, restore more normal neural network function, improve resilience and permit improved development in response to conventional, interdisciplinary therapies and natural play.

“Correcting abnormalities in a mouse is a long way from a cure in humans,” cautioned Naviaux, who is also co-director of the Mitochondrial and Metabolic Disease Center at UC San Diego, “but our study adds momentum to discoveries at the crossroads of genetics, metabolism, innate immunity, and the environment for several childhood chronic disorders. These crossroads represent new leads in our efforts to understand the origins of autism and to develop treatments for children and adults with ASD.”

Co-authors include Jane C. Naviaux, Lin Wang, Kefeng Li, A. Taylor Bright, William A. Alaynick, Kenneth R. Williams and Susan B. Powell, all at UC San Diego.

This study was supported, in part, by the Jane Botsford Johnson Foundation, the UC San Diego Christini Foundation, the UC San Diego Mitochondrial Research Fund, and the Wright Family Foundation.

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Expert in translating autism research into community practice joins UC Davis


Aubyn Stahmer, a licensed clinical psychologist, will be part of the MIND Institute.

Aubyn Stahmer, UC Davis

By Phyllis Brown, UC Davis

Aubyn Stahmer, an expert in the translation of evidence-based autism research to community-based practice and delivery, has joined the UC Davis MIND Institute as an associate professor in the Department of Psychiatry and Behavioral Sciences.

Stahmer, a licensed clinical psychologist, comes to UC Davis from UC San Diego, where she was research director of the Autism Discovery Institute at Rady Children’s Hospital, San Diego, and associate director of the Child and Adolescent Services Research Center.

“We evaluate how to take evidence-based interventions that are effective in research settings and make it possible to deliver them in settings where kids are getting usual care, in schools and early-intervention settings in the community,” Stahmer said.

She is an internationally respected expert in the use of naturalistic developmental behavioral interventions which are validated treatments for autism. Derived from developmental science and applied behavioral analysis (ABA), these interventions are play-based and child-initiated. Goals include the development of communication, language and positive social behaviors.

Stahmer is the principal investigator of two U.S. Department of Education grants designed to examine methods of translating research-based interventions in collaboration with community providers. One adapted model, called Classroom Pivotal Response Teaching, is for classroom use in children 3 to 11. Another, Project ImPACT for Toddlers, provides parent coaching for very young children at risk for autism. Stahmer will continue that research, which is based in public schools and early intervention programs, at the MIND Institute, potentially including Sacramento-area public school and community settings.

At Rady Children’s Hospital Stahmer operated a preschool program for children from 18 months to five years with autism in a setting that also included typically developing peers.

“Dr. Stahmer’s expertise and interests complement and enhance our established programs of research on evidence-based practices in autism treatment,” said Leonard Abbeduto, director of the MIND Institute. “She will extend the reach of the MIND Institute even further into our community, and so ensure we help even more families affected by autism.”

Stahmer said that she plans to work closely with Sally Rogers, professor of psychiatry and behavioral sciences and developer of the Early Start Denver Model (ESDM) approach to early autism intervention. Together they will examine methods of increasing access to evidence-based care to families of children with autism in rural and underserved areas.

“I am very excited to work with Dr. Rogers to examine new ways to increase access to ESDM in the community, both locally and internationally,” Stahmer said.

Rogers said she shares Stahmer’s enthusiasm.

“I am delighted to be able to work with such a wonderful scientist and clinician,” Rogers said. “Her research and expertise in moving interventions from the lab into the community will be a great help to all the intervention scientists at UC Davis.”

Stahmer received her bachelor’s degree from the University of Colorado, Boulder. She received her master’s and doctoral degrees from UC San Diego. She will receive an annual base salary of $126,800. Additional compensation information is available upon request.

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Multiple, short learning sessions strengthen memory formation in fragile X


UC Irvine study suggests the method could aid children with the autism-related condition.

Christine Gall and Gary Lynch found that fragile X model mice trained in three short, repetitious episodes spaced one hour apart performed as well on memory tests as normal mice. (Photo by Chris Nugent, UC Irvine)

By Tom Vasich, UC Irvine

A learning technique that maximizes the brain’s ability to make and store memories may help overcome cognitive issues seen in fragile X syndrome, a leading form of intellectual disability, according to UC Irvine neurobiologists.

Christine Gall, Gary Lynch and colleagues found that fragile X model mice trained in three short, repetitious episodes spaced one hour apart performed as well on memory tests as normal mice. These same fragile X rodents performed poorly on memory tests when trained in a single, prolonged session – which is a standard K-12 educational practice in the U.S.

“These results are dramatic and never seen before. Fragile X model mice trained using this method had memory scores equal to those of control animals,” said Gall, professor of anatomy & neurobiology and neurobiology & behavior. “Our findings suggest an easily implemented, noninvasive strategy for treating an important component of the cognitive problems found in patients with fragile X syndrome.”

Fragile X syndrome is an inherited genetic condition that causes intellectual and developmental disabilities and is commonly associated with autism. Symptoms include difficulty learning new skills or information.

It’s been known since classic 19th century educational psychology studies that people learn better when using multiple, short training episodes rather than one extended session.

Two years ago, the Lynch and Gall labs found out why. They discovered a biological mechanism that contributes to the enhancing effect of spaced training: Brain synapses – which are the connection points among neurons that transfer signals – encode memories in the hippocampus much better when activated briefly at one-hour intervals.

The researchers found that synapses have either low or high thresholds for learning-related modifications and that the high-threshold group requires hourlong delays between activation in order to store new information.

“This explains why prolonged ‘cramming’ is inefficient – only one set of synapses is being engaged,” said Lynch, professor of psychiatry & human behavior and anatomy & neurobiology. “Repeated short training sessions, spaced in time, engage multiple sets of synapses. It’s as if your brain is working at full power.”

The finding was significant, Gall added, because it demonstrated that a ubiquitous and fundamental feature of psychology can, at least in part, be explained by neurobiology.

It also gave the researchers time-sequencing rules for optimizing forms of learning dependent upon the hippocampus – utilized in the current study. Results appear in the Nov. 25 issue of Proceedings of the National Academy of Sciences.

The UCI scientists stress that the new brain-based training protocols, if applied during childhood, have the potential to offset many aspects of fragile X-related autism. “We believe that synaptic memory mechanisms are used during postnatal development to build functional brain circuits for dealing with confusing environments and social interactions,” Lynch said. “Implementing the brain-based rules during childhood training could result in lifelong benefits for patients.”

He and Gall look forward to collaborating with UCI’s Center for Autism Research & Translation to further evaluate the effect of multiple, short training episodes on learning in fragile X children.

Ronald Seese led the study as part of his work toward a Ph.D. and was assisted by Kathleen Wang and Yue Qin Yao. The research was funded by the National Science Foundation (grant 1146708), the National Institutes of Health (grants MH082042 and NS04260), and the William & Nancy Thompson Family Foundation, via UCI’s Center for Autism Research & Translation.

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Preeclampsia during mother’s pregnancy linked with greater autism risk


Likelihood of autism diagnosis even greater if mother experienced more severe disease.

By Phyllis Brown, UC Davis

Children with autism spectrum disorder (ASD) were more than twice as likely to have been exposed in utero to preeclampsia, and the likelihood of an autism diagnosis was even greater if the mother experienced more severe disease, a large study by researchers with the UC Davis MIND Institute has found.

Women with preeclampsia experience hypertension during the latter half of their pregnancies, and may have increased levels of protein in their urine and edema, or fluid retention. Preeclampsia can develop into eclampsia, a life-threatening condition in which seizures may occur.

The study was conducted in more than 1,000 children between the ages of 2 and 3 years enrolled in the Childhood Risks of Autism from Genetics and the Environment (CHARGE) study in Northern California. It is published online today in JAMA Pediatrics.

Cheryl Walker, UC Davis

“We found significant associations between preeclampsia and ASD that increased with severity. We also observed a significant association between severe preeclampsia and developmental delay,” said Cheryl Walker, study senior author, assistant professor, Department of Obstetrics and Gynecology Division of Maternal Fetal Medicine and a researcher affiliated with the UC Davis MIND Institute.

While preeclampsia has previously been examined as a risk factor for autism, the literature has been inconsistent. The current study provides a robust population-based, case-controlled examination of the association between autism and preeclampsia and whether risk was associated with preeclampsia severity.

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New genetic links in autism revealed


For answers, UC San Diego researchers turn to mice, stem cells and the ‘tooth fairy.’

Alysson Muotri, UC San Diego

With the help of mouse models, induced pluripotent stem cells (iPSCs) and the “tooth fairy,” researchers at the UC San Diego School of Medicine have implicated a new gene in idiopathic or non-syndromic autism. The gene is associated with Rett syndrome, a syndromic form of autism, suggesting that different types of autism spectrum disorder (ASD) may share similar molecular pathways.

The findings are published in today’s (Nov. 11) online issue of Molecular Psychiatry.

“I see this research as an example of what can be done for cases of non-syndromic autism, which lack a definitive group of identifying symptoms or characteristics,” said principal investigator Alysson Muotri, Ph.D., associate professor in the UC San Diego departments of pediatrics and cellular and molecular medicine. “One can take advantage of genomics to map all mutant genes in the patient and then use their own iPSCs to measure the impact of these mutations in relevant cell types. Moreover, the study of brain cells derived from these iPSCs can reveal potential therapeutic drugs tailored to the individual. It is the rise of personalized medicine for mental/neurological disorders.”

But to effectively exploit iPSCs as a diagnostic tool, Muotri said researchers “need to compare neurons derived from hundreds or thousands of other autistic individuals.” Enter the “Tooth Fairy Project,” in which parents are encouraged to register for a “Fairy Tooth Kit,” which involves sending researchers like Muotri a discarded baby tooth from their autistic child. Scientists extract dental pulp cells from the tooth and differentiate them into iPSC-derived neurons for study.

“There is an interesting story behind every single tooth that arrives in the lab,” said Muotri.

The latest findings, in fact, are the result of Muotri’s first tooth fairy donor. He and colleagues identified a de novo or new disruption in one of the two copies of the TRPC6 gene in iPSC-derived neurons of a non-syndromic autistic child. They confirmed with mouse models that mutations in TRPC6 resulted in altered neuronal development, morphology and function. They also noted that the damaging effects of reduced TRPC6 could be rectified with a treatment of hyperforin, a TRPC6-specific agonist that acts by stimulating the functional TRPC6 in neurons, suggesting a potential drug therapy for some ASD patients.

The researchers also found that MeCP2 levels affect TRPC6 expression. Mutations in the gene MeCP2, which encodes for a protein vital to the normal function of nerve cells, cause Rett syndrome, revealing common pathways among ASD.

“Taken together, these findings suggest that TRPC6 is a novel predisposing gene for ASD that may act in a multiple-hit model,” Muotri said. “This is the first study to use iPSC-derived human neurons to model non-syndromic ASD and illustrate the potential of modeling genetically complex sporadic diseases using such cells.”

For more information on the Tooth Fairy Project, visit http://muotri.ucsd.edu.

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Study: Dozens of genes associated with autism


Functions of newly identified genes converge on a few important biological processes.

Two major genetic studies of autism, led in part by UC San Francisco scientists and involving more than 50 laboratories worldwide, have newly implicated dozens of genes in the disorder. The research shows that rare mutations in these genes affect communication networks in the brain and compromise fundamental biological mechanisms that govern whether, when, and how genes are activated overall.

The two new studies, published in the advance online edition of Nature today (Oct. 29), tied mutations in more than 100 genes to autism. Sixty of these genes met a “high-confidence” threshold indicating that there is a greater than 90 percent chance that mutations in those genes contribute to autism risk.

The majority of the mutations identified in the new studies are de novo (Latin for “afresh”) mutations, meaning they are not present in unaffected parents’ genomes but arise spontaneously in a single sperm or egg cell just prior to conception of a child.

The genes implicated in the new studies fall into three broad classes: they are involved in the formation and function of synapses, which are sites of nerve-cell communication in the brain; they regulate, via a process called transcription, how the instructions in other genes are relayed to the protein-making machinery in cells; and they affect how DNA is wound up and packed into cells in a structure known as chromatin. Because modifications of chromatin structure are known to lead to changes in how genes are expressed, mutations that alter chromatin, like those that affect transcription, would be expected to affect the activity of many genes.

One of the new Nature studies made use of data from the Simons Simplex Collection (SSC), a permanent repository of DNA samples from nearly 3,000 families created by the Simons Foundation Autism Research Initiative. Each SSC family has one child affected with autism, parents unaffected by the disorder and, in a large proportion, unaffected siblings. The second study was conducted under the auspices of the Autism Sequencing Consortium (ASC), an initiative supported by the National Institute of Mental Health that allows scientists from around the world to collaborate on large genomic studies that couldn’t be done by individual labs.

“Before these studies, only 11 autism genes had been identified with high confidence, and we have now more than quadrupled that number,” said Stephan Sanders, Ph.D., assistant professor of psychiatry at UCSF, co-first author on the SSC study, and co-author on the ASC study. Based on recent trends, Sanders estimates that gene discovery will continue at a quickening pace, with as many as 1,000 genes ultimately associated with autism risk.

“There has been a lot of concern that 1,000 genes means 1,000 different treatments, but I think the news is much brighter than that,” said Matthew W. State, M.D., Ph.D., chair and Oberndorf Family Distinguished Professor in Psychiatry at UCSF. State was co-leader of the Nature study focusing on the SSC and a senior participant in the study organized by the ASC, of which he is a co-founder. ”There is already strong evidence that these mutations converge on a much smaller number key biological functions. We now need to focus on these points of convergence to begin to develop novel treatments.”

Autism, which is marked by deficits in social interaction and language development, as well as by repetitive behaviors and restricted interests, is known to have a strong genetic component. But until a few years ago, genomic research had failed to decisively associate individual genes with the disorder.

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Why are some people with autism hypersensitive to sound?


UC Riverside researchers embark on five-year NIH-funded project.

(From left) Khaleel Razak, Iryna Ethell and Devin Binder. The three researchers are leading a team that will study the mechanisms of auditory hypersensitivity in fragile X syndrome. (Photo by Lille Bose, UC Riverside)

Fragile X syndrome (FXS) is a genetic disorder in humans that causes social impairments and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of intellectual disability and the most common cause of autism.

One aspect of FXS worthy of more research is auditory hypersensitivity – an increased sensitivity to sound through a negative emotional response, resulting in behaviors such as closing the ears with the hands or running away from the sound source. People with FXS also are slow to adapt to constant repetitious sounds in our environment. These hypersensitivity deficits may lead to higher-level auditory deficits such as those involving language.

UC Riverside has received a grant from the National Institutes of Health (NIH) to study the mechanisms of auditory hypersensitivity in FXS from molecules to circuits to therapies.

The five-year $8.7 million grant is awarded to UC Riverside and the University of Texas Southwestern (UTSW) Medical Center, Dallas. UCR will receive approximately $2.7 million of the grant over five years.

NIH recently awarded a total of $35 million to three different centers in the United States to study FXS, allowing the establishment of “Centers for Collaborative Research in FXS.” The UTSW-UCR collaboration is one of the three centers.

The UCR team is being led by Khaleel Razak, an associate professor of psychology; and the School of Medicine’s Iryna Ethell, a professor of biomedical sciences, and Devin Binder, an associate professor of biomedical sciences. The team came together for the project through a collaborative seed grant provided by the Office of Research and Economic Development at UCR and a pilot grant from the FRAXA Research Foundation.

FXS affects 1 in 4,000 boys and is half as prevalent in girls. Symptoms include social and communication deficits, seizures, delayed language development and sensory hypersensitivity.  Despite the prevalence of FXS and the known genetic cause, a cure is yet to be discovered.

“Two recent clinical trials of drugs were suspended because the drugs performed similar to the placebo on outcome measures,” Razak said. “There is, therefore, an urgent need to develop new therapeutic targets and appropriate biomarkers and outcome measures in which the underlying neural mechanism is known at multiple levels of analyses.”

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Moms of kids with autism less likely to take iron supplements while pregnant


First study to examine relationship between maternal iron intake, having a child with autism.

Mothers of children with autism are significantly less likely to report taking iron supplements before and during their pregnancies than the mothers of children who are developing normally, a study by researchers with the UC Davis MIND Institute has found.

Low iron intake was associated with a fivefold greater risk of autism in the child if the mother was 35 or older at the time of the child’s birth or if she suffered from metabolic conditions such as obesity hypertension or diabetes.

The research is the first to examine the relationship between maternal iron intake and having a child with autism spectrum disorder, the authors said. The study, “Maternal intake of supplemental iron and risk for autism spectrum disorders,” is published online in the American Journal of Epidemiology.

Rebecca Schmidt, UC Davis

“The association between lower maternal iron intake and increased ASD risk was strongest during breastfeeding, after adjustment for folic acid intake,” said Rebecca J. Schmidt, assistant professor in the Department of Public Health Sciences and a researcher affiliated with the MIND Institute.

The authors of the current study in 2011 were the first to report associations between supplemental folic acid and reduced risk for autism spectrum disorder, a finding later replicated in larger scale investigations.

“Further, the risk associated with low maternal iron intake was much greater when the mother was also older and had metabolic conditions during her pregnancy.”

The study was conducted in mother-child pairs enrolled in the Northern California-based Childhood Autism Risks from Genetics and the Environment (CHARGE) Study between 2002 and 2009. The participants included mothers of children with autism and mothers of children with typical development.

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Autism early-detection program expands


Developed at UC San Diego, effort seeks to identify at-risk toddlers by first birthday.

Karen Pierce, UC San Diego

Autism spectrum disorder (ASD) is now estimated to impact 1 in every 68 children born in the United States. Yet despite its rising prevalence and the known benefits of early detection and treatment, toddlers in much of the United States are routinely not identified as possibly having ASD until well after their third birthday.

“By that time, much precious brain development has already occurred,” said Karen Pierce, Ph.D., associate professor of neurosciences at the UC San Diego School of Medicine and assistant director of the UC San Diego Autism Center of Excellence.

A new 5-year, $5.1 million grant from the National Institute of Mental Health (NIMH) seeks to remedy that by expanding a program developed by Pierce and colleagues to reduce the mean age of ASD diagnosis in multiple cities across the U.S.

The program, called Get SET Early, is based upon a one-year well-baby check that Pierce first described in a paper published in 2011. In those findings, Pierce and colleagues reported that San Diego toddlers who were systematically assessed for ASD around their first birthday typically began receiving treatment within a few months, years before children in many other cities.

With NIMH funding, the Get SET Early program expands upon Pierce’s original model, adding new features and technologies, such as an iPad-based automatic referral system.

The improved model consists of three stages: In the Screening stage, a network of pediatricians conduct repeat evaluations of toddlers at multiple ages – 12, 18 and 24 months – using standardized testing and scoring. “Since the symptoms of autism can come on slowly between 12 and 24 months, if we screen three times, we are almost guaranteed to detect the overwhelming majority of children with this disorder,” Pierce said.

In the second Evaluation stage, toddlers who may have ASD are immediately referred to local clinics that specialize in ASD for more detailed evaluation.

In the final stage, Treatment, toddlers showing clear signs of ASD are referred to an established network of health care specialists for rapid treatment. “There is evidence that early therapy can have a positive impact on the developing brain,” Pierce said. “The opportunity to diagnose and thus begin treatment for autism around a child’s first birthday has enormous potential to change outcomes for children affected with the disorder.”

The Get SET Early program will expand first to Phoenix, which has one of the oldest average ages of ASD detection in the country. A recent survey conducted by the U.S. Centers for Disease Control found that children with autism living in Phoenix were typically not identified until they were almost 5 years old.

In her 2011 study, published in the Journal of Pediatrics, Pierce and colleagues created a network of 137 pediatricians in the San Diego region and asked them to include a brief assessment at the toddlers’ traditional one-year health checkup. The assessment consisted of parents or caregivers answering a questionnaire called the Communication and Symbolic Behavior Scales Developmental Profile Infant-Toddler Checklist that queried about a child’s use of eye contact, sounds, words, gestures, object recognition and other forms of age-appropriate communication. Any infant who failed the screening was referred to the UC San Diego Autism Center of Excellence for further testing and re-evaluation every six months until age three.

While the NIMH grant will initially test the feasibility of establishing the Get SET Early model in Phoenix, research and testing will also continue in San Diego to assess the efficacy of new improvements, such as repeat triple screenings and Internet-based tracking of referrals and treatment.

“By creating a simple screening, evaluation and treatment initiation and tracking model, we hope to establish national standards so that one day ASD detection and treatment between the first and second birthday will happen for all children,” said Pierce.

Funding for this work comes from the National Institutes of Health and NIMH (grant R01 MH104446-01).

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UC Irvine autism center names executive director


Catherine Brock to spearhead efforts to bring help and hope to patients and families.

Catherine Brock, UC Irvine (Photo by Steve Zylius, UC Irvine)

Catherine M. Brock, a highly regarded clinical and administrative leader in the field of autism spectrum disorders, will become executive director of The Center for Autism & Neurodevelopmental Disorders as of Sept. 15.

Brock will be responsible for overall management of the center, and she’ll focus on positioning it as a center of excellence in the U.S. for clinical care, community engagement and research.

The center is a collaboration of the UC Irvine School of Medicine, CHOC Children’s Hospital, Chapman University’s College of Educational Studies, the Children & Families Commission of Orange County, and the William & Nancy Thompson Family Foundation.

Utilizing an innovative and integrated approach, the center provides assessment, diagnosis, treatment, care coordination, family support and education for children, teens and young adults with autism and other developmental disorders. It’s one of only a few centers in the region to deliver a continuum of support and services until age 22 and to conduct research focused on transforming autism care and treatment.

“I have a clear mission to spearhead The Center for Autism’s efforts to provide help and hope to individuals and families living with autism and neurodevelopmental disorders,” Brock said. “The center comprises world-class clinicians, researchers and practitioners who are completely dedicated to having a meaningful impact on the lives of those here in the community whom we serve, and I am honored to partner with my new colleagues to lead our efforts forward.”

Brock has 20 years of experience in operations and with the treatment of autism. She most recently was associate director of the University of Washington Autism Center, where her responsibilities included operations, administration and clinical leadership. With a master’s degree in clinical psychology from Antioch University Seattle and more than a decade in practice as a licensed mental health counselor, Brock has deep knowledge of autism and possesses the understanding and expertise necessary to forge strong relationships with patients and their families.

“Cathy is a seasoned, highly talented and passionate professional who will be a catalyst and create synergies among the five founding partner organizations and our affiliated UCI research group, the Center for Autism Research & Translation,” said Don Cardinal, chair of the center’s advisory board. “She has an ideal combination of skills, experience and expertise in autism to drive our efforts forward, and our community will be well served by her leadership.”

The center is at 2500 Red Hill Ave. in Santa Ana.

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Treating babies for autism may stave off symptoms


Infant Start therapy treats disabling delays before most kids are diagnosed with autism.

Sally Rogers, UC Davis

Treatment at the earliest age when symptoms of autism spectrum disorder (ASD) appear – sometimes in infants as young as 6 months old – significantly reduces symptoms so that, by age 3, most who received the therapy had neither ASD nor developmental delay, a UC Davis MIND Institute research study has found.

The treatment, known as Infant Start, was administered over a six-month period to 6- to 15-month-old infants who exhibited marked autism symptoms, such as decreased eye contact, social interest or engagement, repetitive movement patterns and a lack of intentional communication. It was delivered by the people who were most in tune with and spent the most time with the babies: their parents.

“Autism treatment in the first year of life: A pilot study of Infant Start, a parent-implemented intervention for symptomatic infants,” is co-authored by UC Davis professors of Psychiatry and Behavioral Sciences Sally J. Rogers and Sally Ozonoff. It is published online today (Sept. 9) in the Journal of Autism and Developmental Disorders.

“Most of the children in the study, six out of seven, caught up in all of their learning skills and their language by the time they were 2 to 3,” said Rogers, the study’s lead author and the developer of the Infant Start therapy. “Most children with ASD are barely even getting diagnosed by then.”

“For the children who are achieving typical developmental rates, we are essentially ameliorating their developmental delays,” Rogers said. “We have speeded up their developmental rates and profiles, not for every child in our sample, but for six of the seven.”

Rogers credited the parents in the small, pilot study with making the difference.

“It was the parents – not therapists – who did that,” she said. “Parents are there every day with their babies. It’s the little moments of diapering, feeding, playing on the floor, going for a walk, being on a swing, that are the critical learning moments for babies. Those moments are what parents can capitalize on in a way that nobody else really can.”

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