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When children behave badly, it’s easy to blame their parents. Sometimes, however, such behavior may be due to a mental disorder.

Mental illnesses are the No. 1 cause of medical disability in youths ages 15 and older in the United States and Canada, according to the World Health Organization.

“One reason we haven’t made greater progress helping people recover from mental disorders is that we get on the scene too late,” said Thomas R. Insel, MD, director of the National Institute of Mental Health (NIMH) and the featured speaker at the American Academy of Pediatrics’ Presidential Plenary during the Pediatric Academic Societies (PAS) annual meeting in Boston.

Dr. Insel discussed signs of mental illnesses in young children and the importance of early diagnosis and intervention in his presentation, “What Every Pediatrician Needs to Know about Mental Disorders,” in the Hynes Convention Center.

As the first line of defense, pediatricians can detect mental disorders early and ensure children get treatment as soon as possible, Dr. Insel said. While questionnaires currently are the best way for doctors to screen for mental illness, better tools are on the horizon, such as cognitive and genetic tests.

It’s also important to understand that mental illnesses are a developmental brain disorder even though they can look like behavior problems, Dr. Insel explained.

“The future of mental illness has to be at the point where we aren’t treating behavior separately from the rest of the person,” he said. “There needs to be full integration of behavior and medical concerns to ensure that we are able to care for the whole person and not just one system.”

In addition to serving as director of the NIMH, Dr. Insel is acting director of the National Center for Advancing Translational Sciences, a new arm of the National Institutes of Health that aims to accelerate the development of diagnostics and therapeutics.

Autism also is an area of interest for Dr. Insel. He chairs the Interagency Autism Coordinating Committee for the U.S. Department of Health and Human Services. Prior to joining NIMH, he was director of the Center for Autism Research and professor of psychiatry at Emory University, where he was the founding director of the Center for Behavioral Neuroscience.

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Exams Tests and Places to Get Help For Those With Asperger’s Syndrome

The doctor will take a medical history and ask questions regarding the child’s development including his or her motor development, language development, and any special interests that the child has expressed.

Making the diagnosis of Asperger’s Syndrome is difficult and takes the input of doctors, teachers, parents and other caregivers in order to make the diagnosis. There are specific criteria that need to be met in order to make the diagnosis of Asperger’s Syndrome including poor social interaction, unusual behavior, obsessive interests, and activities, normal language development, and normal self-help skills and curiosity about the surrounding environment.

The doctor will take a medical history and ask questions regarding the child’s development including his or her motor development, language development, and any special interests that the child has expressed. Social interactions will be noted and a history of the pregnancy and any family medical history or medical conditions will also be ascertained.

Exams and tests will be performed to help determine if Asperger’s syndrome is the correct diagnosis for your child.

Testing will probably include a Psychological Assessment, a communication assessment, and a psychiatric examination. The psychological assessment will look at intellectual function, learning style and intelligence quotient (IQ) as well as an assessment of motor skills. Personality assessment tests may also be performed. The communication assessment involves speech and formal language evaluations where the child will be tested to see how well they understand the use of language and how to communicate ideas. The child will also be tested regarding the ability to understand non-verbal communication and nonliteral language skills, such as humor or metaphor. The child’s voice regarding volume, stress, and pitch will be evaluated.

The psychiatric examination will include the child’s family, peer relationships, reactions to new encounters and the ability to understand and respond to the feelings of others, and also the ability to interpret indirect communication such as sarcasm or teasing. Your child may be observed at home and at school. Signs of conditions such as anxiety and depression will be watched for during observations. Medical personnel will be looking for signs of compliance with the criteria set for Asperger’s Syndrome in the Diagnostic and Statistical Manual of Mental Disorders, which is a publication of the American Psychiatric Association and used to be a standard for diagnosing Asperger’s Syndrome and other Mental Disorders.

Many times a child is misdiagnosed with other conditions prior to be correctly diagnosed with Asperger’s Syndrome. Like most diseases and conditions it is often necessary to rule out other conditions and disorders when making a determination of a diagnosis. It is often a team effort that involves doctors, parents, teachers, psychiatrists, and others who have observed the behavior and communicative abilities of the child.

Places to get help for those with Asperger’s Syndrome:

There are many resources available to gather information concerning Asperger’s Syndrome online and offline.

Online you can find information by going to Aspergerinfo.com or to the Online Asperger Syndrome Information and Support Website located at:

http://www.udel.edu/bkirby/asperger/

Other organizations that can give support and information about Asperger’s Syndrome are:

Global and Regional Asperger Syndrome Partnership located in New York, USA and also online at:

http://www.grasp.org/

Families of Adults Afflicted with Asperger’s Syndrome (FAAAS) located in Centerville, MA USA and on the Web at:

http://www.faaas.org/

MAAP Services for Autism and Asperger Syndrome located in Crown Point Indiana and on the Web at:

http://www.maapservices.org

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Scientists at the Gladstone Institutes have unraveled a process by which depletion of a specific protein in the brain contributes to the memory problems associated with Alzheimer’s disease. These findings provide new insights into the disease’s development and may lead to new therapies that could benefit the millions of people worldwide suffering from Alzheimer’s and other devastating neurological disorders.

The study, led by Gladstone Investigator Jorge J. Palop, PhD, revealed that low levels of a protein, called Nav1.1, disrupt the electrical activity between brain cells. Such activity is crucial for healthy brain function and memory. Indeed, the researchers found that restoring Nav1.1 levels in mice that were genetically modified to mimic key aspects of Alzheimer’s disease (AD-mice) improved learning and memory functions and increased their lifespan. They report their findings in Cell, available online.

“It is estimated that more than 30 million people worldwide suffer from Alzheimer’s disease and that number is expected to rise dramatically in the near future,” said Lennart Mucke, MD, who directs neurological research at Gladstone, an independent and nonprofit biomedical-research organization. “This research improves our understanding of the biological processes that underlie cognitive dysfunction in this disease and could open the door for new therapeutic interventions.”

The researchers’ findings suggest that Nav1.1 levels in special regulatory nerve cells called parvalbumin cells, or PV cells, are essential to generate healthy brain-wave activity – and that problems in this process contribute to cognitive decline in AD-mice and possibly in patients with Alzheimer’s.

In the brain, neurons form highly interconnected networks, using chemical and electrical signals to communicate with each other. The researchers investigated whether this communication between neurons is disrupted in AD-mice, and if so, how this may affect the symptoms of Alzheimer’s disease.

To study this, they performed electroencephalogram (EEG) recordings – a technique that detects abnormalities in the brain’s electrical waves such as those found in patients with epilepsy. They found that similar abnormalities emerged during periods of reduced gamma-wave oscillations – a type of brain wave that is crucial to regulating learning and memory.

“Like a conductor in an orchestra, PV cells regulate brain rhythms by precisely controlling excitatory brain activity,” said Laure Verret, PhD, postdoctoral fellow and lead author. “We found that PV cells in patients with Alzheimer’s and in AD-mice have low levels of the protein Nav1.1 – likely contributing to PV cell dysfunction. As a consequence, AD-mice had abnormal brain rhythms. By restoring Nav1.1 levels, we were able to re-establish normal brain function.”

Indeed, the scientists found that increasing Nav1.1 levels in PV cells improves brain wave activity, learning, memory and survival rates in AD-mice.

“Enhancing Nav1.1 activity, and consequently improving PV cell function, may help in the treatment of Alzheimer’s disease and other neurological disorders associated with gamma-wave alterations and cognitive impairments such as epilepsy, autism and schizophrenia,” said Dr. Palop, who is also an assistant professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. “These findings may allow us to develop therapies to help patients with these devastating diseases.”

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Autism has a strong genetic basis, but so far efforts to identify the responsible genes have had mixed results. The reason for this is that autism is influenced by many different genes, and different genes are involved in different individuals, making it hard to find the common genetic ground between patients.

Now, research conducted at the Hebrew University of Jerusalem has shown that despite this fact, the different genes involved in autism tend to be involved in specific processes in the brain. This can explain, on the one hand, similarities in the behavioral symptoms of different autistics, but also the large spectrum of behaviors observed in different autistic individuals.

The Hebrew University research, conducted by Dr. Sagiv Shifman and his doctoral student Eyal Ben-David of the Department of Genetics at the Alexander Silberman Institute of Life Sciences, has potential implications for early diagnosis as well as for treatment of autism in the future. The study was recently published in the journal PLoS Genetics.

Autism spectrum disorders are neurodevelopmental syndromes characterized by social deficits, language impairments and repetitive behaviors. Recent studies indicate that autism is considerably more common than previously supposed, with a prevalence rate that is high as 1% in some regions.

The main goal of the Hebrew University project was to test the contribution of rare genetic mutations, as well as the genetic variations which are common in the population, and to see whether these different types of genetic risk factors are related. Instead of testing individual genes, the researchers chose to study gene collections, in an attempt to understand general pathways involved in autism.

To that end the scientists constructed a network based on the expression pattern of genes across different brain areas. This allowed them to discover groups of genes with shared function in the brain. Next, based on genetic data from thousands of families with autistic children, the researchers studied the contribution of different groups of genes to autism.

To their surprise, they found — when looking at mutations found in autism as well as thousands of common gene variants that are more frequently seen in autistics — that these mutations and variations are located in specific functional groups.

When looking at families with one autistic individual (sporadic cases), and in families where there is more than one affected individual (multiplex cases), the same variants were seen acting in both cases. These groups of genes are highly active in the first year of life, and are involved in processes of learning, memory, and sensory perception.

The Hebrew University scientists believe that their work could pave the way for large-scale genetic scans in the future that could allow for early diagnosis of autism. Further, the results of their study provide a ray of hope that by concentrating on specific gene groups, it will one day be possible to design drugs which could alleviate symptoms.

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A team of scientists from Johns Hopkins and elsewhere have developed nano-devices that successfully cross the blood-Brain barrier and deliver a drug that tames brain-damaging inflammation in rabbits with cerebral palsy.

A report on the experiments, conducted at Wayne State University in collaboration with the Perinatology Research Branch of the National Institute of Child Health and Human Development, before the lead and senior investigators moved to Johns Hopkins, is published in Science Translational Medicine.

For the study, researchers used tiny, manmade molecules laced with N-acetyl-L-cysteine (NAC), an anti-inflammatory drug used as antidote in acetaminophen poisoning. The researchers precision-targeted brain cells gone awry to halt brain injury. In doing so they improved the animals’ neurologic function and motor skills.

The new approach holds therapeutic potential for a wide variety of neurologic disorders in humans that stem from neuro-inflammation, including Alzheimer’s disease, stroke, autism and multiple sclerosis, the investigators say.

The scientists caution that the findings are a long way from human application, but that the simplicity and versatility of the drug-delivery system make it an ideal candidate for translation into clinical use.

“In crossing the blood-brain barrier and targeting the cells responsible for inflammation and brain injury, we believe we may have opened the door to new therapies for a wide-variety of neurologic disorders that stem from an inflammatory response gone haywire,” says lead investigator Sujatha Kannan, M.D., now a pediatric critical-care specialist at Johns Hopkins Children’s Center.

Cerebral palsy (CP), estimated to occur in three out of 1,000 newborns, is a lifelong, often devastating disorder caused by infection or reduced oxygen to the brain before, during or immediately after birth. Current therapies focus on assuaging symptoms and improving quality of life, but can neither reduce nor reverse neurologic damage and loss of motor function.

Neuro-inflammatory damage occurs when two types of brain cells called microglia and astrocytes – normally deployed to protect the brain during infection and inflammation – actually damage it by going into overdrive and destroying healthy brain cells along with damaged ones. Directly treating cells in the brain has long proven difficult because of the biological and physiological systems that have evolved to protect the brain from blood-borne infections. The quest to deliver the drug to the brain also involved developing a technique to get past the brain-blood barrier, spare healthy brain cells and deliver the anti-inflammatory drug exclusively inside the rogue cells.

To do all this, the scientists used a globular, tree-like synthetic molecule, known as a dendrimer. Its size – 2,000 times smaller than a red blood cell – renders it fit for travel across the blood-brain barrier. Moreover, the dendrimer’s tree-like structure allowed scientists to attach to it molecules of an anti-inflammatory NAC. The researchers tagged the drug-laced dendrimers with fluorescent tracers to monitor their journey to the brain and injected them into rabbits with cerebral palsy six hours after birth. Another group of newborn rabbits received an injection of NAC only.

Not only did the drug-loaded dendrimers make their way inside the brain but, once there, were rapidly swallowed by the overactive astrocytes and microglia.

“These rampant inflammatory cells, in effect, gobbled up their own poison,” Kannan says.

“The dendrimers not only successfully crossed the blood-brain barrier but, perhaps more importantly, zeroed in on the very cells responsible for neuro-inflammation, releasing the therapeutic drug directly into them,” says senior investigator Rangaramanujam Kannan, Ph.D., of the Center for Nanomedicine at the Johns Hopkins Wilmer Eye Institute.

Animals treated with dendrimer-borne NAC showed marked improvement in motor control and coordination within five days after birth, nearly reaching the motor skill of healthy rabbits. By comparison, rabbits treated with dendrimer-free NAC showed minimal, if any, improvement, even at doses 10 times higher than the dendrimer-borne version. Animals treated with the dendrimer-delivered drug also showed better muscle tone and less stiffness in the hind leg muscles, both hallmarks of CP.

Brain tissue analysis revealed that rabbits treated with dendrimer-borne NAC had notably fewer “bad” microglia – the inflammatory cells responsible for brain damage – as well as markedly lower levels of other inflammation markers. They also had better preserved myelin, the protein that sheaths nerves and is stripped or damaged in CP and other neurologic disorders. And even though CP is marked by neuron death in certain brain centers, animals who received dendrimer-borne NAC had higher number of neurons in the brain regions responsible for coordination and motor control, compared with untreated animals and those treated with NAC only.

The findings suggest that the treatment not only reduces inflammation in the cells, but may also prevent cell damage and cell death, the researchers said. The Kannans, who are married, say they plan to follow some treated animals into adulthood to ensure the improvements are not temporary.

A separate study, led by Rangaramanujam Kannan, has already demonstrated the therapeutic benefits of this approach in reversing retinal damage in rats with macular degeneration, the vision-robbing eye disorder that affects millions of older adults.

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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.

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An editorial published in the prestigious journal Environmental Health Perspectives calls for increased research to identify possible environmental causes of autism and other neurodevelopmental disorders in America’s children and presents a list of ten target chemicals including which are considered highly likely to contribute to these conditions.

Philip Landrigan, MD, MSc, a world-renowned leader in children’s environmental health and Director of the Children’s Environmental Health Center (CEHC) at Mount Sinai School of Medicine, co-authored the editorial, entitled “A Research Strategy to Discover the Environmental Causes of Autism and Neurodevelopmental Disabilities,” along with Luca Lambertini, PhD, MPH, MSc, Assistant Professor of Preventive Medicine at Mount Sinai and Linda Birnbaum, Director of the National Institute OF Environmental Health Sciences.

The editorial was published alongside four other papers – each suggesting a link between toxic chemicals and autism. Both the editorial and the papers originated at a conference hosted by CEHC in December 2010.

The National Academy of Sciences reports that 3 percent of all neurobehavioral disorders in children, such as autism spectrum disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD), are caused by toxic exposures in the environment and that another 25 percent are caused by interactions between environmental factors and genetics. But the precise environmental causes are not yet known. While genetic research has demonstrated that ASD and certain other neurodevelopmental disorders have a strong hereditary component, many believe that environmental causes may also play a role – and Mount Sinai is leading an effort to understand the role of these toxins in a condition that now affects between 400,000 and 600,000 of the 4 million children born in the United States each year.

“A large number of the chemicals in widest use have not undergone even minimal assessment of potential toxicity and this is of great concern,” says Dr. Landrigan. “Knowledge of environmental causes of neurodevelopmental disorders is critically important because they are potentially preventable.”

CEHC developed the list of ten chemicals found in consumer products that are suspected to contribute to autism and learning disabilities to guide a research strategy to discover potentially preventable environmental causes. The top ten chemicals are: Lead Methylmercury PCBs Organophosphate pesticides Organochlorine pesticides Endocrine disruptors Automotive exhaust Polycyclic aromatic hydrocarbons Brominated flame retardants Perfluorinated compounds In addition to the editorial, the other four papers also call for increased research to identify the possible environmental causes of autism in America’s children. The first paper, written by a team at the University of Wisconsin – Milwaukee, found preliminary evidence linking smoking during pregnancy to Asperger’s disorder and other forms of high-functioning autism. Two papers, written by researchers at the University of California – Davis, show that PCBs disrupt early brain development. The final paper, also by a team at UC – Davis, suggests further exploring the link between pesticide exposure and autism. 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. Please use one of the following formats to cite this article in your essay, paper or report:

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In a study published in the May 2012 issue of the Journal of the American Academy of Child and Adolescent Psychiatry, led by Mr. Sven Sandin, of the Karolinska Institutet, Sweden and King’s College London, researchers analyzed past studies to investigate possible associations between maternal age and autism. While much research has been done to identify potential genetic causes of autism, this analysis suggests that non-heritable and environmental factors may also play a role in children’s risk for autism.

The researchers compared the risk of autism in different groups of material age (under 20, 24-29, 30-34, and 35+). They found that children of mothers older than 35 years had 30% increased risk for autism. Children of mothers under 20 had the lowest risk of developing autism. The association between advancing maternal age and risk for autism was stronger for male offspring and children diagnosed in more recent years.

The analysis included 25,687 cases of autism spectrum disorder and over 8.6 million control subjects, drawn from the 16 epidemiological papers that fit inclusion criteria for the study as defined by the investigators. The researchers identified and discussed several potential underlying causes of the association between maternal age and risk for autism such as increased occurrence of gene alteration during the aging process and the effects of exposure to environmental toxins over time.

Sandin said of the study, “The study makes us confident there is an increased risk for autism associated with older maternal age, even though we do not know what the mechanism is. It has been observed in high quality studies from different countries, including the US. All studies controlled for paternal age which is an independent risk factor for autism. This finding adds to the understanding that older age of the parents could have consequences to the health of their children.”

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Women who smoke in pregnancy may be more likely to have a child with high-functioning autism, such as Asperger’s Disorder, according to preliminary findings from a study by researchers involved in the U.S. autism surveillance program of the Centers for Disease Control and Prevention.

“It has long been known that autism is an umbrella term for a wide range of disorders that impair social and communication skills,” says Amy Kalkbrenner, assistant professor in the University of Wisconsin-Milwaukee’s Joseph J. Zilber School of Public Health, lead author of the study. “What we are seeing is that some disorders on the autism spectrum, more than others, may be influenced by a factor such as whether a mother smokes during pregnancy.”

The study was published in an advance online release by the journal Environmental Health Perspectives.

Smoking during pregnancy is still common in the U.S. despite its known harmful impacts on babies. Kalkbrenner found that 13 percent of mothers whose children were included in the study had smoked during pregnancy.

Kalkbrenner and colleagues’ population-based study compared smoking data from birth certificates of thousands of children from 11 states to a database of children diagnosed with autism maintained by the CDC’s Autism and Developmental Disabilities Monitoring Network (ADDMN). Of the 633,989 children, born in 1992, 1994, 1996 and 1998, 3,315 were identified as having an autism spectrum disorder at age 8.

“The study doesn’t say for certain that smoking is a risk factor for autism,” Kalkbrenner says. “But it does say that if there is an association, it’s between smoking and certain types of autism,” implicating the disorders on the autism spectrum that are less severe and allow children to function at a higher level. That connection, she adds, needs further study.

April is Autism Awareness Month, and several studies of possible links between environmental factors and autism are being published by Environmental Health Perspectives at the same time as Kalkbrenner’s study. “The CDC recently released data indicating that 1 in 88 children has an autism spectrum disorder, making such environmental studies even more timely,” says Kalkbrenner.

Because autism involves a broad spectrum of conditions and the interplay of genetics and environment is so complex, no one study can explain all the causes of autism, she adds. “The goal of this work is to help provide a piece of the puzzle. And in this we were successful.”

Other research articles published in Environmental Health Perspectives show that polychlorinated biphenyls disrupt early brain development by interfering with the signals that promote normal neuron branching. A review article suggests research directions for exploring a potential link between pesticides and autism. An editorial calls for increased discovery research to identify possible environmental causes of autism in America’s children.

“PCB 95 Promotes Dendritic Growth via Ryanodine Receptor-Dependent Mechanisms”

“PCB 95 Modulates Calcium-Dependent Signaling Pathway Responsible for Activity-Dependent Dendritic Growth”

“Tipping the Balance of Autism Risk: Potential Mechanisms Linking Pesticides and Autism”

“A Research Strategy to Discover the Environmental Causes of Autism and Neurodevelopmental Disabilities”

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A new study, published by Cell Press in the journal Neuron, discovers several genes associated with autism and finds evidence for a shared genetic mechanism underlying autism and fragile X syndrome, the most common genetic cause of intellectual disability.

It is well established that genetic variation caused by mutation can lead to autism spectrum disorders, and research has repeatedly implicated “de novo” (new) mutations, those that show up for the first time in affected children, as being particularly relevant. Identification of the specific genes associated with autism may lead to much needed advances in the diagnosis and treatment of autism spectrum disorders. The current study, led by Dr. Michael Wigler from Cold Spring Harbor Laboratory, used gene sequencing methods to look at nearly 350 families with healthy children and children on the autistic spectrum, part of the larger Simons Simplex Collection. Specifically, the researchers looked for mutations that were present in the children but not in their parents.

The team found that autism is linked with the types of new mutations that are likely to disrupt the function of a gene. By disrupting one of the pair of healthy genes that we normally inherit, such mutations alter “gene dosage.” There was a 2-fold higher incidence of such mutations in the affected child than in the healthy child, but little to no difference in the overall incidence of much more prevalent types of mutations. The results also showed that children with older parents have more new mutations. This is consistent with other recent reports and perhaps explains why older parents are more likely to have children on the autism spectrum. “More generally, this work and the work preceding it point to the importance of new mutations and gene dosage in so-called complex genetic disorders,” says Dr. Wigler.

Importantly, the study also identified many new autism candidate genes, and these genes showed a strong overlap with genes linked to the pathway involved in fragile X syndrome, one of the best studied cognitive-behavioral disorders in humans. “We observe strong statistical evidence for the link between autism and fragile X syndrome, first suggested by study coauthors Dr. Jennifer Darnell and Dr. Robert Darnell, in a paper they published in Cell last year,” explains Dr. Wigler. “Our finding has important implications for therapy and shows that autism is in large part a molecular disorder of neuroplasticity, the mechanisms by which our nervous system adapts to change.”

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