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Extra Brain Cells May Explain Autism

Posted: November 9th, 2011 | Author: | Filed under: Applied Science, Medicated, Michael Courtenay, Science, Science News | Tags: , , , , , , , , , , , , | Comments Off on Extra Brain Cells May Explain Autism

A new study suggests that Autism starts in the womb, researchers have found a remarkable 67 per cent increase in the total number of brain cells in the prefrontal cortex of new born babies with ASD.

Extra Brain Cells May Explain AutismChildren with autism appear to have too many cells in a key area of the brain needed for communication and emotional development, say US researchers. Their findings help explain why young children with autism often develop brains that are larger or heavier than normal. Dr Eric Courchesne says the finding of excess brain cells in the prefrontal cortex explains brain overgrowth in autism, and hints at why brain function in this area is disrupted. Courchesne, of the University of California San Diego Autism Center of Excellence, and colleagues, have also found dozens of genes that may raise the risk of autism. But genetic causes only explain 10 per cent to 20 per cent of cases, and recent studies have pointed to environmental factors, possibly in the womb, as a potential trigger. The team found excess brain cells in each child with autism they studied, says Courchesne. And the brains of the autistic children also weighed more than those of typically developing children of the same age.

Researchers searching for an early indicator of autism say they’ve discovered a promising possibility, an impairment in the ability of the brain’s right and left hemispheres to communicate with each other. The researchers did brain imaging scans – fMRIs – on 29 sleeping toddlers with autism, 30 typically developing kids and 13 children with significant language delays, but not autism. All were between 1 and 4 years old. The scans showed that the language areas of the left and right hemispheres of the autistic toddlers’ brains were less “in sync” than the hemispheres of the typical kids and the children with other language delays. The weaker the synchronization, the more severe the autistic child’s communication difficulties ::::

The new study suggests the condition starts in the womb because brain cells in this area known as the prefrontal cortex typically develop during the second trimester of pregnancy. The findings could help narrow the search for a cause of autism. Courchesne and colleagues carefully counted the number of brain cells in tissue from seven boys with autism who had died and six boys who did not have autism at the time of their deaths. They focused on the prefrontal cortex, a part of the brain which is thought to grow too large and too fast in children with autism.

“We found a really remarkable 67 per cent increase in the total number of brain cells in the prefrontal cortex,” says Courchesne.

“No one really knows why synchronization is important, but it’s clearly a robust phenomenon apparent in the brains of animals and humans of all ages,” said lead study author Ilan Dinstein, a neurobiologist at the Weizmann Institute of Science in Rehovot, Israel, and a member of the Autism Center of Excellence at the University of California, San Diego.

“The main theory is that it is important for the proper communication between different brain areas,” Dinstein added. “Such communication is thought to be essential for normal brain function and for normal behavior.”

The study is published in the June 23 issue of the journal Neuron.

Neural synchronization refers to the coordinated timing of neural activity across distinct brain areas, Dinstein explained. In a normal brain, neurons in separate areas belonging to a system with a particular function, such as vision or language, always stay in sync, even during sleep.

“The brain is always active, even when you’re sleeping. So you can assess synchronization both during wake and sleep,” Dinstein said.

Think of it like a series of lightbulbs on the same circuit, explained Dr. Gary Goldstein, president and chief executive officer of the Kennedy Krieger Institute in Baltimore, who was not involved in the research. In the brains of normally developing children and kids with language difficulties, the lightbulbs on the circuits oscillate, that is, all get brighter or dimmer in the right and left hemispheres at the same time. In the kids with autism, the hemispheres are out of sync. The circuits on the left side get brighter as those on the right side get dimmer. Specifically, researchers found communication differences in the left and right inferior frontal gyrus, which is involved with speech, and the superior temporal gyrus, which is involved in receptive language, or understanding what people say, Goldstein said.

Researchers said the findings could help in the search for methods to screen for autism even before obvious symptoms emerge.

“The idea is that our measure would be one of several measures developed over the next few years, which together would give good accuracy in identifying autism in extremely young toddlers,” Dinstein said. “Having biological measures for diagnosing autism would revolutionize the field.”

Goldstein said it was unlikely fMRIs would be used to diagnosis autism. Most hospitals don’t have the equipment. It’s expensive, time consuming, and interpreting the images requires extensive training, he said.

Even so, the study is intriguing in that it fits with genetic research that’s identified more than 20 autism risk genes. “Those genes, by and large, code for proteins that make the synapses work, or the connections between neurons,” Goldstein said. “These researchers are looking at the next step up, which are the circuits, or the connections between the brain regions.”

It would be interesting to study whether learning and behavioral therapy can change those patterns, he added.

Geraldine Dawson, chief science officer of Autism Speaks, said the study adds to the evidence that autism may be, at least in part, a “developmental disconnection syndrome.” Prior research has also found connectivity problems between different brain regions in autism.

“This helps explain why people with autism have trouble with complex behaviors, such as social interaction and language, which require coordinated activity across several brain regions,” Dawson said. “This study suggests that faulty neural connectivity is an early characteristic of autism and helps explain some of the symptoms that emerge in the first couple of years of life. Even early gestures and social games require coordinated activity among several brain regions.”

source: uc sandiego

source: abc

source: jama

History:  A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic.  Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report. The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair’s marriage to gain Blair’s inheritance. The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation. The New Latin word autismus (English translation autism) was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word autós (αὐτός, meaning self), and used it to mean morbid self-admiration, referring to “autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance”. The word autism first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler’s terminology autistic psychopaths in a lecture in German about child psychology. Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981. Leo Kanner of the Johns Hopkins Hospital first used autism in its modern sense in English when he introduced the label early infantile autism in a 1943 report of 11 children with striking behavioral similarities. Almost all the characteristics described in Kanner’s first paper on the subject, notably “autistic aloneness” and “insistence on sameness”, are still regarded as typical of the autistic spectrum of disorders. It is not known whether Kanner derived the term independently of Asperger. Kanner’s reuse of autism led to decades of confused terminology like infantile schizophrenia, and child psychiatry’s focus on maternal deprivation led to misconceptions of autism as an infant’s response to “refrigerator mothers”. Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy. As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions. Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, parents continue to feel social stigma in situations where their autistic children’s behaviors are perceived negatively by others, and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research. The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely. Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.

Autism is a disorder of neural development characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old. Autism affects information processing in the brain by altering how nerve cells and their synapses connect and organize; how this occurs is not well understood. It is one of three recognized disorders in theautism spectrum (ASDs), the other two being Asperger syndrome, which lacks delays in cognitive development and language, and Pervasive Developmental Disorder-Not Otherwise Specified (commonly abbreviated as PDD-NOS), which is diagnosed when the full set of criteria for autism or Asperger syndrome are not met.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations, or by rare combinations of common genetic variants. In rare cases, autism is strongly associated with agents that cause birth defects. Controversies surround other proposed environmental causes, such as heavy metals, pesticides or childhood vaccines; the vaccine hypotheses are biologically implausible and lack convincing scientific evidence. The prevalence of autism is about 1–2 per 1,000 people worldwide; however, the Centers for Disease Control and Prevention (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD. The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.

Parents usually notice signs in the first two years of their child’s life. The signs usually develop gradually, but some autistic children first develop more normally and then regress. Early behavioral or cognitive intervention can help autistic children gain self-care, social, and communication skills. Although there is no known cure, there have been reported cases of children who recovered. Not many children with autism live independently after reaching adulthood, though some become successful. An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.

Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders. People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling “like an anthropologist on Mars”.

Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn taking, and do not have the ability to use simple movements to express themselves, such as the deficiency to point at things. Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers. Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD. Older children and adults with ASD perform worse on tests of face and emotion recognition.

Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect the quality of life more deeply.

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in non-autistic children with language impairments. A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs. Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others’ words (echolalia) or reverse pronouns. Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD: for example, they may look at a pointing hand instead of the pointed-at object, and they consistently fail to point at objects in order to comment on or share an experience.  Autistic children may have difficulty with imaginative play and with developing symbols into language.

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well as, and adults better than, individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior. These symptoms do not imply sickness, fragility, or emotional disturbance.

Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) is diagnosed when the criteria are not met for a more specific disorder. Unlike with autism, people with Asperger syndrome have no substantial delay in language development. The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD) or sometimes the autistic disorders, whereas autism itself is often called autistic disorderchildhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder; in clinical practice, though, autismASD, and PDD are often used interchangeably. ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary. Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds, or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided intosyndromal and non-syndromal autism; the syndromal autism is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis. Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible thatregressive autism is a specific subtype, or that there is a continuum of behaviors between autism with and without regression.

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.

Newer technologies such as fMRIand diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism; one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects. It has been proposed to classify autism using genetics as well as behavior.

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, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants. Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA but are heritable and influence gene expression. Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population. However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality like fragile X syndrome, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD. Numerous candidate genes have been located, with only small effects attributable to any particular gene. The large number of autistic individuals with unaffected family members may result from copy number variations—spontaneous deletions or duplications in genetic material during meiosis. Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.

Several lines of evidence point to synaptic dysfunction as a cause of autism. Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion. Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes. All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.

Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies, extensive searches are underway. Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important 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, vaccines, and prenatal stress, although no links have been found, and some have been completely disproven.

Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine “overload”, a vaccine preservative, or the MMR vaccine for causing autism. The latter theory was supported by a litigation-funded study that has since been shown to have been “an elaborate fraud”. Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.

Autism’s symptoms result from maturation-related changes in various systems of the brain. How autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors. The behaviors appear to have multiple pathophysiologies.

What are some common signs of autism? The hallmark feature of ASD is impaired social interaction. As early as infancy, a baby with ASD may be unresponsive to people or focus intently on one item to the exclusion of others for long periods of time. A child with ASD may appear to develop normally and then withdraw and become indifferent to social engagement.

Children with an ASD may fail to respond to their names and often avoid eye contact with other people. They have difficulty interpreting what others are thinking or feeling because they can’t understand social cues, such as tone of voice or facial expressions, and don’t watch other people’s faces for clues about appropriate behavior. They lack empathy.

Many children with an ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging. They also tend to start speaking later than other children and may refer to themselves by name instead of “I” or “me.” Children with an ASD don’t know how to play interactively with other children. Some speak in a sing-song voice about a narrow range of favorite topics, with little regard for the interests of the person to whom they are speaking.

Children with characteristics of an ASD may have co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis, epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder. About 20 to 30 percent of children with an ASD develop epilepsy by the time they reach adulthood. .

How is autism diagnosed? ASD varies widely in severity and symptoms and may go unrecognized, especially in mildly affected children or when it is masked by more debilitating handicaps. Very early indicators that require evaluation by an expert include:

no babbling or pointing by age 1 no single words by 16 months or two-word phrases by age 2 no response to name loss of language or social skills poor eye contact excessive lining up of toys or objects no smiling or social responsiveness.

Later indicators include:

impaired ability to make friends with peers impaired ability to initiate or sustain a conversation with others absence or impairment of imaginative and social play stereotyped, repetitive, or unusual use of language restricted patterns of interest that are abnormal in intensity or focus preoccupation with certain objects or subjects inflexible adherence to specific routines or rituals.

Health care providers will often use a questionnaire or other screening instrument to gather information about a child’s development and behavior. Some screening instruments rely solely on parent observations, while others rely on a combination of parent and doctor observations. If screening instruments indicate the possibility of an ASD, a more comprehensive evaluation is usually indicated.

A comprehensive evaluation requires a multidisciplinary team, including a psychologist, neurologist, psychiatrist, speech therapist, and other professionals who diagnose children with ASDs. The team members will conduct a thorough neurological assessment and in-depth cognitive and language testing. Because hearing problems can cause behaviors that could be mistaken for an ASD, children with delayed speech development should also have their hearing tested.

Children with some symptoms of an ASD but not enough to be diagnosed with classical autism are often diagnosed with PDD-NOS. Children with autistic behaviors but well-developed language skills are often diagnosed with Asperger syndrome. Much rarer are children who may be diagnosed with childhood disintegrative disorder, in which they develop normally and then suddenly deteriorate between the ages of 3 to 10 years and show marked autistic behaviors.

What causes autism? Scientists aren’t certain about what causes ASD, but it’s likely that both genetics and environment play a role. Researchers have identified a number of genes associated with the disorder. Studies of people with ASD have found irregularities in several regions of the brain. Other studies suggest that people with ASD have abnormal levels of serotonin or other neurotransmitters in the brain. These abnormalities suggest that ASD could result from the disruption of normal brain development early in fetal development caused by defects in genes that control brain growth and that regulate how brain cells communicate with each other, possibly due to the influence of environmental factors on gene function. While these findings are intriguing, they are preliminary and require further study. The theory that parental practices are responsible for ASD has long been disproved.

What role does inheritance play? Twin and family studies strongly suggest that some people have a genetic predisposition to autism. Identical twin studies show that if one twin is affected, there is up to a 90 percent chance the other twin will be affected. There are a number of studies in progress to determine the specific genetic factors associated with the development of ASD. In families with one child with ASD, the risk of having a second child with the disorder is approximately 5 percent, or one in 20. This is greater than the risk for the general population. Researchers are looking for clues about which genes contribute to this increased susceptibility. In some cases, parents and other relatives of a child with ASD show mild impairments in social and communicative skills or engage in repetitive behaviors. Evidence also suggests that some emotional disorders, such as bipolar disorder, occur more frequently than average in the families of people with ASD.

Do symptoms of autism change over time? For many children, symptoms improve with treatment and with age. Children whose language skills regress early in life—before the age of 3—appear to have a higher than normal risk of developing epilepsy or seizure-like brain activity. During adolescence, some children with an ASD may become depressed or experience behavioral problems, and their treatment may need some modification as they transition to adulthood. People with an ASD usually continue to need services and supports as they get older, but many are able to work successfully and live independently or within a supportive environment.

How is autism treated? There is no cure for ASDs. Therapies and behavioral interventions are designed to remedy specific symptoms and can bring about substantial improvement. The ideal treatment plan coordinates therapies and interventions that meet the specific needs of individual children. Most health care professionals agree that the earlier the intervention, the better.

Educational/behavioral interventions: Therapists use highly structured and intensive skill-oriented training sessions to help children develop social and language skills, such as Applied Behavioral Analysis. Family counseling for the parents and siblings of children with an ASD often helps families cope with the particular challenges of living with a child with an ASD.

Medications: Doctors may prescribe medications for treatment of specific autism-related symptoms, such as anxiety, depression, or obsessive-compulsive disorder. Antipsychotic medications are used to treat severe behavioral problems. Seizures can be treated with one or more anticonvulsant drugs. Medication used to treat people with attention deficit disorder can be used effectively to help decrease impulsivity and hyperactivity.

Other therapies: There are a number of controversial therapies or interventions available, but few, if any, are supported by scientific studies. Parents should use caution before adopting any unproven treatments. Although dietary interventions have been helpful in some children, parents should be careful that their child’s nutritional status is carefully followed.

What research is being done? In 1997, at the request of Congress, the National Institutes of Health (NIH) formed its Autism Coordinating Committee (NIH/ACC) to enhance the quality, pace and coordination of efforts at the NIH to find a cure for autism (http://www.nimh.nih.gov/health/topics/autism-spectrum-disorders-pervasive-developmental-disorders/nih-initiatives/nih-autism-coordinating-committee.shtml). The NIH/ACC involves the participation of seven NIH Institutes and Centers: the National Institute of Neurological Disorders and Stroke (NINDS), the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institute of Mental Health, the National Institute on Deafness and Other Communication Disorders, the National Institute of Environmental Health Sciences, the National Institute of Nursing Research, and the National Center on Complementary and Alternative Medicine. The NIH/ACC has been instrumental in the understanding of and advances in ASD research. The NIH/ACC also participates in the broader Federal Interagency Autism Coordinating Committee (IACC) that is composed of representatives from various component agencies of the U.S. Department of Health and Human Services, as well as the U.S. Department of Education and other government organizations.

In fiscal years 2007 and 2008, NIH began funding the 11 Autism Centers of Excellence (ACE), coordinated by the NIH/ACC. The ACEs are investigating early brain development and functioning, social interactions in infants, rare genetic variants and mutations, associations between autism-related genes and physical traits, possible environmental risk factors and biomarkers, and a potential new medication treatment.

Where can I get more information? For more information on neurological disorders or research programs funded by the National Institute of Neurological Disorders and Stroke, contact the Institute’s Brain Resources and Information Network (BRAIN) at:

BRAIN P.O. Box 5801 Bethesda, MD 20824 (800) 352-9424


Information also is available from the following organizations:

Association for Science in Autism Treatment P.O. Box 188 Crosswicks, NJ   08515-0188 info@asatonline.org http://www.asatonline.org Autism National Committee (AUTCOM) P.O. Box 429 Forest Knolls, CA   94933 http://www.autcom.org
Autism Network International (ANI) P.O. Box 35448 Syracuse, NY   13235-5448 jisincla@syr.edu http://www.ani.ac Autism Research Institute (ARI) 4182 Adams Avenue San Diego, CA   92116 director@autism.com http://www.autismresearchinstitute.com Tel: 866-366-3361 Fax: 619-563-6840
Autism Science Foundation 419 Lafayette Street 2nd floor New York, NY   10003 contactus@autismsciencefoundation.org http://www.autismsciencefoundation.org/ Tel: 646-723-3978 Fax: 212-228-3557 Autism Society of America 4340 East-West Highway Suite 350 Bethesda, MD   20814 http://www.autism-society.org Tel: 301-657-0881 800-3AUTISM (328-8476) Fax: 301-657-0869
Autism Speaks, Inc. 2 Park Avenue 11th Floor New York, NY   10016 contactus@autismspeaks.org http://www.autismspeaks.org Tel: 212-252-8584 California: 310-230-3568 Fax: 212-252-8676 Birth Defect Research for Children, Inc. 800 Celebration Avenue Suite 225 Celebration, FL   34747 betty@birthdefects.org http://www.birthdefects.org Tel: 407-566-8304 Fax: 407-566-8341
MAAP Services for Autism, Asperger Syndrome, and PDD P.O. Box 524 Crown Point, IN   46308 info@aspergersyndrome.org http://www.aspergersyndrome.org/ Tel: 219-662-1311 Fax: 219-662-1315 National Dissemination Center for Children with Disabilities U.S. Dept. of Education, Office of Special Education Programs 1825 Connecticut Avenue NW, Suite 700 Washington, DC   20009 nichcy@aed.org http://www.nichcy.org Tel: 800-695-0285 202-884-8200 Fax: 202-884-8441
National Institute of Child Health and Human Development (NICHD) National Institutes of Health, DHHS 31 Center Drive, Rm. 2A32 MSC 2425 Bethesda, MD   20892-2425 http://www.nichd.nih.gov Tel: 301-496-5133 Fax: 301-496-7101 National Institute on Deafness and Other Communication Disorders Information Clearinghouse 1 Communication Avenue Bethesda, MD   20892-3456 nidcdinfo@nidcd.nih.gov http://www.nidcd.nih.gov Tel: 800-241-1044 800-241-1055 (TTD/TTY)
National Institute of Environmental Health Sciences (NIEHS) National Institutes of Health, DHHS 111 T.W. Alexander Drive Research Triangle Park, NC   27709 webcenter@niehs.nih.gov http://www.niehs.nih.gov Tel: 919-541-3345 National Institute of Mental Health (NIMH) National Institutes of Health, DHHS 6001 Executive Blvd. Rm. 8184, MSC 9663 Bethesda, MD   20892-9663 nimhinfo@nih.gov http://www.nimh.nih.gov Tel: 301-443-4513/866-415-8051 301-443-8431 (TTY) Fax: 301-443-4279

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