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Autism Speaks Grants Related to Potential Environmental Factors in Autism

Autism Speaks is committed to facilitating research that will uncover the causes of autism, develop effective biomedical treatments, and hasten the discovery of a cure. As part of this commitment, Autism Speaks has funded research projects that explore potential environmental factors in autism.

For the years 2005-2007, Autism Speaks and Cure Autism Now are funding $4,351,716 in grants for environmental research.

These current grants build on previous commitments by the National Alliance for Autism Research, or NAAR, and Cure Autism Now.

From 1997-2004, NAAR funded $881,984 in grants on environmental factors while from 2000-2004 Cure Autism Now funded $748,041 in such research. The combined funding commitment to date on autism environmental sciences is $5,981,741. 

Also, learn more about Autism Speaks’ current grants for treatment research.

Current Autism Speaks Grants on Environmental Factors (2005-2007)

Total Funding Commitment: $4,351,716 

A. Some examples where toxicant, environmental factor or vaccine exposure is directly examined (direct part of the research question) include: 

PI: Adams (Mentor-based fellowship, 2005)

Early Markers of Autism and Social-Cognitive Processing in Infants Exposed to Valproic Acid During Prenatal Development ($54,000)

The use of drugs to control epilepsy (such as valprioc acid) during pregnancy has been suggested to increase the risk for autism spectrum disorders in offspring. Thus far, data on autism risk has been based primarily on case reports, retrospective sample studies, and suggestions from animal research. This study will assess the developmental outcomes in a group of infants prenatally exposed to VPA, as well as a comparison group of infants matched by age, maternal age and demographic characteristics. It will also examine the effects of prenatal VPA exposure on motor, mental, and social-emotional development, as well as social-cognitive processing. 

What this means for people with autism: This study will help clarify if there is indeed an increased risk of autism in children exposed to valproic acid in utero . Determination of environmental or pharmaceutical contributions to autism will contribute to development of better animal models and intervention strategies to prevent VPA associated cases of autism. 

PI: Briscoe (Pilot Award, 2006)

Teratogen-Induced ASD and Brainstem Development. ($59,948) 

While the etiology of autism and ASD is unknown, prenatal exposure to chemical teratogens including the antiseizure medications thalidomide and valproate are associated with increased incidences of ASD. Exposure to these agents is known to produce brainstem abnormalities which are reflected in individuals with autism. While the mechanism by which these defects are caused by these chemicals is being explored, the findings do raise the possibility that they may be similar to that which contributes to autism neuropathology. This project proposes to initiate a detailed analysis of the effect of thalidomide and valproate on different species of animals, including the rat, mouse, chick and zebrafish. The investigators will examine a panel of molecular markers – genes which will identify specific structures in the developing brainstem. The identification of chemical induced brain defects in these organisms will offer the opportunity for many follow up studies to determine the exact nature of the flaws and how they cause the symptoms of ASD. 

What this means for people with autism:
 Because exposure to thalidomide and valproate has been associated with symptoms of autism spectrum disorder, an understanding of the specific biochemical and molecular effects of these teratogens during early brainstem development will help better identify disease mechanism. This information is likely to have far-reaching implications for understanding and diagnosing ASD and may aid the development of therapeutic interventions to treat or ameliorate ASD symptoms. 

PI: Croen (Augmentation and Bridge Award, 2006)

Augmentation of CA CADDRE Studies ( $200,000) 

Since 2001, the California Center for Autism and Developmental Disabilities Research and Epidemiology (CA CADDRE) has been one of the largest, most extensive datasets of information on children with autism living in California.

CA CADDRE, funded by the Centers for Disease Control and Prevention, is run collaboratively by Dr. Croen from Kaiser Permanente’s Division of Research and Drs. Grether and Windham from the Department of Health Services. The CA CADDRE center has also used Kaiser Permanente medical records to investigate autism risk factors during pregnancy and early childhood. 

This grant will fund several new analyses of this rich dataset to examine risk factors for autism that have been speculated about in the literature. For example, Dr. Croen and her colleagues will investigate the risk of autism from: 

  • prenatal exposure to the immunization RhoGAM, which is given to women who deliver a Rh+ baby;
  • maternal illnesses such as infections, inflammation and endocrine disorders;
  • maternal hormone use, ultrasound exams and maternal use of the asthma drug terbutaline;
  • maternal exposure to environmental chemicals, including airborne chemicals and workplace exposure.

What this means for people with autism: Data from this study will fill important gaps in understanding environmental risk factors for autism spectrum disorders. Researchers will be able to use the results from these analyses to design future autism studies and, potentially, to design strategies to prevent autism spectrum disorders 

PI: Freedman (Pilot Award, 2004)

Double Hit Hypothesis of Autism: Genetic Susceptibility and Environmental Exposure to Metals. ($120,000) (Received extension 2005 due to change in investigator to Ed Levin) 

High level exposure to the heavy metals mercury and copper can lead to neuropsychological impairments in adults. Of concern, children are more susceptible to these cognitive impairments. While the levels at which exposure has led to dysfunction in motor and memory functions is considerably high, there are conditions under which an individual can not properly metabolize/detoxify metals, leading to a high bioburden compared to exposure level. Drs. Freedman and Levin will test whether a defect in metal metabolism (genetic) combined with exposure to copper or mercury (environmental) are causative factors in the development of autism like behaviors using an animal model. They will test the hypothesis that a disruption in normal metal metabolism and concomitant metal intoxication during development contributes to persistent cognitive and social impairment. Changes in cognitive and social behavior in response to exposure to copper or inorganic mercury will be examined in wild type mice and a transgenic strain in which a central component in metal metabolism, metallothionein, has been inactivated. The enzyme metallothionein is essential for removing heavy metals from the body, therefore this genetic manipulation may serve as a susceptibility factor to the deleterious effects of heavy metals such as mercury and copper. 

What this means for people with autism: The information and improved mechanistic under­standing obtained from the proposed studies will help define the roles of metal toxicants in the etiology of neurodevelopmental and neurobehavioral disorders. This information may be applied to the clinical intervention and possible prevention of metal-induced neurological disorders. 

PI: Hall (CAN Pilot Project Grant, 2007)

Impact of Maternal Infection on Neurodevelopment – Structural and Functional Changes. ($119,760)

Although autism has a strong genetic component, early exposure to environmental insult may be a significant risk factor for the disorder. Exposure to known viruses during the first trimester of pregnancy has been connected to higher rates of autism. Animal modeling can be used to directly test if early exposure to immune challenges causes changes in brain structure, function and behavior that resemble changes seen in individuals with autism. Dr. Hall is interested in studying the behavior of mice that have been exposed to viral infection in-utero. Importantly, he will be assessing the neurological origins of these behaviors. Using recently available animal imaging methods he plans to assess the outcomes of maternal infection upon brain pathways key to autism, focusing especially on the dopamine and serotonin neurotransmitter systems. These methods offer the advantage over other techniques that the same animal can be studied across time. This provides the exciting opportunity to also study the effects of environmental manipulations on behavioral outcomes, and connect these results to the neurological changes seen throughout development. The overall objective of this study is to localize and quantify molecular events that occur in offspring as a result of maternal infection. This work holds promise for the development of new diagnostic tools and improvements in intervention. 

PI: Hertz-Piccioto (Augmentation and Bridge Award, 2006)

Bridge Award to the CHARGE study ($25,000) 

This study was awarded to Dr. Hertz-Piccioto to bridge NIEHS funding to her CHARGE study (Childhood Autism Risks from Genetics and the Environment). The CHARGE study has so far enrolled over 500 participants affected with autism, developmentally delayed, or not-affected. Her study examines toxicological exposures through biosampling as well as in depth interviews, monitors medical records as well as banks biosamples for genetic studies in order to examine gene-environment interactions.

PI: Hertz-Picciotto (CAN Pilot Project Award, 2006)

Polybrominated Diphenyl Ethers as a Potential Neurodevelopmental Toxicant ($118,012)

Both genetic and environmental factors contribute to autism in the majority of cases, yet few specific causes have been identified. In the search for relevant environmental exposures, chemicals affecting neurodevelopment are prime suspects. One such group of chemicals is the polybrominated diphenyl ether (PBDEs). These are flame-retardants used widely in consumer products, including plastic casings for television sets and computers, construction materials, carpeting and foam cushions. Levels of PBDEs are rapidly increasing in the environment and in human tissues, with body burdens in California among the highest worldwide. Of foremost concern is the neurodevelopmental toxicity of PBDEs demonstrated in animal studies. Prenatal exposures alter spontaneous behaviors, adversely affect learning and memory, and result in a lack of ability to habituate to a novel situation. PBDEs cross the placenta, accumulate in the fetus, and disrupt thyroid hormones, which are crucial for early brain, motor, language and sensory development. Thus, we will measure PBDEs in serum collected from children participating in a large epidemiologic study of autism. The CHARGE (Childhood Autism Risk from Genetics and the Environment) Study has enrolled over 400 subjects, including children with autism, children with developmental delay, and children from the general population. Over 300 of these children gave blood samples, from which we will select 90 (30 from each group) for measurement of PBDEs. This project will provide preliminary data to determine whether children with autism have higher concentrations of PBDEs than those from the general population or those with developmental delay but not autism. 

PI: Keller (Interdisciplinary Award, 2005)

Comparative Analysis of Cerebellar Neuropathology in Human Autistic Patients and in Cerebellar Mouse Mutants ($292,02024) 

Neuroanatomical and neuroimaging studies in autism conducted by several research groups show faulty development of neural structures, particularly in a structure at the base of the brain called the cerebellum. The cerebellum is a particularly interesting research target because its structure and function has remained consistent throughout evolution. In addition, the development of the cerebellum takes place during late pregnancy and early postnatal life, which is a period that is believed to be critical for autism. Specifically, the size of the cerebellum is reported to be smaller in individuals with autism and the number of cells which direct messages to other brain areas, Purkinje cells, are shown to be reduced in number. 
While the mechanism that affects Purkinje cell number and cerebellar size is not yet well described, preliminary data suggests that reelin, an autism candidate gene, interacts with gonadal sex hormones during cerebellar development. An interaction of abnormal reelin expression coupled with exposure to differing levels of testosterone during brain development may contribute to the reduced number of Purkinje cells in individuals with autism. This study will look for alterations of enzymes and receptors involved in gonadal steroid signaling in human brain tissue to determine the interaction between testosterone levels, reelin expression, and Purkinje cell development. The results of human brain tissue research will be followed by examining the effects of estrogen in a genetic strain of mouse named Reeler mice. Reeler mice lack the reelin protein which leads to a malformed cerebellum with disorganized Purkinje cells. By using this approach, the effects changes in gestational environment, including testosterone levels with genetic mutations on human pathology can be investigated in a multifaceted way. 

What this means for people with autism: This study will investigate the interaction between genetic vulnerability and gonadal steroid hormones on Purkinje cell survival, migration, and/or differentiation, which would account for the biased sex ratio of autism. This hypothesis has not yet been tested and these researchers will examine the role of reelin, a candidate gene for autism, and 17beta-Estradiol, on mouse Purkinje cells. Dr. Keller’s group will be linking animal models with human pathological studies in an interdisciplinary fashion and studying the possible protective role of estrogen on genetic susceptibility to autism spectrum disorders. 

PI: McCaffrey (Pilot Award, 2005)

Disruption of Organization of the Cerebral Cortex by Retinoic Acid ($119,200) 

Summary: Dysfunction of the cerebral cortex is likely to be a significant contributor to the pathogenesis of autism. One mechanism by which changes in cortical function may occur is by too much activity, leading to “overexcitation.” This may be caused by a dysregulation in systems that normally turn off neurons. In this study, Dr. McCaffery and associates will investigate the influence of retinoic acid, which inhibits the migration of specific neurons to the cortex and so would reduce the number of neurons that regulate brain activity. Retinoic acid has been suggested as one possible candidate of an environmental input that, in excess, may result in some features of autistic pathology. Fetal exposure to retinoic acid can occur through the use of a number of drugs that can influence the levels or potency of retinoic acid, including Accutane, alcohol, or valproate. 

What this means for people with autism: Studying the effects of pharmaceutical agents and teratogens on brain development will help illustrate the mechanisms by which environmental factors may contribute to the neuropathology of autism. 

PI: Newschaffer (Pilot Award, 2005)

Autism, Autoimmunity and the Environment ($120,000) 

Summary: There is some evidence regarding an association between autism and autoimmunity, but the nature of this connection is still unclear. At the same time, given apparent upsurges in autism prevalence, interest into environmental risk factors continues to build. Because autism pathology likely begins early in development, the prenatal period is a critical time window for exposures to environmental risk factors. This study will look at two potentially related factors contributing to the fetal environment: maternal antibody levels and chemical exposures during pregnancy. The results of this research will add to the understanding of immunologic and environmental risk factors in autism. 

What this means for people with autism: A reliable biomarker to enhance diagnosis of autism has not yet been well characterized or established. This study will explore autoantibodies as potential biomarkers of autism risk and will link biomarker data with ecologic data on environmental exposures. 

PI: Newschaffer (Pilot Award, 2005) 

Autism risk and Exposures/Biomarkers Measured During the pre-, peri-, and neonatal periods: a Baby Sibs Pilot Investigation ($120,000) 

Given the strong evidence supporting the early origins of ASD, exposure and biomarker data collected during the pre-, peri- and neonatal time periods could be more strongly associated with ASD risk because they are measured during an etiologically more significant time period than those collected later in life. Also, although it is possible to collect interview data on pre-, peri- and neonatal exposures retrospectively, prospective collection offers substantive advantages in reducing error and limiting recall bias. 
Collection of biomarker and exposure data in a high-risk cohort offers some distinct advantages over collecting these data in a population-based cohort. Most obvious is that, in a high-risk cohort, informative analyses can be completed with a relatively smaller sample size because clinical events are more common and there is greater variation in subclinical (continuously measured) endpoints. A second advantage of a high-risk cohort is compliance. Motivation to sustain study participation in the high-risk cohort would likely be higher on average then in a population-based cohort (although compliance and sample collection logistics are still a major challenge in this study design). Finally, studying a genetically susceptible population may allow for observation of associations between biomarkers and/or risk factors and ASD that would be more difficult to detect in a population-based sample.

What this means for people with autism: This investigation will demonstrate the feasibility of assembling and retaining a study population to determine if a larger study is possible. The pilot effort will also focus on data collection areas anticipated to present particular challenges – for example: the collection of biosamples during the labor and delivery, post-partum, and early neonatal periods. Finally, the pilot investigation will provide some data on the distribution of exposure and biomarker values observed during the pre-natal period, critical for brain development.

PI: Noble (CAN Pilot Project Grant, 2007)

Cellular, Physiological and Molecular Mechanisms Underlying Alterations in CNS Development Caused by Exposure to Clinically-Relevant Levels of Mercury-Containing Compounds ($120,000)

Dr. Noble’s research aims to understand the mechanisms by which genetic factors and environmental insults combine to disrupt normal brain development and cause complex neurological syndromes such as autism spectrum disorders (ASD). His laboratory is interested in understanding how identical insults can have different outcomes in different individuals. The goal of the research is to provide a mechanistic understanding of vulnerability to physiological stressors implicated in ASD. Previous work from the Noble lab has shown that the state of oxidative stress of individual cells (“redox state”) controls how they react to various environmental agents. The importance of redox states in controlling multiple cell functions is of potential interest given the observations that some data suggests individuals with ASD show signs of being in a more oxidized status. This condition may make them more vulnerable to physiological stressors. These studies will focus on thimerosal and methyl mercury in order to understand the cellular basis for vulnerability to these toxicants, and are designed to provide general principles relevant to understanding how any toxicant impinges on normal cell development. As a part of the proposed research, Dr. Noble aims to uncover approaches to identifying oxidative stress that could provide the basis for early identification of children at particular risk of damage from environmental toxins. They will further apply this knowledge to the identification of a means to protect such individuals by studying the efficacy of anti-oxidant compounds in protecting against the cellular effects of thimerosal and methyl mercury. 

PI: Wagner (Pilot Award, 2005)

Animal Model of autism Using Engrailed2 Knockout Mice. ($98,880) 

Autism is a neurobiological disorder with primary symptoms include impaired communication and social interaction with restricted or repetitive motor movements. Dr. Wagner and his colleagues have developed a model that examines the neurobehavioral development of mice in three core areas: motor, cognitive, and social. As the EN2 gene has been shown to be associated with autism, Dr. Wagner’s lab will examine behavioral development in a mouse model where this gene is not expressed. Furthermore, the effects of two environmental toxicants, VPA and DEHP will be examined to determine if this gene confers susceptibility to environmental exposures. He predicts that disruption of the En2 gene will alter the developmental path of the brain and lead to widespread behavioral changes that may be made worse in the presence of these toxicants. 

What this means for people with autism: These studies may help clarify the genetic, neurobiological and environmental influences in autism. Finding genes involved in autism susceptibility and learning how they contribute to disease development will provide information that could lead to more effective treatments and interventions.

B. Other studies which indirectly examine toxicant exposure/immune function: 

PI: Ashwood (CAN Pilot Project Award, 2006)

Immunological Phenotyping in Autism: A Screen for Potential Early Biomarkers of Activation ($120,000) 
It is thought that the interaction of genetic susceptibility and exposure to nongenetic influences during critical periods of neurodevelopment plays a part in the development of autism. Virtually the entire research literature on autism emphasizes the multiple facets of this disorder. Taken together, these data indicate that ASD is, in reality, a group of disorders that share a common behavioral profile. To make progress in identifying the causes of these disorders it will be essential to develop diagnostic markers that will lead to unequivocal differentiation of the various phenotypes. We aim to demonstrate the presence of distinct immune phenotypes in ASD based on the level of activation of their immune response. We will identify and characterize the immune response in ASD by comparing the activation status and function of lymphocyte cell populations and their cytokine/chemokine profiles, firstly in peripheral blood and secondly in isolated cell cultures that receive immunological challenge. Immunological findings will be correlated with behavioral and biomedical factors to examine the relationship between the immune responses and clinical characteristics of autism. By elucidating the medical and biological correlates of autism, we hope to contribute to a clearer understanding of the early biological processes underlying this increasingly common disorder. A better understanding of the underlying biology may contribute to earlier identification and the development of more individual-based treatment regimens.

PI: Boulanger (Mentor-based Fellowship, 2006)

Modulation of Glutamate Receptor Trafficking in Autism: Role of MHC class I ($84,000)

There is growing evidence of an imbalance in neuronal signaling in the brains of some individuals with autism. The neurotransmitter glutamate is an important chemical that “turns on” neurons. Direct measures of glutamate neurotransmission have been used to measure proper neuronal signaling in animal models. Recent studies have linked the ability of neurons to respond to the neurochemical glutamate to the changes in immune response. Because maternal immune challenge during pregnancy may be a risk factor for autism in children, this raises the possibility that maternal immune challenge may alter glutamatergic neurotransmission. This is may be accomplished through modification of MHC class I molecules (major histocompatibility complex class I) in the developing fetal brain. MHC-I molecules are an essential part of the immune response which are now known to be expressed in the brain and modulate neuronal function.

Using a mouse model, Drs. Boulanger and Fourgeaud will test whether changes in MHC class I in the developing brain effects glutamate receptors, and whether these changes can be induced in the fetal brain by maternal immune challenge. Together with the projects mentored by Dr. McAllister and Dr. Patterson, the role of alterations in immune function on brain development and later behavioral function will be better understood.

What this means for people with autism: These studies could also provide a mechanistic link between maternal immune challenge, a significant environmental risk factor for autism, and glutamatergic dysfunction, a hallmark symptom of this disorder. Furthermore, the results of these studies may suggest new, immune-based strategies for the diagnosis, treatment, and prevention of autism.

PI: Boulanger (CAN Pilot Project Award, 2006)

Immune Genes and Abnormal Brain Development in Autism ($120,000)

In this study Dr. Boulanger outlines the connections between autism and immunological challenges. She will study how a variety of material infections, such as influenza, may affect the development and behavior of the fetus, even when the fetus shows no signs of direct infection itself. The fetal impact appears to be the result of a relatively nonspecific aspect of the maternal immune response, but is reflected in altered cytokines in the fetal brain. This study will use mouse models and autistic children to explore whether the expression of immune genes is altered in the autistic brain, perhaps highlighting the potential for immune-based diagnostics, treatment and prevention.

PI: Deth (CAN Pilot Project Award, 2006)

Glutathione-dependent Synthesis of Methylcobalamin: A Target for Neurodevelopmental Toxins ($117,880)

While the exact cause of autism is not yet known, research during the past several years has focused on the possibility that many cases of autism result from exposure to the ethylmercury-containing vaccine preservative thimerosal. A subgroup of exposed individuals may be less able to detoxify and eliminate heavy metals, placing them at higher risk. Previous work from our lab has shown that thimerosal and other heavy metals potently inhibit an enzyme that uses vitamin B12, and that this inhibition could lead to developmental disorders like autism. Thimerosal interferes with the process that converts dietary B12 to its active form, known as methylB12. MethylB12 has proven to be quite helpful in treating autism, which reinforces the idea that impaired methyl B12 synthesis may be an important contributing cause. Thus this project will investigate the biochemical pathway that makes methylB12 and will elucidate the mechanism by which thimerosal causes its inhibition. It will also compare the thimerosal susceptibility of this pathway in cells from siblings who did or did not develop autism. Preliminary results suggest that the autistic children’s cells show greater sensitivity. Results from this study will help to clarify what causes autism and what makes one child more likely to develop autism than another. 

PI: Holtzman (CAN Pilot Award, 2007)

Oxidative Phosphorylation in Cells from Autistic Individuals Compared to Non-Autistic Siblings ($120,000) 

This study analyzes whether metabolic abnormalities contribute directly to the pathogenesis of autism. Using patient cell lines, the project is designed to identify any abnormalities in mitochondria and the generation of ATP, the chemical form of energy. If successful, these results will lead directly to studies of the genetic mutations or toxic reactions important in the development of autism.

PI: Jonakait (CAN Pilot Project Award, 2006)

Microglial Regulation of Cholinergic Development in the Basal Forebrain ($112,778)

While the neurobiological basis for autism remains poorly understood, neuropathological studies have detected structural abnormalities in certain brain regions suggesting that disruption of normal brain development may play a role in the disorder. Our work highlights one of those abnormal brain regions, the so-called cholinergic basal forebrain, that innervates important brain areas serving cognitive function. Autistic children have too many neurons in this region, but how such changes might occur in development has not been explained. Increasing evidence also suggests that fetal exposure to infectious agents or toxins with associated inflammation may play a role in the development of autism. Such infection or toxicity can extend to the embryonic brain where local inflammation might prove detrimental to the developing brain. Our own work performed on cultured rodent cells suggests that abnormal embryonic brain inflammation during development leads directly to abnormal neurodevelopmental outcomes. Specifically, it leads to the excess production of cholinergic neurons in the basal forebrain. Thus, we have shown directly that brain inflammation has important neurodevelopmental consequences. Our proposal seeks to extend those studies by investigating in vivo whether maternal infection will lead to a similar excess of cholinergic neurons in the fetal brain. We will also seek to determine whether several known inflammatory signals will act similarly in culture and what developmental mechanisms they might use to create excess numbers of these neurons. Finally, we hope to begin to identify the specific molecules that cause the basal forebrain to develop abnormally. 

PI: Kawikova (Pilot Award, 2006)

Does Autoimmunity play a Role in the Pathogenesis of Autism ($120,000) 

Many neuropathological studies in autism have reported a reduction in numbers of cells in the brain in areas which control motor coordination and cognitive functioning. While the mechanism of this loss in cell number is unknown, a recent study demonstrated the presence of inflammation in the same brain areas. This suggests that an autoimmune process may play a role in the neuronal loss observed in autism. Autoimmunity occurs when the immune system not only protects the body against infectious microorganisms, but mounts an immune response against one’s own tissue. This experiment will investigate whether the mechanisms which regulate autoimmunity are inadequate in children with autism and whether this is accompanied by signs of immune system activation. Measures of immune function will also be coupled with diagnostic instruments to shed light on whether changes in immune system activation is related to the severity of autism symptoms which is different from individual to individual. 

PI: Le Belle (CAN Pilot Project Award, 2006)

Molecular and Environmental Influences on Autism Pathophysiology (CAN Young Investigator Award, 2006; $80,000) 
The incidence of macrocephaly (enlarged head) in the population of autistic patients is considerably higher than in control populations and indicates that this may contribute to the development of ASD. We are interested in what genetic and environmental changes underlie the development of macrocephaly and autism. Mutations in PTEN can be found in some autistic patients with macrocephaly. We have a mouse model of macrocephaly in which the gene PTEN has been deleted, resulting in the abnormal growth of brain cells, producing animals with large heads. We have recently shown that PTEN has a role in the ability of normal brain stem cells to self-renew, proliferate, and grow. We will use a relatively new technology in the study of gene expression in the brain, called microarray, to identify genes that are changed in our macrocephalic PTEN mutant mice. These experiments may identify genes and gene networks that contribute to ASD. We will also study how PTEN activity is affected by environmental factors. One such factor is oxidative stress. Oxidative stress is a general term used to describe oxidative damage to a cell, tissue, or organ, caused by reactive oxygen species. Most reactive oxygen species come from the internal sources as byproducts of normal cellular metabolism, such as energy generation from mitochondria. External sources include exposure to cigarette smoke, environmental pollutants such as emission from automobiles and industries, consumption of alcohol in excess, asbestos, exposure to ionizing radiation, and bacterial, fungal or viral infections. We and others have found that low levels of oxidative stress can enhance the self-renewal and proliferation of brain stem cells when grown in a culture dish, and this also results in decreased amounts of PTEN gene expression. We propose to look further at this potential mechanism by over-expressing pro-oxidant genes and disrupting anti-oxidant genes in cultured cells and in developing mouse embryos to determine if oxidative stress is a key environmental factor in the development of ASD with macrocephaly.

PI: Lipkin (CAN Pilot Project Award, 2006)

Histologic, Microbiological and Molecular Analyses of Bowel Disease in ASDs ($120,000) 

Debilitating gastrointestinal (GI) dysfunction is described in some autistic children, possibly at higher frequency in individuals with a regressive phenotype. Its cause is unknown; however, some studies have implicated inflammation or infection. The significance of gastrointestinal dysfunction for brain dysfunction is controversial; some investigators have proposed that differences in GI microflora induce inflammation, influence permeability of the GI tract, or release novel neuroactive peptides that have remote effects in brain. Our project will use sensitive new assays for gene expression, microbiology and immunology to survey GI tract biopsies and blood from two groups of children: one group with GI dysfunction and autism, and one group with GI dysfunction but no neurological disturbance. The implication of an infectious agent (or agents) as factors (or cofactors) in autism or associated GI comorbidity could lead to new strategies for prophylaxis or therapeutic intervention. Discovery of distinct profiles of gene expression in GI tract or of soluble factors in peripheral blood may provide insights into pathogenesis; inform genetic analyses; and facilitate management by providing therapeutic targets and objective criteria for diagnosis and treatment response.

PI: McAllister (Mentor-based Fellowship, 2006)

The role of MHC class I molecules in synapse formation: possible implications for the pathogenesis of autism ($78,000)

Although there is a strong genetic component to autism and autism spectrum disorder, there are non-genetic causal factors. Maternal viral infection has been put forward as one such factor. During an infection, the immune system releases molecules called cytokines which then trigger an increase in MHC-I molecules. Dr MacAllister’s team has previously shown that altered MHC-I levels can affect the brain by reducing the ability of neurons to form synapses and modifying existing connections. Therefore, it is possible that modifications of immune function may alter normal brain development and possibly produce symptoms of ASD.

This new research will investigate the specific role of cytokines on MHC-I expression and how these changes affect neuronal development. This will be done by measuring MHC-I levels after administration of cytokines as well as examining the number of synapses following exposure. Finally, the function of these neuronal connections will be tested to determine whether the immune response, possibly altered in autism, leads to impaired connectivity and circuitry.

What this means for people with autism: Changes in immune system function have been reported in individuals with autism, but the consequences of this hyperactivity on brain development are not yet well understood. These studies will lead to a better understanding of the neurobiological consequences of altered immune activity, and how they relate to ASD.

PI: McAllister (CAN Pilot Project Award, 2006)

A Role for Immune Proteins in Early Stages of Neural Development: Possible Implications for the Pathogenesis of Autism (CAN Pilot Project Award, 2006; $120,000)

Proper formation of connections in the brain during childhood provides the substrate for adult perception, learning, memory, and cognition. Tragically, improper formation or function of these connections leads to many neurodevelopmental disorders, including autism. Autism spectrum disorder is a highly prevalent severe neurobehavioral syndrome with a heterogeneous phenotype. Although there is a strong genetic component to autism, the syndrome can also be caused or influenced by nongenetic factors. Specifically, maternal viral infection has been identified as the principle nongenetic cause of autism. Several studies have even indicated a genetic link between autism and immune system genes. Since immune molecules are increased following infection and are present in the developing brain, it is possible that changes in these immune molecules lead to changes in neuronal connectivity that underlie some forms of autism. This proposal will test this idea by studying the function of altered levels of a specific kind of immune molecule on the initial formation of connections and their subsequent plasticity in the developing brain. Thus, our results should reveal a mechanism for the primary nongenetic cause of autism and thereby illuminate potential preventive therapies for this devastating disease.What this means for people with autism: Determining the precise role of specific immune activity may elucidate an important immune mechanism leading to inflammation in CNS of autistic patients, as well as open new therapeutic possibilities for these patients.

PI: Pessah(CAN Environmental Initiative Innovator Award, 2006)

Contribution of Calcium Channel Mutations to Autism Risk and Mercury Susceptibility ($140,000) 

The goal of this research is to understand the genetic and environmental risk factors contributing to the incidence and severity of core symptoms and comorbidity seen in childhood autism. Dr. Pessah hypothesizes that mutations in specific types of calcium (Ca2+) channels may contribute to certain forms of autism and significantly increased susceptibility to adverse effects of environmental toxicants. This hypothesis is based on evidence from the Pessah lab that organic mercury, polychlorinated biphenyls, and flame retardants (PBDEs) can alter the intracellular Ca2+ signals generated by ryanodine receptors, an important type of calcium channel, and that these receptors are essential for normal maturation and function of both the immune and nervous systems. To attain these goals, mice that contain mutations for calcium channels will be studied for abnormal social behavior and their possible heightened susceptibility to organic mercury compounds such as thimerosal will be studied in detail. One mouse currently being developed possesses a mutation within a specific calcium channel (Cavl.2) that has been found to cause Timothy Syndrome (TS). Children with TS have a 60% rate of an autism diagnosis, with up to 80% of the children showing some signs of autism. Two additional mouse models are currently being studied that possess a mutation within the type 1 or type 2 ryanodine receptor Ca2+ channel (RyR1 and RyR2, respectively). Dr. Pessah’s lab has found that mice possessing mutations in RyR channels have heightened susceptibility to chemically-induced adverse reactions of the immune and nervous systems. Together, the Cavl.2 and RyR2 receptors form a signaling unit in heart, neurons and T lymphocytes. This project will investigate whether these three lines of mice, which have an underlying genetic defect in Ca2+ signaling, will have increased behavioral and immunological problems when exposed to mercury, and will also examine whether mercury directly affects the development of nerve cells from these animals. Finally, the Pessah lab will determine whether children with autism have a higher frequency of Cavl.2 or RyR mutations. Collectively these experiments will provide important new information on the possible contribution of Cavl.2 or RyR mutations to autism risk in humans and launch studies of enhanced susceptibility of the developing nervous and immune systems to organic forms of mercury in mice carrying mutations relevant to autism. 

PI: Rosenspire (CAN Pilot Award, 2007)

The Overlap Between Celiac Disease and Autism – Potential Inflammatory Responses Exacerabated by Exposure to Toxicants Such as Mercury ($60,000) 

The aim of this grant is to research the connection between autism and celiac disease (CD), an autoimmune disorder of the small intestine characterized by intolerance to dietary gluten. Establishing an unambiguous link of CD to autism will allow them to pursue their hypothesis that CD may lead to inappropriate inflammation in the brain, and that patients with CD may also be especially prone to adverse inflammatory responses upon exposure to environmental toxicants such as mercury. 

PI: Silbergeld (CAN Pilot Project Award, 2006)

Genetic Susceptibility to Mercury-induced Immune Dysfunction in Autism and Autism- Spectrum Disorders ($120,000) 

The goal of this project is to examine genes that may affect responses to environmental risk factors in autism and autism spectrum disorders (ASD). These are complex diseases that are known to involve interactions between genetic susceptibility and acquired (or environmental) exposures. However, most research on autism/ASD development has not examined these interactions, but rather focused on either genetic or environmental risk factors, including mercury compounds. The failure to include gene-environment interactions may be one reason why we have not yet identified either key genes or significant environmental risk factors associated with autism/ASD. We plan to examine whether there are differences in how children with autism/ASD respond to one environmental contaminant (mercury) compared to their unaffected siblings and parents. We hypothesize that mercury does not cause autism by itself, but that individuals who carry certain variations in specific genes may have heightened responses to mercury, and that these variations will increase the likelihood that those children exposed to mercury will develop autism/ASD. In order to accomplish our goal, we will first develop and validate a panel of tests using immune cells found in human blood to quantitate immune responses to mercury in vitro by using the blood of healthy volunteers. Then we will apply this panel to cells obtained from children diagnosed with autism/ASD, their unaffected siblings, their parents, and unrelated community controls. This project will be the first study on this topic conducted in cells from human subjects. Eventually, we hope to identify variations in specific genes related to these responses to mercury for use in epidemiological studies of autism/ASD. 

PI: Singer (Pilot Award, 2005)

Autoimmune Abnormalities in Autism: a Family Study ($120,000) 

Several theories have been proposed based on the presence of antineurononal antibodies (ANAb) in individuals with autism. One study suggests that autism may be caused by the placental transfer of antibodies that, in turn, interfere with the development of the fetal brain. A second hypothesis suggests that identifying antibodies against specific central nervous system (CNS) proteins is essential in providing clues about the underlying pathophysiology. In order to further investigate the possibility of placental transfer of antibodies as a cause for autism, Dr. Singer’s research will compare antibody levels in mothers of children with autism to those of unaffected children. He will also study both adult and fetal postmortem brain tissue to look at differentiation based on developmental factors. 

What this means for people with autism: The identification of autoimmune abnormalities can aid in the definition of the autism phenotype, and provide new insight for physiological mechanisms behind the cause of autism as well as potential preventative therapy. 

PI: Wills-Karp, Malloy, Manning-Courtney (Pilot Award, 2006)

Does Immune System Dysfunction Play a Role in Autism? ($100,000) 

Recent evidence suggests that the immune system, which normally protects the body against many diseases, may malfunction in people with autism and actually contribute to or produce this disorder. “Adaptive” immune “T” cells are summoned by ‘innate” immune cells to attack invaders. Immune T cells in some people, however, mistake the body’s own tissues as foreign and attack them, a process called “autoimmunity.” Immune T cells also can over-react to otherwise harmless substances, such as pollen, and produce allergies. Usually these potentially errant responses by immune T cells are kept under control by ‘regulatory T cells.” Regulatory T cells are produced by the Foxp3 gene. According to the collaborating researchers, who combine expertise in autism, immunity, and patterns of disease (“epidemiology”), a disproportionate number of children with autism have immune system malfunctions that are similar to those seen in autoimmunity, allergy, or both conditions. They hypothesize that regulatory T cells in people with autism may be too few, or too weak, to provide a generalized ability to control errant immune responses, which contributes to, or causes, autism.

The collaborators will study immune T cells, which circulate through the bloodstream, in blood samples taken from 20 children with autism and 20 healthy (“control”) children. They will compare the number of regulatory T cells, and how effectively these cells control the “attacker” T cells, in blood samples from the two groups of children. The investigators also will find out whether differences exist in the two groups of blood samples in the amount of chemicals, called ‘cytokines,” produced by attacking T cells. Excessive amounts of these cytokines, suggesting incomplete control of T cells by their regulators, may have consequences for the brain, providing a link between immune dysfunction and autism. Alternatively, some other factor may be common to both immune regulation and to autism. 

What this means for people with autism:
 If this study indicates that a failure to properly regulate immune T cells is involved in autism, the research will provide a better understanding of immune system involvement in autism. The findings also may provide an immune “marker” to diagnose autism, and lead to development of specific immune-based therapies to prevent or treat autism. 

PI: Vogel (Pilot Award, 2006)

Neuroinflammation, the Kynurenine Pathway, and Autism($118, 692) 

Although the causes of autism are still unknown, there is growing evidence that genetic, environmental, and immunological factors may contribute to the development of the disorder. Many cases of autism are reported to be associated with chronic activation of the immune system. This experiment will investigate markers of chronic neuroinflammation in brain tissue from individuals affected with autism. These markers will be compared to levels of two newly studied neuroactive compounds which have been associated with cell death: kynurenic acid (KYNA) and quinolinic acid (QUIN). Dr. Vogel and his colleagues will investigate if alterations in the relative abundance of KYNA and/or QUIN affect the development and functioning of neural circuits or induce damage in the nervous system thereby contributing to the development of autism. 

What this means for people with autism: Alterations in immune system function has been associated with autism, however, the link between immune reactivity and onset of autism spectrum disorder has not been clearly defined. Changes in KYNA and QUIN in human postmortem tissue along with other neuropathological alterations would help better define the relationship of the immune system in brain development and neurodevelopmental disorders. These results could lead to new targets, possibly those in the immune system, for the development of novel treatments for autism. 

PI: Vogt (Pilot Award, 2005)

Immune Biomarkers in Serum and Newborn Dried Blood Spots ($118,880)

At present, there are no biological tests that can be performed to diagnose autism. This study will help develop methods and establish reference ranges for measuring immune biomarkers in infants, children, and mothers that could aid in early recognition and diagnosis of autism. The researchers will investigate if autism may be caused by immune and inflammatory reactions that influence neural development during gestation and infancy. They will use the microbead suspension array (MSA), which is a flexible, highly sensitive assay system that can be used to measure multiple biomarkers simultaneously from a very small sample, such as a drop of blood. Dr. Vogt and his colleagues hope to develop a panel of reliable, transferable laboratory methods for measuring selected biological markers of the immune system in serum and dried blood spots (DBS). 

What this means for people with autism: This study will help establish tests and reference ranges that are readily transferable to other laboratories, so that all research and public health investigators can make use of them. Ideally, these population- based research activities will implicate specific environmental triggers of autism and help lead to preventive measures. 

C. Studies which investigates other environmental factors: 

PI: Chen (Pilot Award, 2006)

Testing the “Extreme Male Brain” Theory of Autism ($100,000) 

Autism occurs four times more frequently in males compared to females, suggesting that a complex genetic predisposition, involving hormones, is involved. According to these researchers, since females have stronger emphasizing capability, while males have stronger systemizing capability, an “extreme male brain” (EMB) theory may explain the genetic basis of autism. This theory proposes that individuals along the autism spectrum are characterized by impairments in empathy alongside intact or even exceptional systematizing capacities. The researchers suggest that endogenous hormone levels of either or both the parent and the fetus during development are important. They hypothesize that inherited genetic variations in androgen metabolism modify the risk of autism, that there is a critical time when fetal exposure to androgens, specifically testosterone, is related to later development of autism spectrum disorder. 

They will test the EMB theory by undertaking genetic studies in 260 mother-child pairs in which the child has autism. First, the researchers will identify different forms of androgen-metabolizing genes that are biomarkers for integrated hormone levels. They then will assess this relationship between androgen metabolism and autism risk by analyzing forms of genes that favor the production and accumulation of testosterone. Thereafter, they will confirm whether the forms of genes identified occur in 300 healthy mother-child pairs, and whether maternal or fetal hormonal levels are key. Through this process, the researchers will derive direct evidence on whether or not the EMB theory is valid. 

What this means for people with autism: If the EMB theory is validated, it would lead to further clinical efforts to assess genetic or individual susceptibility factors that increase the risk of autism, and to explore whether contributing hormonal, environmental or dietary exposures might be minimized. 

PI: Dodds (CAN Pilot Project Award, 2007)

Risk for Developing Autism: A Population-Based Longitudinal Study of Obstetric and Neonatal Factors ($119,662) 

Autism is part of a spectrum of disorders that are characterized by severe impairment in social interaction and communication and by the presence of inflexible behavior. Numerous reports suggest a trend of increasing rates of autism in Canada and in other countries, although it is not clear whether this increase reflects increased awareness of autism and changes in the way autism is diagnosed or whether the increase reflects true population increases in the disorder. Little is known about the causes of this disorder. Several recent studies have suggested that problems in pregnancy or in the newborn period may play a role in the development of autism. The purpose of this study is to use a population-based approach to identify pregnancy and newborn factors that are associated with the subsequent development of autism. Understanding the role of early life factors that are related to the development of autism is a first step towards early diagnosis and intervention. 

PI: Happe (Mentor-based Fellowship, 2006)

From Genes to Behavior: A Multidisciplinary Investigation of the Autism Triad ($82,000) 

Most research on autism spectrum disorders (ASDs) has assumed that the three core behaviors that represent ASDs—social impairments, communication, and restricted/repetitive behaviors – the “triad” are interrelated. However, it is possible that these three domains may be very different and caused by different mechanisms. This implies that different features of autism may be caused by different genes, associated with different brain regions and related to different core cognitive impairments. Dr. Happe and her colleagues, therefore propose that research is likely to learn more about ASDs by examining each of these behaviors separately. 

Dr. Angelica Ronald, the post-doctoral fellow, will conduct new analyses to examine individual differences in affected and non-affected people in three domains of cognitive processing. She will also identify genetic markers and environmental factors which are associated with each core behavior. This will help better identify the causes for each symptom of autism, and determine if they can be separated from one another. Data and resources from the Twins Early Development Study, will be used to expedite findings. The post-doctoral fellow is well qualified for this project, having already published several papers on autism research and recently received the 2006 Young Investigator Award by the International Society for Autism Research. 

What this means for people with autism: This research will take a novel approach to studying the gene-brain-behavior pathways in ASDs by examining the three core behavioral traits of ASD separately. If the theory holds up and different features of autism are caused by different genes, associated with different brain regions, and related to different core cognitive impairments, the findings from this study may lead to tailored interventions designed to address specific characteristics of each behavioral trait. 

PI: Kinney (CAN Pilot Project Award, 2005)

Do Environmental Factors Play a Role in Autism? A Test Using Natural Experiments ($80,000) 

Whether environmental factors play an important role in causing autism is a crucial – and hotly debated – question. Many studies report unusually high rates of medical problems during the gestations and births of persons who later developed autism, suggesting that environmental factors occurring before or around the time of birth may contribute to the development of the disorder. Skeptics, however, argue that the same genes that cause autism also cause these high rates of pregnancy and birth complications. The most powerful scientific approach to deciding this issue — an experiment in which pregnant women were randomly assigned to low vs. high stress conditions – would clearly be unethical. We use an alternative strategy that uses natural disasters as “experiments of nature” to test the hypothesis that exposure to stressful events during vulnerable weeks of gestation significantly increases risk of developing autism. Anonymous data on more than 4,000 persons with autism from three different states, as well as on 2 million general population births in these same states, will be studied to investigate whether autism rates are significantly increased among individuals who were in certain weeks of gestation at the time their mothers were exposed to natural disasters such as extremely destructive earthquakes, hurricanes, and severe blizzards. Confirmation that pre- and perinatal environmental stressors play a significant role in causing autism would have important implications for the treatment and prevention of autism. 

PI: Nair (Special Project, 2006)

Neurodevelopmental disabilities among children in India($100,000) 

Given current epidemiologic estimates, there are approximately 1.7 million individuals with autism in India. The primary objective of this research project is to assess the screening and diagnostic prevalence of neurodevelopmental disorders, including autism, in children between the ages of 2-9 in India and gain information on risk factors in these children. The investigators will develop a novel neurodevelopmental disability screening tool and consensus clinical criteria, and validate these instruments so that they can be used in as a diagnostic instrument for further evaluation of the prevalence of autism in this country. In addition to studying the prevalence of autism in Indian, the investigators will also identify the full clinical spectrum of autism using their test instruments. In addition to case ascertainment, potential risk factors for autism, including infections, nutritional deficiencies and genetic factors will be identified through open ended interviews with health personnel. 

What this means for people with autism:
 The identification of an initial nation-wide developmental disability cohort would allow more refined characterization of the Indian autistic population, setting the stage for exploring future scientific opportunities in causes (more comprehensive epidemiology and genetic studies), diagnosis (Baby Sibs), and treatment (clinical trials) in that country. By generating valid data from India, capturing socio-cultural and geographical variability, researchers can better identify the true worldwide prevalence of autism and further quantify risk factors which may contribute to these differences. 

PI: Patterson (Mentor-based Fellowship, 2006)

Role of Cytokines in Mediating the Role of Maternal Immune Activation in the Fetal Brain ($52,000) 

Children whose mothers develop infections during pregnancy are at increased risk for autism, schizophrenia or other neurodevelopmental disorders. However the molecular pathway that leads from infection to autism is unclear. Using an animal model of maternal viral infection, Dr. Patterson have shown that the maternal immune reaction, rather than the virus itself, interferes with fetal development leading to behavioral symptoms of heightened anxiety and decreased social interaction. 

This experiment will establish which specific immune factors interfere with fetal brain development. Four different immune factors will be tested to produce and then reverse early behavioral deficits in offspring exposed in utero to these immune factors. Any immune factor that meets both criteria will be a leading candidate for continued research into specific molecular pathways that interfere with normal development and lead to autism-like symptoms. 

What this means for people with autism: This project will use a mouse model of a known risk factor for autism—maternal viral infection—to determine a mechanism that elicits changes in fetal brain development and leads to the autistic phenotype. These findings could lead to a better understanding of what goes wrong in autism, and suggest potential methods of preventing the disorder. 

PI: Rakic (Mentor-based Fellowship, 2006)

Effects of a Non-Steroidal Anti-Inflammatory Drug on Neuronal Migration ($101,000)

While the precise causes of autism is not yet known, multiple genetic and environmental factors are thought to play an important impact on the development of the disorder. The site where certain neurons connect, called gap junctions, are sensitive to environmental agents and have downstream effects on cell growth and reproduction, and possibly on migration of neuronal precursors to their appropriate destinations. In order to manipulate the function of the gap junction in an animal model, the investigators will test the effects of an NSAID which alters the function of gap junctions on the activity of neurons during development and migration. Deficits in neuronal migration and formation of different layers of the cortex may lead to the neuropathological and behavioral features observed by other scientists. 

The mentor and the fellow will use advanced molecular biology techniques to trace the position of the migrated neurons during critical periods of neuronal development. They will also study properties of the misplaced neurons to determine their abilities to participate in a functional network. Finally, behavioral analysis of offspring exposed to prenatal NSAIDS will be performed. This will help better link any neurobiological differences with functional outcomes, especially as they relate to the symptoms of autism spectrum disorder. 

What this means for people with autism: Using disruption of the gap junction by biophysical and environmental factors will help identify the cause of cortical malformation. This will be relevant to a better understanding of brain development as well as the causes of autism spectrum disorders 

PI: Schmitz (Pilot Award, 2005)

Cytoarchitectural Alterations in the Cerebral Cortex in Autism($120,000) 

Dr. Schmitz’s lab has been studying the neuropathological characteristics of autism for many years. His group has reported abnormalities in size, number, and organization of neurons in the cerebral cortex. This current study will utilize novel tools to view the organization of cells in the cortex in three dimensions, specifically examining the connectivity of neurons between different areas of the cortex. Furthermore, his lab will compare these changes with those of a current animal model of autism: in utero maternal influenza virus exposure. 

What this means for people with autism: The results of the proposed project will contribute to a better understanding of the neuropathology of autism using software which will be made available to the research community. In addition, this study will investigate the validity of an animal model of autism where environmental factors play a key role. 

PI: Windham (Pilot Award, 2006)

Autism and Prenatal Hormone Markers($60,000) 

The California Department of Health Services is currently tracking the prevalence and demographic characteristics of autism. This data will be linked to hormone and protein markers measured during pregnancy. This is made possible though the California prenatal screening program, in which several hormones or protein markers were measured in maternal blood during the second trimester. In the proposed study, the levels of these hormone/protein in nearly 2,000 pregnant women and their offspring who are later diagnosed with autism, compared to the nearly 600,000 screened births during the same two years. Although hormonal factors have been frequently suggested as contributing to the occurrence or severity of autism, few studies have investigated this hypothesis. 

What this means for people with autism: The results will help shape further research to rigorously evaluate complex interactions between genetic factors, in utero hormonal factors, and environmental factors in relation to autism. In addition to the analyses proposed, the investigators have numerous opportunities for follow-up, including examining similar parameters in other birth years, examining other newborn screening markers, and potentially obtaining newborn blood spots for genotyping. The proposed study provides a unique and cost-effective opportunity explore important data on a very large population.


Autistic people have fought the inclusion of ABA in therapy for us since before Autism Speaks, and other non-Autistic-led autism organizations, started lobbying legislation to get it covered by insurances and Medicaid. 

ABA is a myth originally sold to parents that it would keep their Autistic child out of an institution. Today, parents are told that with early intervention therapy their child will either be less Autistic or no longer Autistic by elementary school, and can be mainstreamed in typical education classes. ABA is very expensive to pay out of pocket. Essentially, Autism Speaks has justified the big price tag up front will offset the overall burden on resources for an Autistic’s lifetime. The recommendation for this therapy is 40 hours a week for children and toddlers.

The original study that showed the success rate of ABA to be at 50% has never been replicated. In fact, the study of ABA by United States Department of Defense was denounced as a failure. Not just once, but multiple times. Simply stated: ABA doesn’t workIn study after repeated study: ABA (conversion therapy) doesn’t work. 

What more recent studies do show: Autistics who experienced ABA therapy are at high risk to develop PTSD and other lifelong trauma-related conditions. Historically, the autism organizations promoting ABA as a cure or solution have silenced Autistic advocates’ opposition. ABA is also known as gay conversion therapy.

The ‘cure’ for Autistics not born yet is the prevention of birth. 

The ‘cure’ is a choice to terminate a pregnancy based on ‘autism risk.’ The cure is abortion. This is the same ‘cure’ society has for Down Syndrome. 

This is eugenics 2021. Instead of killing Autistics and disabled children in gas chambers or ‘mercy killings’ like in Aktion T4, it’ll happen at the doctor’s office, quietly, one Autistic baby at a time. Different approaches yes, but still eugenics and the extinction of an entire minority group of people.

Fact: You can’t cure Autistics from being Autistic.

Fact: You can’t recover an Autistic from being Autistic.

Fact: You can groom an Autistic to mask and hide their traits. Somewhat. … however, this comes at the expense of the Autistic child, promotes Autistic Burnout (this should not be confused with typical burnout, Autistic Burnout can kill Autistics), and places the Autistic child at high risk for PTSD and other lifelong trauma-related conditions.

[Note: Autism is NOT a disease, but a neurodevelopmental difference and disability.]

Fact: Vaccines Do Not Cause Autism.

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