Autism Speaks | 2009 Weatherstone Predoctoral Fellowships | #AutisticHistory #BanABA

Autism Speaks is NOT an autistic ally

[Note: Shared for #AutisticHistory archive purposes. This is NOT An Autistic Ally.]

2009 Weatherstone Predoctoral Fellowships *

Meaghan V. Parladé,
Mentor: Jana M. Iverson
University of Pittsburgh

Temporal Coordination of Social Communicative Behaviors in Infant Siblings of Children with Autism

The ability to coordinate use of gestures, eye contact, facial expressions, and language to communicate to others is a skill that typically develops in infancy. Older children with ASD have communicative impairments that reflect difficulty in producing coordinations of this sort. Identifying disruptions in development of this ability in infancy may help predict later ASD diagnosis.

This project examines the production and coordination of gestures, eye contact, facial expressions, communicative non-word vocalizations, and words in infants who, because they have an older sibling with autism, are at heightened risk for developing ASD. Infants will be observed monthly at home from 8 to 14 months, with follow-up visits at 18 and 24 months. The goals are to: a) document infants’ changing ability to coordinate communicative behaviors; b) observe differences in communicative coordinations between situations in which the child is interacting with an unfamiliar adult and those in which interaction is with a familiar caregiver; and c) evaluate delay and/or impairment in communicative coordination in infancy as a predictor of later ASD diagnosis.

Identifying indicators of autism at a significantly earlier point in development than is currently possible will allow for earlier initiation of treatment services. In addition, finding out when and how infants at risk for autism develop difficulties in integrating communicative behaviors will help us understand the nature of social communication impairments in older children with ASD and contribute to the development of more tailored interventions.

Lisa B. Wilson
Mentor: Donald C. Rojas
University of Colorado Denver

MEG Investigation of Phonological Processing in Autism

Deficits involving phonology, the sound system of language, are seen in a large subset of individuals with autism. There is also behavioral evidence for phonological processing deficits in the unaffected first-degree relatives of individuals with autism. Despite this, no neuroimaging studies, which enable a direct examination of brain structure and function, have investigated phonological processing in autism.

Using magnetoencephalography (MEG) and magnetic resonance imaging (MRI), the fellow will investigate the temporal dynamics and spatial localization of phonological processing in parents of children with autism and in adults with autism. In addition, several behavioral measures of phonological processing will be collected. Given the importance of language deficits in the symptomatology and clinical outcome of children with autism, the proposed work focuses on understanding impairments in structural levels of language processing that can diminish or even preclude subsequent language development.

By examining the brain mechanisms underlying phonological processing in parents of children with autism and in adults with autism, the aim of this research is to identify a neurophysiological biomarker of the language deficits seen in autism. A biomarker of structural language deficits could be used to guide and strengthen future genetic studies of autism. It would also allow for subgroup identification to aid clinical interventions.

Jennifer Foss-Feig
Mentor: Wendy Stone
Vanderbilt University

Neural mechanisms underlying an extended multisensory temporal binding window in ASD

It has long been reported that individuals with autism spectrum disorders (ASD) experience high rates of sensory disturbances, including sensory fascinations, sensitivities, and aversions, as well as difficulty integrating and understanding information occurring simultaneously across multiple senses. Previous studies in our lab have found that children with ASD have difficulty discriminating presentation order of rapidly-occurring sensory information and ?bind together? information from multiple senses across an extended time window. The timing of brain responses to basic sensory information could underlie the everyday sensory difficulties so commonly reported in ASD, as well as other core symptoms such as communication and social difficulties.

The proposed study will use noninvasive measures of brain electrical activity (EEG) to examine differences in brain processes that underlie: (1) processing of timing information in basic sensory information, and (2) binding together of multisensory stimuli (i.e., sights and sounds occurring close together in time). The study will also examine how differences in sensory and multisensory processing and the brain functions that underlie them relate to observed and reported individual differences in social, communication, and sensory symptoms. Finding out how the brain responds to and integrates rapidly-presented sensory information is essential for understanding sensory disturbances commonly reported in ASD and how these differences may relate to core deficits (i.e., communication, reciprocal social interaction, restricted/repetitive behaviors) in ASD. Understanding the nature and level of sensory processing difficulties may eventually lead to targeted diagnostic and intervention strategies.

M. Bangash
Mentor: Paul Worley
Johns Hopkins University

The role of SHANK3 in the etiology of autism spectrum disorder

Mutations in the SHANK3 gene have been implicated in a subset of patients with Autism spectrum disorder (ASD) in a gene-dosage dependent manner. Shank3 is a putative scaffold molecule found at the post-synaptic density (PSD), binds multiple partners and has been termed the master scaffolding molecule of the PSD. One of the key interactors of Shank3 is the Homer class of signaling and scaffold molecules. Shank3 and Homer act in concert to regulate spine maturation. Here we describe a novel Homer-dependent mechanism to stabilize Shank3 at the PSD. Both genetic and pharmacological tools can modulate this pathway thus having implications for ASD therapy. Finally, we are making a novel mouse model of SHANK3 that mimics a reported deletion of the Homer-binding domain of Shank3 in patients with ASD. This mouse model will be a useful tool to study the in vivo function of Shank3. Based on our data, we make predictions on the stability of Shank3 in this mouse model and propose a repertoire of biochemical and behavioral tests to link our molecular model with ASD-like behavior.

Elaine Hsiao
Mentor: Paul Patterson
California Institute of Technology

How Does IL-6 Mediate the Development of Autism-Related Behaviors?

Maternal infection is an environmental factor that can increase the incidence of autism in the offspring. In an animal model of this risk factor, respiratory infection of pregnant mice yields offspring that develop behavioral abnormalities and neuropathology consistent with those observed in autistic patients. These changes can be mimicked by maternal injection of the dsRNA, poly(I:C), which evokes an anti-viral inflammatory response. Recent studies have shown that the cytokine interleukin-6 (IL-6) is necessary and sufficient for mediating the development of behavioral and transcriptional changes in this maternal immune activation (MIA) model. While IL-6 is critical for mediating the effects of MIA, the mechanism by which IL-6 acts to alter neural development is unknown. Preliminary results indicate that IL-6 activates cells in the placenta and fetal brain, causing the induction of IL-6 response genes and IL-6 mRNA as well. This project will identify the cells that respond to IL-6 and localize the source(s) of IL-6 production. The long-term goals are to elucidate the molecular mechanisms by which IL-6 alters fetal brain development and to discover how these defects influence postnatal behavioral dysfunction.

Anna-Maria D’Cruz
Mentor: John A. Sweeney
University of Illinois at Chicago

Neurobiological Mechanisms of Insistence on Sameness in Autism

Insistence on Sameness (IS) is a core feature of autism, characterized by compulsive adherence to routine, and stereotyped, repetitive behaviors. IS makes it hard for individuals with autism to adjust to the dynamic demands of their environment. Their preference for sameness is typically accompanied by considerable distress when preferred behavioral patterns are interrupted. Consequently, IS in autism leads to serious behavioral management problems, has adverse effects on social relations and the capacity for independent living, and is a common reason why individuals with autism require psychiatric care. At present, we lack understanding of the alterations in functional brain systems that contribute to IS.

The fellow will test two hypotheses about abnormalities in brain function that may contribute to IS, using functional magnetic resonance imaging (fMRI) and behavioral studies. While the cognitive model of impaired set-shifting implicates dorsolateral prefrontal cortex (PFC) and dorsal striatum, altered reward processes implicate ventral striatum and ventrolateral PFC. The first hypothesis is that the brain systems responsible for changing from repetitive behaviors to more flexible ones are impaired. Alternatively, individuals with autism may not recognize or respond to external cues or rewards intended to promote changes in behavior. The fellow will use tests that require individuals to change from one set of behaviors to another, based on reward, to examine behavioral flexibility in autism.

Understanding the brain systems involved in changing behavior and their dysfunction will ultimately help guide treatment for this understudied yet disabling aspect of autism. Further, investigating reward processes in this context has broad relevance, given the reduced impact of social and other cues that are typically used to reinforce and support adaptive behavior in autism.

Bradford Elmer
Mentor: Kimberley McAllister
University of California at Davis

A role for immune molecules in cortical connectivity: potential implications for autism

Autism is a pervasive developmental disorder resulting from altered brain development and connectivity. It is thought that defects in synapse formation cause improper wiring in the brain, resulting in the cognitive and behavioral deficits typical in autism. The formation of synapses—synaptogenesis—is a very complex process. Only two proteins are currently known to decrease the number of these connections during early brain development. Interestingly, one of these proteins, the major histocompatibility complex class I (MHCI), happens to be very important in regulating the immune response while also being able to inhibit the establishment of synapses in the brain. The other protein, myocyte enhancer factor 2 (MEF2), is required for normal brain development and alters the expression of genes that are linked to autism.

The fellow proposes to use molecular biology and biochemical techniques to alter the function of MHCI and MEF2 in brain cells to probe the molecular pathway underlying their function. One of the most common themes among the environmental factors thought to lead to autism is their ability to activate the immune system. By defining the relationship between these two proteins with respect to synapse formation, this study will help us better understand how the immune system could alter connections in the developing brain to give rise to neurodevelopmental disorders. Most importantly, results from our work could identify novel drug targets for treating diseases that are influenced by immune dysregulation, such as autism.

Joshua Hailpern
Mentor: Karrie G. Karahalios (Co-mentors: James Halle and Laura DeThrone)
University of Illinois at Urbana Champaign

Visualizing Voice

The goal of this work is to develop and evaluate a set of voice visualization software tools that specifically target multi-syllabic word production in children autism spectrum disorders (ASD). The use of technology has the potential to alleviate some apprehension experienced by many ASD children when interacting with humans. In addition, it can provide teachers/therapists with new techniques to complement and/or supplement their existing approaches. Our goal with this work is to develop and evaluate a set of software programs that “paint” an individual’s voice on the screen, showing volume and pitch changes as well as when syllables occur.

Our preliminary studies lead us to believe there is potential to create a new direction of research utilizing real-time visualizations to teach language skills. We aim to develop these software tools using Task Centered User Interface Design method, in which subjects of the target population are involved with the software development from the beginning to the end of the design phase. This approach emphasizes building not simply what engineers think is needed, but building what the intended users demonstrate they need. In effect, the users become part of the development team. Interactions with computer technology can help to motivate children with ASD and may help to eliminate some apprehension experienced by many children when interacting with humans. Finally, due to the profile of strengths and weaknesses of children with ASD, the introduction of human-computer interaction may shed new light on a field that has been almost exclusively experienced through human-to-human interaction.

* The term of each fellowship is two years at $28,000 annually. The proposed training projects total $448,000.


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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