Social conformity and autism spectrum disorder : a child-friendly take on a classic study

Perhaps surprisingly, given the importance of conformity as a theoretical construct in social psychology and the profound implications autism has for social function, little research has been done on whether autism is associated with the propensity to conform to a social majority. This study is a modern, child-friendly implementation of the classic Asch conformity studies. The performance of 15 children with autism was compared to that of 15 typically developing children on a line judgement task. Children were matched for age, gender and numeracy and literacy ability. In each trial, the child had to say which of three lines a comparison line matched in length. On some trials, children were misled as to what most people thought the answer was. Children with autism were much less likely to conform in the misleading condition than typically developing children. This finding was replicated using a continuous measure of autism traits, the Autism Quotient questionnaire, which showed that autism traits negatively correlated with likelihood to conform in the typically developing group. This study demonstrates the resistance of children with autism to social pressure

A Qualitative Study of the Effects of the University of Arkansas Autism Support Program

Abstract Individuals who have been diagnosed with autism spectrum disorder are often united by the following characteristics: difficulty communicating and interacting with others, inhibited ability to function socially, difficulty functioning academically or at work, and trouble transitioning to independent lifestyles (Lord, 2013). The purpose of this study was to determine how undergraduate students with Autism Spectrum Disorder perceive the helpfulness of the University of Arkansas Autism Support Program in the following areas: reducing college- related stress, facilitating academic success, facilitating social success, and preparing individuals for independent adult roles. In short, the study sought to determine the effects of the University of Arkansas Autism Support Program on participating undergraduate students with Autism Spectrum Disorder. Data was collected via a paper and pencil questionnaire and an oral interview for undergraduate members of the University of Arkansas Autism Support Program to complete. The results of this study are beneficial to any individual who has a connection to autism in academia (i.e. students with autism spectrum disorders, autism support program employees, peers, professors, researchers, family members, etc.) and provides useful qualitative data on the strengths and weaknesses of one of many college-level autism support programs through the eyes of participating students

Exaggerated CpH methylation in the autism-affected brain.

BackgroundThe etiology of autism, a complex, heritable, neurodevelopmental disorder, remains largely unexplained. Given the unexplained risk and recent evidence supporting a role for epigenetic mechanisms in the development of autism, we explored the role of CpG and CpH (H = A, C, or T) methylation within the autism-affected cortical brain tissue.MethodsReduced representation bisulfite sequencing (RRBS) was completed, and analysis was carried out in 63 post-mortem cortical brain samples (Brodmann area 19) from 29 autism-affected and 34 control individuals. Analyses to identify single sites that were differentially methylated and to identify any global methylation alterations at either CpG or CpH sites throughout the genome were carried out.ResultsWe report that while no individual site or region of methylation was significantly associated with autism after multi-test correction, methylated CpH dinucleotides were markedly enriched in autism-affected brains (~2-fold enrichment at p < 0.05 cutoff, p = 0.002).ConclusionsThese results further implicate epigenetic alterations in pathobiological mechanisms that underlie autism

Social Difficulties in Youth with Autism With and Without Anxiety and ADHD Symptoms

Social difficulties inherent to autism spectrum disorder are often linked with co‐occurring symptoms of anxiety and attention deficit hyperactivity disorder (ADHD). The present study sought to examine the relation between such co‐occurring symptoms and social challenges. Parents of adolescents with autism (N = 113) reported upon social challenges via the social responsiveness scale (SRS) and anxiety and ADHD symptomatology via the Child Behavior Checklist. Results revealed differences in SRS scores across co‐occurring symptom subgroups (Anxiety, ADHD, Both, Neither)—namely, adolescents with autism and anxiety as well as those with autism, anxiety, and ADHD showed greater scores on the SRS than the other groups. Implications for research and clinical practice are discussed and recommendations are offered. Lay Summary Anxiety and attention deficit hyperactivity disorder (ADHD) symptoms are related to greater social challenges for adolescents with autism spectrum disorder. The present study found that autism with anxiety and autism with anxiety and ADHD, was related to greater social difficulties than autism alone. Findings provide further support for the intertwined nature of anxiety and ADHD symptoms in autism. What this may mean for research and clinical practice is considered and recommendations are suggested

Autism-associated SNPs in the clock genes _npas2_, _per1_ and the homeobox gene _en2_ alter DNA sequences that show characteristics of microRNA genes.

Intronic single nucleotide polymorphisms (SNPs) in the clock genes _npas2_ and _per1_ and the homeobox gene _en2_ are reported to be associated with autism. This bioinformatics analysis of the intronic regions which contain the autism-associated SNPs rs1861972 and rs1861973 in _en2_, rs1811399 in _npas2_, and rs885747 in _per1_, shows that these regions encode RNA transcripts with predicted structural characteristics of microRNAs. These microRNA-like structures are disrupted _in silico_ by the presence of the autism enriched alleles of rs1861972, rs1861973, rs1811399 and rs885747 specifically, as compared with the minor alleles of these SNPs. The predicted gene targets of these microRNA-like structures include genes reported to be implicated in autism (_gabrb3_, _shank3_) and genes causative of diseases co-morbid with autism (_mecp2_ and _rai1_). The inheritance of the AC haplotype of rs1861972 - rs1861973 in _en2_, the C allele of rs1811399 in _npas2_, and the C allele of rs1234747 in _per1_ may contribute to the causes of autism by affecting microRNA genes that are co-expressed along with the homeobox gene _en2_ and the circadian genes _npas2_ and _per1_

Reduced face identity aftereffects in relatives of children with autism.

Autism is a pervasive developmental condition with complex aetiology. To aid the discovery of genetic mechanisms, researchers have turned towards identifying potential endophenotypes - subtle neurobiological or neurocognitive traits present in individuals with autism and their "unaffected" relatives. Previous research has shown that relatives of individuals with autism exhibit face processing atypicalities, which are similar in nature albeit of lesser degree, to those found in children and adults with autism. Yet very few studies have examined the underlying mechanisms responsible for such atypicalities. Here, we investigated whether atypicalities in adaptive norm-based coding of faces are present in relatives of children with autism, similar to those previously reported in children with autism. To test this possibility, we administered a face identity aftereffect task in which adaptation to a particular face biases perception towards the opposite identity, so that a previously neutral face (i.e., the average face) takes on the computationally opposite identity. Parents and siblings of individuals with autism showed smaller aftereffects compared to parents and siblings of typically developing children, especially so when the adapting stimuli were located further away from the average face. In addition, both groups showed stronger aftereffects for adaptors far from the average than for adaptors closer to the average. These results suggest that, in relatives of children with autism, face-coding mechanism are similar (i.e., norm-based) but less efficient than in relatives of typical children. This finding points towards the possibility that diminished adaptive mechanisms might represent a neurocognitive endophenotype for autism

Modeling Autistic Features in Animals

A variety of features of autism can be simulated in rodents, including the core behavioral hallmarks of stereotyped and repetitive behaviors, and deficits in social interaction and communication. Other behaviors frequently found in autism spectrum disorders (ASDs) such as neophobia, enhanced anxiety, abnormal pain sensitivity and eye blink conditioning, disturbed sleep patterns, seizures, and deficits in sensorimotor gating are also present in some of the animal models. Neuropathology and some characteristic neurochemical changes that are frequently seen in autism, and alterations in the immune status in the brain and periphery are also found in some of the models. Several known environmental risk factors for autism have been successfully established in rodents, including maternal infection and maternal valproate administration. Also under investigation are a number of mouse models based on genetic variants associated with autism or on syndromic disorders with autistic features. This review briefly summarizes recent developments in this field, highlighting models with face and/or construct validity, and noting the potential for investigation of pathogenesis, and early progress toward clinical testing of potential therapeutics. Wherever possible, reference is made to reviews rather than to primary articles

Environmental pre-requisites and social interchange : the participation experience of adolescents with autism spectrum disorder in Zurich

Aim: Participation of adolescents with autism spectrum disorder hardly occurs in settings outside of home and school. Little is known about how their participation is influenced by environmental factors. This study explored how and why adolescents with autism spectrum disorder perceive aspects of their environment as facilitators or barriers to their participation outside of home and school. Method: This explanatory case study explored the participation experiences of adolescents with autism spectrum disorder (15-21 years) from Zurich and surroundings with in-depth interviews and photo-elicitation, using photos made by the participants during activities outside of home and school. Data was analysed with a 7-step procedure. Result: The presence of two main themes seemed necessary to facilitate participation outside of home and school: "environmental prerequisites to attend activities", which consists of five subthemes, such as "the company of trusted persons" and "the provision of knowledge and information", and "social interchange and engagement", which consists of three subthemes and describes how actual involvement can be supported. Conclusion: Our findings highlight the influence of trusted persons on adolescents with autism spectrum disorder, and the need to extend the support network for these adolescents to other individuals, services and society so that their participation in activities can be encouraged. IMPLICATIONS FOR REHABILITATION: Adolescents with autism spectrum disorder perceive every kind of participation outside of home and school as social. We recommend using the company of trusted persons to encourage adolescents with autism spectrum disorder to actively participate outside of home and school. Rehabilitation professionals should promote environment-based approaches to achieve participation of adolescents with autism spectrum disorder. Rehabilitation professionals should actively approach, acknowledge and gently guide adolescents with autism spectrum disorder to support engagement in participation

The temporal binding deficit hypothesis of autism

Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication