1. Bambini-Junior V, Rodrigues L, Behr GA, Moreira JC, Riesgo R, Gottfried C. {{Animal model of autism induced by prenatal exposure to valproate: Behavioral changes and liver parameters}}. {Brain Res}. 2011 Aug 23;1408:8-16.
Autism is characterized by behavioral impairments in three main domains: social interaction; language, communication and imaginative play; and range of interests and activities. This syndrome has attracted social attention by its high prevalence. The animal model induced by prenatal exposure to valproic acid (VPA) has been proposed to study autism. Several characteristics of behavioral abnormalities found in the VPA rats, such as repetitive/stereotypic-like activity and deficit in social interaction have been correlated with autism. Features like flexibility to change strategy, social memory and metabolic status of the induced rats have not been examined. Thus, the main aim of this work was to investigate additional behavioral rodent similarities with autism, as well as, liver redox parameters after prenatal exposure to VPA. Young rats from the VPA group presented aberrant approach to a stranger rat, decreased conditioned place preference to conspecifics, normal spatial learning and a lack of flexibility to change their strategy. As adults, they presented inappropriate social approach to a stranger rat, decreased preference for social novelty, apparently normal social recognition and no spatial learning deficits. Examination of the liver from the VPA group presented significantly increased (12%) levels of catalase (CAT) activity, no alteration in superoxide dismutase (SOD) activity and a decrease in the SOD/CAT ratio. TBARS, sulfhydril and carbonyl contents, and serum levels of aminotransferases remained unchanged. In summary, rats prenatally exposed to VPA presented decreased flexibility to change strategy and social impairments similar to the autism symptoms, contributing to the understanding of neurodevelopmental symptoms and oxidative imbalance associated to the autism spectrum disorder.
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2. Dykens EM, Lee E, Roof E. {{Prader-Willi syndrome and autism spectrum disorders: an evolving story}}. {J Neurodev Disord}. 2011 Aug 20.
Prader-Willi syndrome (PWS) is well-known for its genetic and phenotypic complexities. Caused by a lack of paternally derived imprinted material on chromosome 15q11-q13, individuals with PWS have mild to moderate intellectual disabilities, repetitive and compulsive behaviors, skin picking, tantrums, irritability, hyperphagia, and increased risks of obesity. Many individuals also have co-occurring autism spectrum disorders (ASDs), psychosis, and mood disorders. Although the PWS 15q11-q13 region confers risks for autism, relatively few studies have assessed autism symptoms in PWS or directly compared social, behavioral, and cognitive functioning across groups with autism or PWS. This article identifies areas of phenotypic overlap and difference between PWS and ASD in core autism symptoms and in such comorbidities as psychiatric disorders, and dysregulated sleep and eating. Though future studies are needed, PWS provides a promising alternative lens into specific symptoms and comorbidities of autism.
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3. Facon B, Magis D, Belmont JM. {{Beyond matching on the mean in developmental disabilities research}}. {Res Dev Disabil}. 2011 Aug 17.
The matching of groups is a traditional way to control for confounding variables in developmental disabilities research. The equivalency of means across groups is routinely checked for these variables, but not the homogeneity of their variances or the shapes of their distributions. In the present paper, it is argued that group matching can go seriously wrong unless it directly confronts the distributional concerns by the use of well-known statistical indices and very simple graphical displays of the distributions. The question of the equivalency of item response profiles is also addressed since two participants or two groups of participants can obtain the same overall score on the matching variable by passing different items. In this case, the matching cannot be considered satisfactory because of poor concordance between the molar (overall score) and molecular (item scores) levels of matching. Angoff’s Delta plot method, a statistical approach for detecting differential item functioning across small groups is described. It is promising as a simple way to prove whole test/individual item correspondence and, in addition, a useful tool for making post hoc statistical analyses at the item level on the dependent variables.
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4. Geschwind DH. {{Genetics of autism spectrum disorders}}. {Trends Cogn Sci}. 2011 Aug 18.
Characterized by a combination of abnormalities in language, social cognition and mental flexibility, autism is not a single disorder but a neurodevelopmental syndrome commonly referred to as autism spectrum disorder (ASD). Several dozen ASD susceptibility genes have been identified in the past decade, collectively accounting for 10-20% of ASD cases. These findings, although demonstrating that ASD is etiologically heterogeneous, provide important clues about its pathophysiology. Diverse genetic and genomic approaches provide evidence converging on disruption of key biological pathways, many of which are also implicated in other allied neurodevelopmental disorders. Knowing the genes involved in ASD provides us with a crucial tool to probe both the specificity of ASD and the shared neurobiological and cognitive features across what are considered clinically distinct disorders, with the goal of linking gene to brain circuits to cognitive function.
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5. Laugeson EA, Frankel F, Gantman A, Dillon AR, Mogil C. {{Evidence-Based Social Skills Training for Adolescents with Autism Spectrum Disorders: The UCLA PEERS Program}}. {J Autism Dev Disord}. 2011 Aug 20.
The present study examines the efficacy and durability of the PEERS Program, a parent-assisted social skills group intervention for high-functioning adolescents with ASD. Results indicate that teens receiving PEERS significantly improved their social skills knowledge, social responsiveness, and overall social skills in the areas of social communication, social cognition, social awareness, social motivation, assertion, cooperation, and responsibility, while decreasing autistic mannerisms and increasing the frequency of peer interactions. Independent teacher ratings revealed significant improvement in social skills and assertion from pre-test to follow-up assessment. Examination of durability of improvement revealed maintenance of gains in nearly all domains with additional treatment gains at a 14-week follow-up assessment.
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6. Norris M, Lecavalier L, Edwards MC. {{The Structure of Autism Symptoms as Measured by the Autism Diagnostic Observation Schedule}}. {J Autism Dev Disord}. 2011 Aug 20.
The current study tested several competing models of the autism phenotype using data from modules 1 and 3 of the ADOS. Participants included individuals with ASDs aged 3-18 years (N = 1,409) from the AGRE database. Confirmatory factor analyses were performed on total samples and subsamples based on age and level of functioning. Three primary models were tested, including a one-factor model, the DSM-IV model, and the anticipated DSM-V model. Results indicated all models fit similarly. Module 1 ratings yielded better indices of fit across all models and higher inter-factor correlations than Model 3. Model fits were impacted by age and level of functioning. The lack of differentiation between models suggests that the structure of ASD symptoms is complex to measure statistically.
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7. Testa-Silva G, Loebel A, Giugliano M, de Kock CP, Mansvelder HD, Meredith RM. {{Hyperconnectivity and Slow Synapses during Early Development of Medial Prefrontal Cortex in a Mouse Model for Mental Retardation and Autism}}. {Cereb Cortex}. 2011 Aug 19.
Neuronal theories of neurodevelopmental disorders (NDDs) of autism and mental retardation propose that abnormal connectivity underlies deficits in attentional processing. We tested this theory by studying unitary synaptic connections between layer 5 pyramidal neurons within medial prefrontal cortex (mPFC) networks in the Fmr1-KO mouse model for mental retardation and autism. In line with predictions from neurocognitive theory, we found that neighboring pyramidal neurons were hyperconnected during a critical period in early mPFC development. Surprisingly, excitatory synaptic connections between Fmr1-KO pyramidal neurons were significantly slower and failed to recover from short-term depression as quickly as wild type (WT) synapses. By 4-5 weeks of mPFC development, connectivity rates were identical for both KO and WT pyramidal neurons and synapse dynamics changed from depressing to facilitating responses with similar properties in both groups. We propose that the early alteration in connectivity and synaptic recovery are tightly linked: using a network model, we show that slower synapses are essential to counterbalance hyperconnectivity in order to maintain a dynamic range of excitatory activity. However, the slow synaptic time constants induce decreased responsiveness to low-frequency stimulation, which may explain deficits in integration and early information processing in attentional neuronal networks in NDDs.
