1. Davis MAC, Spriggs A, Rodgers A, Campbell J. {{The Effects of a Peer-Delivered Social Skills Intervention for Adults with Comorbid Down Syndrome and Autism Spectrum Disorder}}. {J Autism Dev Disord};2017 (Dec 22)
Deficits in social skills are often exhibited in individuals with comorbid Down syndrome (DS) and autism spectrum disorder (ASD), and there is a paucity of research to help guide intervention for this population. In the present study, a multiple probe study across behaviors, replicated across participants, assessed the effectiveness of peer-delivered simultaneous prompting in teaching socials skills to adults with DS-ASD using visual analysis techniques and Tau-U statistics to measure effect. Peer-mediators with DS and intellectual disability (ID) delivered simultaneous prompting sessions reliably (i.e., > 80% reliability) to teach social skills to adults with ID and a dual-diagnoses of DS-ASD with small (Tau Weighted = .55, 90% CI [.29, .82]) to medium effects (Tau Weighted = .75, 90% CI [.44, 1]). Statistical and visual analysis findings suggest a promising social skills intervention for individuals with DS-ASD as well as reliable delivery of simultaneous prompting procedures by individuals with DS.
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2. Feczko E, Balba N, Miranda-Dominguez O, Cordova M, Karalunas SL, Irwin L, Demeter DV, Hill AP, Langhorst BH, Grieser Painter J, Van Santen J, Fombonne EJ, Nigg JL, Fair DA. {{Subtyping cognitive profiles in Autism Spectrum Disorder using a random forest algorithm}}. {Neuroimage};2017 (Dec 20)
DSM-5 Autism Spectrum Disorder (ASD) comprises a set of neurodevelopmental disorders characterized by deficits in social communication and interaction and repetitive behaviors or restricted interests, and may both affect and be affected by multiple cognitive mechanisms. This study attempts to identify and characterize cognitive subtypes within the ASD population using a random forest (RF) machine learning classification model. We trained our model on measures from seven tasks that reflect multiple levels of information processing. 47 ASD diagnosed and 58 typically developing (TD) children between the ages of 9 and 13 participated in this study. Our RF model was 72.7% accurate, with 80.7% specificity and 63.1% sensitivity. Using the RF model, we measured the proximity of each subject to every other subject, generating a distance matrix between participants. This matrix was then used in a community detection algorithm to identify subgroups within the ASD and TD groups, revealing 3 ASD and 4 TD putative subgroups with unique behavioral profiles. We then examined differences in functional brain systems between diagnostic groups and putative subgroups using resting-state functional connectivity magnetic resonance imaging (rsfcMRI). Chi-square tests revealed a significantly greater number of between group differences (p<.05) within the cingulo-opercular, visual, and default systems as well as differences in inter-system connections in the somato-motor, dorsal attention, and subcortical systems. Many of these differences were primarily driven by specific subgroups suggesting that our method could potentially parse the variation in brain mechanisms affected by ASD. Lien vers le texte intégral (Open Access ou abonnement)
3. Jawaid S, Kidd GJ, Wang J, Swetlik C, Dutta R, Trapp BD. {{Alterations in CA1 hippocampal synapses in a mouse model of fragile X syndrome}}. {Glia};2017 (Dec 23)
Fragile X Syndrome (FXS) is the major cause of inherited mental retardation and the leading genetic cause of Autism spectrum disorders. FXS is caused by mutations in the Fragile X Mental Retardation 1 (Fmr1) gene, which results in transcriptional silencing of Fragile X Mental Retardation Protein (FMRP). To elucidate cellular mechanisms involved in the pathogenesis of FXS, we compared dendritic spines in the hippocampal CA1 region of adult wild-type (WT) and Fmr1 knockout (Fmr1-KO) mice. Using diolistic labeling, confocal microscopy, and three-dimensional electron microscopy, we show a significant increase in the diameter of secondary dendrites, an increase in dendritic spine density, and a decrease in mature dendritic spines in adult Fmr1-KO mice. While WT and Fmr1-KO mice had the same mean density of spines, the variance in spine density was three times greater in Fmr1-KO mice. Reduced astrocyte participation in the tripartite synapse and less mature post-synaptic densities were also found in Fmr1-KO mice. We investigated whether the increase in synaptic spine density was associated with altered synaptic pruning during development. Our data are consistent with reduced microglia-mediated synaptic pruning in the CA1 region of Fmr1-KO hippocampi when compared with WT littermates at postnatal day 21, which is the peak period of synaptic pruning in the mouse hippocampus. Collectively, these results support abnormal synaptogenesis and synaptic remodeling in mice deficient in FMRP. Deficits in the maturation and distribution of synaptic spines on dendrites of CA1 hippocampal neurons may play a role in the intellectual disabilities associated with FXS.
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4. Shen L, Zhang K, Feng C, Chen Y, Li S, Iqbal J, Liao L, Zhao Y, Zhai J. {{iTRAQ based proteomic analysis reveals protein profile in plasma from children with autism}}. {Proteomics Clin Appl};2017 (Dec 23)
PURPOSE: Autism is a childhood neurological disorder with poorly understood etiology and pathology. This study is designed to identify differentially expressed proteins which might serve as potential biomarkers for autism. EXPERIMENTAL DESIGN: We performed iTRAQ (isobaric tags for relative and absolute quantitation) analysis for normal and autistic children’s plasma of the same age group. RESULTS: The results showed that 24 differentially expressed proteins were identified between autistic subjects and controls. For the first time, differential expression of complement C5 (C5) and fermitin family homolog 3 (FERMT3) were related to autism. Five proteins i.e., complement C3 (C3), C5, integrin alpha-IIb (ITGA2B), talin-1 (TLN1), and vitamin D-binding protein (GC), were validated via enzyme-linked immunosorbent assay (ELISA). By ROC (receiver operating characteristic) analysis, combinations of these four proteins C3, C5, ITGA2B and TLN1 distinguished autistic children from healthy controls with a high AUC (area under the ROC curve) value (0.982, 95% CI, 0.957-1.000, P < 0.000). CONCLUSION: These above described proteins are found involved in different pathways that have previously been linked to the pathophysiology of autism spectrum disorders (ASDs). The results strongly support that focal adhesions, acting cytoskeleton, cell adhesion, motility and migration, synaptogenesis, and complement system are involved in the pathogenesis of autism, and highlight the important role of platelet function in the pathophysiology of autism. This article is protected by copyright. All rights reserved. Lien vers le texte intégral (Open Access ou abonnement)
5. Song Y, Hakoda Y. {{Selective Impairment of Basic Emotion Recognition in People with Autism: Discrimination Thresholds for Recognition of Facial Expressions of Varying Intensities}}. {J Autism Dev Disord};2017 (Dec 22)
Autism spectrum disorders (ASD) are characterized by early onset qualitative impairments in reciprocal social development. However, whether individuals with ASD exhibit impaired recognition of facial expressions corresponding to basic emotions is debatable. To investigate subtle deficits in facial emotion recognition, we asked 14 children diagnosed with high-functioning autism (HFA)/AS and 17 typically developing peers to complete a new highly sensitive test of facial emotion recognition. The test stimuli comprised faces expressing increasing degrees of emotional intensity that slowly changed from a neutral to a full-intensity happiness, sadness, surprise, anger, disgust, or fear expression. We assessed individual differences in the intensity of stimuli required to make accurate judgments about emotional expressions. We found that, different emotions had different identification thresholds and the two groups were generally similar in terms of the sequence of discrimination threshold of six basic expressions. It was easier for individuals in both groups to identify emotions that were relatively fully expressed (e.g., intensity > 50%). Compared with control participants, children with ASD generally required stimuli with significantly greater intensity for the correct identification of anger, disgust, and fear expressions. These results suggest that individuals with ASD do not have a general but rather a selective impairment in basic emotion recognition.
