1. Alverson CY, Yamamoto SH. {{VR Employment Outcomes of Individuals with Autism Spectrum Disorders: A Decade in the Making}}. {J Autism Dev Disord}. 2017.
This study utilized hierarchical linear modeling analysis of a 10-year extant dataset from Rehabilitation Services Administration to investigate significant predictors of employment outcomes for vocational rehabilitation (VR) clients with autism. Predictor variables were gender, ethnicity, attained education level, IEP status in high school, secondary disability status, and total number of VR services. Competitive employment was the criterion variable. Only one predictor variable, Total Number of VR Services, was significant across all 10 years. IEP status in high school was not significant in any year. The remaining predictors were significant in one or more years. Further research and implications for researchers and practitioners are included.
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2. Arnett AB, Cairney BE, Wallace AS, Gerdts J, Turner TN, Eichler EE, Bernier RA. {{Comorbid symptoms of inattention, autism, and executive cognition in youth with putative genetic risk}}. {J Child Psychol Psychiatry}. 2017.
BACKGROUND: Symptoms of autism spectrum disorder (ASD) and inattention (IA) are highly comorbid and associated with deficits in executive cognition. Cognitive deficits have been posited as candidate endophenotypes of psychiatric traits, but few studies have conceptualized cognitive deficits as psychiatric comorbidities. The latter model is consistent with a latent factor reflecting broader liability to neuropsychological dysfunction, and explains heterogeneity in the cognitive profile of individuals with ASD and IA. METHODS: We tested competing models of covariance among symptoms of ASD, IA, and cognition in a sample of 73 youth with a known genetic mutation. RESULTS: A common executive factor fit best as a cognitive comorbidity, rather than endophenotype, of the shared variance between measures of IA and ASD symptoms. Known genetic risk explained a third of the shared variance among psychiatric and cognitive measures. CONCLUSIONS: Comorbid symptoms of ASD, IA, and cognitive deficits are likely influenced by common neurogenetic factors. Known genetic risk in ASD may inform future investigation of putative genetic causes of IA.
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3. Cheng CH, Chan PS, Hsu SC, Liu CY. {{Meta-analysis of sensorimotor gating in patients with autism spectrum disorders}}. {Psychiatry Res}. 2017.
Prepulse inhibition (PPI) of startle response is a well-established neurophysiological marker of sensorimotor gating ability in psychiatric patients including those with autism spectrum disorders (ASD). PPI has been utilized as an indicator of the central inhibitory function and is potentially linked to the clinical features of this disease. However, it remains inconclusive whether ASD patients exhibit PPI deficits compared with healthy controls. The present meta-analysis aimed to explore the pooled effect sizes of PPI in ASD patients. We searched major electronic databases from 1990 to January 2017. Seven studies, consisting of 21 individual investigations with 135 healthy controls and 99 ASD patients, were obtained. The effect size, calculated as Hedges’s g and 95% confidence interval, were estimated. Overall, we found ASD patients exhibited an impaired PPI compared with healthy controls (p = 0.008). Specifically, significant PPI deficits were observed among ASD children/adolescents, compared with their healthy counterparts (p = 0.019). However, differences in PPI responses were not observed among adults. Conclusively, our results reconciled the previous studies and showed that ASD children/adolescents, but not adults, exhibit reduced sensorimotor gating function compared to healthy controls. We also suggest that the parameters of PPI are particularly important and the results should be interpreted with cautions.
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4. Cidav Z, Xie M, Mandell DS. {{Foster Care Involvement Among Medicaid-Enrolled Children with Autism}}. {J Autism Dev Disord}. 2017.
The prevalence and risk of foster care involvement among children with autism spectrum disorder (ASD) relative to children with intellectual disability (ID), children with ASD and ID, and typically developing children were examined using 2001-2007 Medicaid data. Children were followed up to the first foster care placement or until the end of 2007; a discrete time logistic regression analysis was conducted. Both the prevalence and risk of foster care involvement were greatest for children with ASD, and the prevalence increased substantially over the study period among children with ASD. Continued examination of the factors contributing to the higher risk of foster placement is warranted to unravel the complex circumstances facing these vulnerable children and their families.
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5. Collins PY, Pringle B, Alexander C, Darmstadt GL, Heymann J, Huebner G, Kutlesic V, Polk C, Sherr L, Shih A, Sretenov D, Zindel M. {{Global services and support for children with developmental delays and disabilities: Bridging research and policy gaps}}. {PLoS Med}. 2017; 14(9): e1002393.
Pamela Collins and colleagues explain the research and policy approaches needed globally to ensure children with developmental delays and disabilities are fully included in health and education services.
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6. Conner CM, White SW. {{Brief Report: Feasibility and Preliminary Efficacy of Individual Mindfulness Therapy for Adults with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2017.
Intervention research on adults with autism spectrum disorder (ASD) is sparse. Many adults with ASD experience impaired emotion regulation (ER), which is thought to contribute to higher rates of psychiatric comorbidities among adults with ASD and indirect effects upon adaptive functioning, interpersonal relationships, and vocational status. The purpose of this study was to investigate feasibility and initial efficacy of an adapted mindfulness-based individual therapy targeting ER difficulties for adults with ASD. There is evidence for feasibility based on acceptable treatment fidelity and participant satisfaction ratings. Of nine participants, seven demonstrated improvement in at least one of the following domains; impulse control, access to ER strategies, and emotional acceptance. Further research is recommended, including additional timepoints and a clinical cutoff-derived sample.
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7. Finch KH, Tager-Flusberg H, Nelson CA. {{Neural responses to linguistic stimuli in children with and without autism spectrum disorder}}. {Eur J Neurosci}. 2017.
Atypical neural responses to language have been found in toddlers with autism spectrum disorder (ASD) and in their unaffected siblings. However, given that language difficulties are often seen in these children, it is difficult to interpret whether these neural differences are a result of the diagnosis of ASD or impairments in their language abilities. In this current study, we recorded event-related potentials (ERPs) from four groups of 36-month-olds: low-risk control (LRC), high-risk for ASD defined as having an older sibling with ASD (HRA) but who do not have ASD or milder autism-like symptoms (HRA-Typ), HRA children who do not have ASD but exhibit milder autism-like symptoms (HRA-Atyp), and HRA children diagnosed with ASD (ASD). Children listened to words expected to be acquired early (e.g. ball) and words expected to be acquired late (e.g. calf). ERPs were analyzed over time windows sensitive to word processing as well as frontal and temporo-parietal sites over the left and right hemisphere. When controlling for language abilities, there were group differences within the temporo-parietal sites. Specifically, the HRA-Atyp group showed a different timed response to late words compared to the ASD and LRC groups. In addition we found a relation between neural responses in the left frontal sites and ASD severity. Our results suggest that both language abilities and ASD diagnoses are important to consider when interpreting neural differences in lexical processing. This article is protected by copyright. All rights reserved.
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8. Ganz JB, Morin KL, Foster MJ, Vannest KJ, Genc Tosun D, Gregori EV, Gerow SL. {{High-technology augmentative and alternative communication for individuals with intellectual and developmental disabilities and complex communication needs: a meta-analysis}}. {Augment Altern Commun}. 2017: 1-15.
The use of mobile technology is ubiquitous in modern society and is rapidly increasing in novel use. The use of mobile devices and software applications (« apps ») as augmentative and alternative communication (AAC) is rapidly expanding in the community, and this is also reflected in the research literature. This article reports the social-communication outcome results of a meta-analysis of single-case experimental research on the use of high-tech AAC, including mobile devices, by individuals with intellectual and developmental disabilities, including autism spectrum disorder. Following inclusion determination, and excluding studies with poor design quality, raw data from 24 publications were extracted and included 89 A-B phase contrasts. Tau-U nonparametric, non-overlap effect size was used to aggregate the results across all studies for an omnibus and moderator analyses. Kendall’s S was calculated for confidence intervals, p-values, and standard error. The omnibus analysis indicated overall low to moderate positive effects on social-communication outcomes for high-tech AAC use by individuals with intellectual and developmental disabilities.
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9. Goncalves J, Violante IR, Sereno J, Leitao RA, Cai Y, Abrunhosa A, Silva AP, Silva AJ, Castelo-Branco M. {{Testing the excitation/inhibition imbalance hypothesis in a mouse model of the autism spectrum disorder: in vivo neurospectroscopy and molecular evidence for regional phenotypes}}. {Mol Autism}. 2017; 8: 47.
BACKGROUND: Excitation/inhibition (E/I) imbalance remains a widely discussed hypothesis in autism spectrum disorders (ASD). The presence of such an imbalance may potentially define a therapeutic target for the treatment of cognitive disabilities related to this pathology. Consequently, the study of monogenic disorders related to autism, such as neurofibromatosis type 1 (NF1), represents a promising approach to isolate mechanisms underlying ASD-related cognitive disabilities. However, the NF1 mouse model showed increased gamma-aminobutyric acid (GABA) neurotransmission, whereas the human disease showed reduced cortical GABA levels. It is therefore important to clarify whether the E/I imbalance hypothesis holds true. We hypothesize that E/I may depend on distinct pre- and postsynaptic push-pull mechanisms that might be are region-dependent. METHODS: In current study, we assessed two critical components of E/I regulation: the concentration of neurotransmitters and levels of GABA(A) receptors. Measurements were performed across the hippocampi, striatum, and prefrontal cortices by combined in vivo magnetic resonance spectroscopy (MRS) and molecular approaches in this ASD-related animal model, the Nf1+/- mouse. RESULTS: Cortical and striatal GABA/glutamate ratios were increased. At the postsynaptic level, very high receptor GABA(A) receptor expression was found in hippocampus, disproportionately to the small reduction in GABA levels. Gabaergic tone (either by receptor levels change or GABA/glutamate ratios) seemed therefore to be enhanced in all regions, although by a different mechanism. CONCLUSIONS: Our data provides support for the hypothesis of E/I imbalance in NF1 while showing that pre- and postsynaptic changes are region-specific. All these findings are consistent with our previous physiological evidence of increased inhibitory tone. Such heterogeneity suggests that therapeutic approaches to address neurochemical imbalance in ASD may need to focus on targets where convergent physiological mechanisms can be found.
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10. Graf WD, Miller G, Epstein LG, Rapin I. {{Author response: The autism « epidemic »: Ethical, legal, and social issues in a developmental spectrum disorder}}. {Neurology}. 2017; 89(12): 1310-1.
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11. Johnson BS, Zhao YT, Fasolino M, Lamonica JM, Kim YJ, Georgakilas G, Wood KH, Bu D, Cui Y, Goffin D, Vahedi G, Kim TH, Zhou Z. {{Biotin tagging of MeCP2 in mice reveals contextual insights into the Rett syndrome transcriptome}}. {Nat Med}. 2017.
Mutations in MECP2 cause Rett syndrome (RTT), an X-linked neurological disorder characterized by regressive loss of neurodevelopmental milestones and acquired psychomotor deficits. However, the cellular heterogeneity of the brain impedes an understanding of how MECP2 mutations contribute to RTT. Here we developed a Cre-inducible method for cell-type-specific biotin tagging of MeCP2 in mice. Combining this approach with an allelic series of knock-in mice carrying frequent RTT-associated mutations (encoding T158M and R106W) enabled the selective profiling of RTT-associated nuclear transcriptomes in excitatory and inhibitory cortical neurons. We found that most gene-expression changes were largely specific to each RTT-associated mutation and cell type. Lowly expressed cell-type-enriched genes were preferentially disrupted by MeCP2 mutations, with upregulated and downregulated genes reflecting distinct functional categories. Subcellular RNA analysis in MeCP2-mutant neurons further revealed reductions in the nascent transcription of long genes and uncovered widespread post-transcriptional compensation at the cellular level. Finally, we overcame X-linked cellular mosaicism in female RTT models and identified distinct gene-expression changes between neighboring wild-type and mutant neurons, providing contextual insights into RTT etiology that support personalized therapeutic interventions.
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12. Kerin T, Volk H, Li W, Lurmann F, Eckel S, McConnell R, Hertz-Picciotto I. {{Association Between Air Pollution Exposure, Cognitive and Adaptive Function, and ASD Severity Among Children with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2017.
Prenatal exposure to air pollution has been associated with autism spectrum disorder (ASD) risk but no study has examined associations with ASD severity or functioning. Cognitive ability, adaptive functioning, and ASD severity were assessed in 327 children with ASD from the Childhood Autism Risks from Genetics and the Environment study using the Mullen Scales of Early Learning (MSEL), the Vineland Adaptive Behavior Scales (VABS), and the Autism Diagnostic Observation Schedule calibrated severity score. Estimates of nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), ozone, and near-roadway air pollution were assigned to each trimester of pregnancy and first year of life. Increasing prenatal and first year NO2 exposures were associated with decreased MSEL and VABS scores. Increasing PM10 exposure in the third trimester was paradoxically associated with improved performance on the VABS. ASD severity was not associated with air pollution exposure.
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13. Lanphear NE. {{Autism Diagnosis: The Local Context Matters}}. {J Dev Behav Pediatr}. 2017.
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14. Linstead E, Dixon DR, Hong E, Burns CO, French R, Novack MN, Granpeesheh D. {{An evaluation of the effects of intensity and duration on outcomes across treatment domains for children with autism spectrum disorder}}. {Transl Psychiatry}. 2017; 7(9): e1234.
Applied behavior analysis (ABA) is considered an effective treatment for individuals with autism spectrum disorder (ASD), and many researchers have further investigated factors associated with treatment outcomes. However, few studies have focused on whether treatment intensity and duration have differential influences on separate skills. The aim of the current study was to investigate how treatment intensity and duration impact learning across different treatment domains, including academic, adaptive, cognitive, executive function, language, motor, play, and social. Separate multiple linear regression analyses were used to evaluate these relationships. Participants included 1468 children with ASD, ages 18 months to 12 years old, M=7.57 years, s.d.=2.37, who were receiving individualized ABA services. The results indicated that treatment intensity and duration were both significant predictors of mastered learning objectives across all eight treatment domains. The academic and language domains showed the strongest response, with effect sizes of 1.68 and 1.85 for treatment intensity and 4.70 and 9.02 for treatment duration, respectively. These findings are consistent with previous research that total dosage of treatment positively influences outcomes. The current study also expands on extant literature by providing a better understanding of the differential impact that these treatment variables have across various treatment domains.
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15. Machado C, Estevez M, Rodriguez R, Leisman G. {{Letter re: The autism « epidemic »: Ethical, legal, and social issues in a developmental spectrum disorder}}. {Neurology}. 2017; 89(12): 1310.
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16. Martella G, Meringolo M, Trobiani L, De Jaco A, Pisani A, Bonsi P. {{The Neurobiological Bases of Autism Spectrum Disorders The R451C-Neuroligin 3 mutation hampers the expression of long-term synaptic depression in the dorsal striatum}}. {Eur J Neurosci}. 2017.
Autism spectrum disorders (ASDs) comprise a heterogeneous group of disorders with a complex genetic etiology. Current theories on the pathogenesis of ASDs suggest that they might arise from an aberrant synaptic transmission affecting specific brain circuits and synapses. The striatum, which is part of the basal ganglia circuit, is one of the brain regions involved in ASDs. Mouse models of ASDs have provided evidence for an imbalance between excitatory and inhibitory neurotransmission. Here we investigated the expression of long-term synaptic plasticity at corticostriatal glutamatergic synapses in the dorsal striatum of the R451C-NL3 phenotypic mouse model of autism. This mouse model carries the human R451C mutation in the neuroligin3 (NL3) gene, that has been associated with highly penetrant autism in a Swedish family. The R451C-NL3 mouse has been shown to exhibit autistic-like behaviors and alterations of synaptic transmission in different brain areas. However, excitatory glutamatergic transmission and its long-term plasticity have not been investigated in the dorsal striatum so far. Our results indicate that the expression of long-term synaptic depression (LTD) at corticostriatal glutamatergic synapses in the dorsal striatum is impaired by the R451C-NL3 mutation. A partial rescue of LTD was obtained by exogenous activation of cannabinoid CB1 receptors or enhancement of the endocannabinoid tone, suggesting that an altered cannabinoid drive might underlie the deficit of synaptic plasticity in the dorsal striatum of R451C-NL3 mice. This article is protected by copyright. All rights reserved.
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17. Mundy P. {{A Review of Joint Attention and Social-Cognitive Brain Systems in Typical Development and Autism Spectrum Disorder}}. {Eur J Neurosci}. 2017.
This article provides a review of the increasingly detailed literature on the neurodevelopment of joint attention. Many findings from this literature support and inform the hypothesis that the neurodevelopment of joint attention contributes to the functional development of neural systems for human social cognition. Joint attention begins to develop by 5 months of age and is tantamount to the ability to adopt a common perspective with another person. It involves a whole-brain system with nodes in the: (a) dorsal and medial frontal cortex, (b) orbital frontal/insula cortex, (c) anterior/ posterior cingulate cortex, (d) superior temporal cortex, (e) precuneus/parietal cortex, and (f) amygdala and striatum. This system integrates triadic information processing about: (a) self-attention/action, (b) information about others’ attention/action during social interactions that involve, (c) coordinated attention as well as processing a common referent in space. The results of this new imaging literature have the potential to advance current models of social cognition and the social brain, which rarely consider the contribution of the cognitive neurodevelopment of joint attention. The new neuroscience of joint attention is also extremely valuable for clinical research on social-cognitive neurodevelopmental disorders. This is most clearly the case for autism spectrum disorder (ASD) because it is consistent with the hypothesis of substantial functional neurodevelopmental continuity between the preschool impairments of joint attention, and childhood theory of mind ability that characterize the development of ASD. This article is protected by copyright. All rights reserved.
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18. Pappaianni E, Siugzdaite R, Vettori S, Venuti P, Job R, Grecucci A. {{Three shades of grey: detecting brain abnormalities in children with autism by using Source-, Voxel- and Surface-based Morphometry}}. {Eur J Neurosci}. 2017.
Autistic spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social interactions, communication and stereotyped behavior. Recent evidence from neuroimaging supports the hypothesis that ASD deficits in adults may be related to abnormalities in a specific frontal-temporal network (Autism-specific Structural Network, ASN). To see whether these results extend to younger children and to better characterize these abnormalities, we applied three morphometric methods on brain grey matter of children with and without ASD. We selected 39 sMRI images of male children with ASD and 42 typically developing (TD) from the ABIDE database. We used Source-Based Morphometry (SoBM), a whole-brain multivariate approach to identify grey matter networks, Voxel-Based Morphometry (VBM), a voxel-wise comparison of the local grey matter concentration, and Surface-Based Morphometry (SuBM) for the estimation of the cortical parameters. SoBM showed a bilateral frontal-parietal-temporal network different between groups, including the inferior-middle temporal gyrus, the inferior parietal lobule and the postcentral gyrus; VBM returned differences only in the right temporal lobe; SuBM returned a thinning in the right inferior temporal lobe thinner in ASD, a higher gyrification in the right superior parietal lobule in TD and in the middle frontal gyrus in ASD. For the first time, we investigated the brain abnormalities in children with ASD by using three morphometric techniques. The results were relatively consistent between methods, stressing the role of an Autism-specific Structural Network in ASD individuals. We also make methodological speculations on the relevance of using multivariate and whole brain neuroimaging analysis to capture ASD complexity. This article is protected by copyright. All rights reserved.
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19. Sadybekov A, Tian C, Arnesano C, Katritch V, Herring BE. {{An autism spectrum disorder-related de novo mutation hotspot discovered in the GEF1 domain of Trio}}. {Nat Commun}. 2017; 8(1): 601.
The Rho guanine nucleotide exchange factor (RhoGEF) Trio promotes actin polymerization by directly activating the small GTPase Rac1. Recent studies suggest that autism spectrum disorder (ASD)-related behavioral phenotypes in animal models of ASD can be produced by dysregulation of Rac1’s control of actin polymerization at glutamatergic synapses. Here, in humans, we discover a large cluster of ASD-related de novo mutations in Trio’s Rac1 activating domain, GEF1. Our study reveals that these mutations produce either hypofunctional or hyperfunctional forms of Trio in rodent neurons in vitro. In accordance with pathological increases or decreases in glutamatergic neurotransmission observed in animal models of ASD, we find that these mutations result in either reduced synaptic AMPA receptor expression or enhanced glutamatergic synaptogenesis. Together, our findings implicate both excessive and reduced Trio activity and the resulting synaptic dysfunction in ASD-related pathogenesis, and point to the Trio-Rac1 pathway at glutamatergic synapses as a possible key point of convergence of many ASD-related genes.Trio is a RhoGEF protein that promotes actin polymerization and is implicated in the regulation of glutamatergic synapses in autism spectrum disorder (ASD). Here the authors identify a large cluster of de novo mutations in the GEF1 domain of Trio in whole-exome sequencing data from individuals with ASD, and confirm that some of these mutations lead to glutamatergic dysregulation in vitro.
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20. Sare RM, Harkless L, Levine M, Torossian A, Sheeler CA, Smith CB. {{Deficient Sleep in Mouse Models of Fragile X Syndrome}}. {Front Mol Neurosci}. 2017; 10: 280.
In patients with fragile X syndrome (FXS), sleep problems are commonly observed but are not well characterized. In animal models of FXS (dfmr1 and Fmr1 knockout (KO)/Fxr2 heterozygote) circadian rhythmicity is affected, but sleep per se has not been examined. We used a home-cage monitoring system to assess total sleep time in both light and dark phases in Fmr1 KO mice at different developmental stages. Fmr1 KOs at P21 do not differ from controls, but genotype x phase interactions in both adult (P70 and P180) groups are statistically significant indicating that sleep in Fmr1 KOs is reduced selectively in the light phase compared to controls. Our results show the emergence of abnormal sleep in Fmr1 KOs during the later stages of brain maturation. Treatment of adult Fmr1 KO mice with a GABAB agonist, R-baclofen, did not restore sleep duration in the light phase. In adult (P70) Fmr1 KO/Fxr2 heterozygote animals, total sleep time was further reduced, once again in the light phase. Our data highlight the importance of the fragile X genes (Fmr1 and Fxr2) in sleep physiology and confirm the utility of these mouse models in enhancing our understanding of sleep disorders in FXS.
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21. Semino S, Ring M, Bowler DM, Gaigg SB. {{The Influence of task Demands, Verbal Ability and Executive Functions on Item and Source Memory in Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2017.
Autism Spectrum Disorder (ASD) is generally associated with difficulties in contextual source memory but not single item memory. There are surprising inconsistencies in the literature, however, that the current study seeks to address by examining item and source memory in age and ability matched groups of 22 ASD and 21 comparison adults. Results show that group differences in source memory are moderated by task demands but not by individual differences in verbal ability, executive function or item memory. By contrast, unexpected group differences in item memory could largely be explained by individual differences in source memory. These observations shed light on the factors underlying inconsistent findings in the memory literature in ASD, which has important implications for theory and practice.
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22. Tin LNW, Lui SSY, Ho KKY, Hung KSY, Wang Y, Yeung HKH, Wong TY, Lam SM, Chan RCK, Cheung EFC. {{High-functioning autism patients share similar but more severe impairments in verbal theory of mind than schizophrenia patients}}. {Psychol Med}. 2017: 1-12.
BACKGROUND: Evidence suggests that autism and schizophrenia share similarities in genetic, neuropsychological and behavioural aspects. Although both disorders are associated with theory of mind (ToM) impairments, a few studies have directly compared ToM between autism patients and schizophrenia patients. This study aimed to investigate to what extent high-functioning autism patients and schizophrenia patients share and differ in ToM performance. METHODS: Thirty high-functioning autism patients, 30 schizophrenia patients and 30 healthy individuals were recruited. Participants were matched in age, gender and estimated intelligence quotient. The verbal-based Faux Pas Task and the visual-based Yoni Task were utilised to examine first- and higher-order, affective and cognitive ToM. The task/item difficulty of two paradigms was examined using mixed model analyses of variance (ANOVAs). Multiple ANOVAs and mixed model ANOVAs were used to examine group differences in ToM. RESULTS: The Faux Pas Task was more difficult than the Yoni Task. High-functioning autism patients showed more severely impaired verbal-based ToM in the Faux Pas Task, but shared similar visual-based ToM impairments in the Yoni Task with schizophrenia patients. CONCLUSIONS: The findings that individuals with high-functioning autism shared similar but more severe impairments in verbal ToM than individuals with schizophrenia support the autism-schizophrenia continuum. The finding that verbal-based but not visual-based ToM was more impaired in high-functioning autism patients than schizophrenia patients could be attributable to the varied task/item difficulty between the two paradigms.
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23. Travers BG, Mason AH, Mrotek LA, Ellertson A, Dean DC, 3rd, Engel C, Gomez A, Dadalko OI, McLaughlin K. {{Biofeedback-Based, Videogame Balance Training in Autism}}. {J Autism Dev Disord}. 2017.
The present study examined the effects of a visual-based biofeedback training on improving balance challenges in autism spectrum disorder (ASD). Twenty-nine youth with ASD (7-17 years) completed an intensive 6-week biofeedback-based videogame balance training. Participants exhibited training-related balance improvements that significantly accounted for postural-sway improvements outside of training. Participants perceived the training as beneficial and enjoyable. Significant moderators of training included milder stereotyped and ritualistic behaviors and better starting balance. Neither IQ nor BMI moderated training. These results suggest that biofeedback-based balance training is associated with balance improvements in youth with ASD, most robustly in those with less severe repetitive behaviors and better starting balance. The training was perceived as motivating, further suggesting its efficacy and likelihood of use.
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24. Uljarevic M, Richdale AL, McConachie H, Hedley D, Cai RY, Merrick H, Parr JR, Le Couteur A. {{The Hospital Anxiety and Depression scale: Factor structure and psychometric properties in older adolescents and young adults with autism spectrum disorder}}. {Autism Res}. 2017.
Despite the high frequency of anxiety and depression symptoms in individuals with Autism Spectrum Disorder (ASD) and a significant impact of these comorbidities on both individuals with ASD and their families, research on the validity of anxiety and depression measures in the ASD population is currently lacking. The aim of this study was to explore the psychometric properties of the Hospital Anxiety and Depression Scale [HADS; Zigmond & Snaith, ] in a sample of older adolescents and young adults with ASD. One hundred and fifty one participants (UK Transition longitudinal study: N = 106; 75 males, Mage = 16.04 years, SD = 1.28; Longitudinal Study of Australian Schools Leavers with ASD: N = 45, 30 males; Mage = 18.35 years, SD = 2.55) completed the HADS and a range of mental health and well-being measures. Combination of the Principal Component Analysis and Parallel Analysis indicated two factors as an optimal solution in our sample, accounting for 43.77% of variance with factors being identical in terms of content with the structure found in the general population. Internal consistency was good for the HADS anxiety scale (HADS-A; .82-.84) and acceptable for the HADS depression scale (HADS-D; .60-.72). Convergent validity of both HADS-A and HADS-D scales was excellent and divergent validity was acceptable. Our study represents a significant contribution to the literature by providing an initial validation of the HADS in older adolescents and younger adults with ASD. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Research on the validity of measurement of anxiety and depression in ASD is currently lacking. The aim of this study was to explore the properties of the Hospital Anxiety and Depression Scale (HADS) in a sample of 151 young people with ASD. Participants completed HADS and a range of mental health and well-being measures. Encouragingly, our findings suggest that HADS provides a reliable and valid assessment of anxiety and depression in ASD.
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25. van Tilborg E, Achterberg EJM, van Kammen CM, van der Toorn A, Groenendaal F, Dijkhuizen RM, Heijnen CJ, Vanderschuren L, Benders M, Nijboer CHA. {{Combined fetal inflammation and postnatal hypoxia causes myelin deficits and autism-like behavior in a rat model of diffuse white matter injury}}. {Glia}. 2017.
Diffuse white matter injury (WMI) is a serious problem in extremely preterm infants, and is associated with adverse neurodevelopmental outcome, including cognitive impairments and an increased risk of autism-spectrum disorders. Important risk factors include fetal or perinatal inflammatory insults and fluctuating cerebral oxygenation. However, the exact mechanisms underlying diffuse WMI are not fully understood and no treatment options are currently available. The use of clinically relevant animal models is crucial to advance knowledge on the pathophysiology of diffuse WMI, allowing the definition of novel therapeutic targets. In the present study, we developed a multiple-hit animal model of diffuse WMI by combining fetal inflammation and postnatal hypoxia in rats. We characterized the effects on white matter development and functional outcome by immunohistochemistry, MRI and behavioral paradigms. Combined fetal inflammation and postnatal hypoxia resulted in delayed cortical myelination, microglia activation and astrogliosis at P18, together with long-term changes in oligodendrocyte maturation as observed in 10 week old animals. Furthermore, rats with WMI showed impaired motor performance, increased anxiety and signs of autism-like behavior, i.e. reduced social play behavior and increased repetitive grooming. In conclusion, the combination of fetal inflammation and postnatal hypoxia in rats induces a pattern of brain injury and functional impairments that closely resembles the clinical situation of diffuse WMI. This animal model provides the opportunity to elucidate pathophysiological mechanisms underlying WMI, and can be used to develop novel treatment options for diffuse WMI in preterm infants.
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26. Vanmarcke S, van de Cruys S, Moors P, Wagemans J. {{Intact animacy perception during chase detection in ASD}}. {Sci Rep}. 2017; 7(1): 11851.
We explored the strength of implicit social inferences in adolescents with and without Autism Spectrum Disorder (ASD) using a chasing paradigm in which participants judged the absence/presence of a chase within a display of four seemingly randomly moving dots. While two of these dots always moved randomly, the two others could fulfill the role of being either the chasing (wolf) or chased (sheep) dot. In the chase-present (but not the chase-absent) trials the wolf displayed chasing behavior defined by the degree to which the dot reliably moved towards the sheep (chasing subtlety). Previous research indicated that chasing subtlety strongly influenced chase detection in typically developing (TD) adults. We intended to replicate and extend this finding to adolescents with and without ASD, while also adding either a social or a non-social cue to the displays. Our results confirmed the importance of chasing subtlety and indicated that adding social, but not non-social, information further improved chase detection performance. Interestingly, the performance of adolescents with ASD was less dependent on chasing subtlety than that of their TD counterparts. Nonetheless, adolescents with and without ASD did not differ in their use of the added social (or non-social) cue.
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27. Wang M, Jiang L, Tang X. {{Levetiracetam is associated with decrease in subclinical epileptiform discharges and improved cognitive functions in pediatric patients with autism spectrum disorder}}. {Neuropsychiatr Dis Treat}. 2017; 13: 2321-6.
OBJECTIVE: Subclinical epileptiform discharges (SEDs) are common in pediatric patients with autism spectrum disorder (ASD), but the effect of antiepileptic drugs on SEDs in ASD remains inconclusive. This physician-blinded, prospective, randomized controlled trial investigated an association between the anticonvulsant drug levetiracetam and SEDs in children with ASD. METHODS: A total of 70 children with ASD (4-6 years) and SEDs identified by electroencephalogram were randomly divided into two equal groups to receive either levetiracetam and educational training (treatment group) or educational training only (control). At baseline and after 6 months treatment, the following scales were used to assess each individual’s behavioral and cognitive functions: the Chinese version of the Psychoeducational Profile – third edition (PEP-3), Childhood Autism Rating Scale (CARS), and Autism Behavior Checklist (ABC). A 24-hour electroencephalogram was recorded on admission (baseline) and at follow-up. The degree of satisfaction of each patient was also evaluated. RESULTS: Relative to baseline, at the 6-month follow-up, the PEP-3, CARS, and ABC scores were significantly improved in both the treatment and control groups. At the 6-month follow-up, the PEP-3 scores of the treatment group were significantly higher than those of the control, whereas the CARS and ABC scores were significantly lower, and the rate of electroencephalographic normalization was significantly higher in the treatment group. CONCLUSION: Levetiracetam appears to be effective for controlling SEDs in pediatric patients with ASD and was also associated with improved behavioral and cognitive functions.
