1. Barbaro J, Dissanayake C. {{Early markers of autism spectrum disorders in infants and toddlers prospectively identified in the Social Attention and Communication Study}}. {Autism}. 2012.
The Social Attention and Communication Study involved the successful implementation of developmental surveillance of the early markers of autism spectrum disorders in a community-based setting. The objective in the current study was to determine the most discriminating and predictive markers of autism spectrum disorders used in the Social Attention and Communication Study at 12, 18 and 24 months of age, so that these could be used to identify children with autism spectrum disorders with greater accuracy. The percentage of ‘yes/no’ responses for each behavioural marker was compared between children with autistic disorder (n = 39), autism spectrum disorder (n = 50) and developmental and/or language delay (n = 20) from 12 to 24 months, with a logistic regression also conducted at 24 months. Across all ages, the recurring key markers of both autistic disorder and autism spectrum disorder were deficits in eye contact and pointing, and from 18 months, deficits in showing became an important marker. In combination, these behaviours, along with pretend play, were found to be the best group of predictors for a best estimate diagnostic classification of autistic disorder/autism spectrum disorder at 24 months. It is argued that the identified markers should be monitored repeatedly during the second year of life by community health-care professionals.
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2. Callan MA, Clements N, Ahrendt N, Zarnescu DC. {{Fragile X Protein is required for inhibition of insulin signaling and regulates glial-dependent neuroblast reactivation in the developing brain}}. {Brain Res}. 2012; 1462: 151-61.
Fragile X syndrome (FXS) is the most common form of inherited mental disability and known cause of autism. It is caused by loss of function for the RNA binding protein FMRP, which has been demonstrated to regulate several aspects of RNA metabolism including transport, stability and translation at synapses. Recently, FMRP has been implicated in neural stem cell proliferation and differentiation both in cultured neurospheres as well as in vivo mouse and fly models of FXS. We have previously shown that FMRP deficient Drosophila neuroblasts upregulate Cyclin E, prematurely exit quiescence, and overproliferate to generate on average 16% more neurons. Here we further investigate FMRP’s role during early development using the Drosophila larval brain as a model. Using tissue specific RNAi we find that FMRP is required sequentially, first in neuroblasts and then in glia, to regulate exit from quiescence as measured by Cyclin E expression in the brain. Furthermore, we tested the hypothesis that FMRP controls brain development by regulating the insulin signaling pathway, which has been recently shown to regulate neuroblast exit from quiescence. Our data indicate that phosphoAkt, a readout of insulin signaling, is upregulated in dFmr1 brains at the time when FMRP is required in glia for neuroblast reactivation. In addition, dFmr1 interacts genetically with dFoxO, a transcriptional regulator of insulin signaling. Our results provide the first evidence that FMRP is required in vivo, in glia for neuroblast reactivation and suggest that it may do so by regulating the output of the insulin signaling pathway. This article is part of a Special Issue entitled: RNA-Binding Proteins.
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3. Centelles L, Assaiante C, Etchegoyhen K, Bouvard M, Schmitz C. {{[Understanding social interaction in children with autism spectrum disorders: Does whole-body motion mean anything to them?]}}. {Encephale}. 2012; 38(3): 232-40.
BACKGROUND: Autism spectrum disorders (ASD) are characterized by difficulties in social interaction and verbal and non verbal reciprocal communication. Face and gaze direction, which participate in non verbal communication, are described as atypical in ASD. Also body movements carry multiple social cues. Under certain circumstances, for instance when seeing two persons from far, they constitute the only support that allows the grasping of a social content. Here, we investigated the contribution of whole-body motion processing in social understanding. OBJECTIVE: The aim of the study was to evaluate whether children with ASD make use of information carried by body motion to categorize dynamic visual scenes that portrayed social interactions. METHODOLOGY: In 1973, Johansson devised a technique for studying the perception of biological motion that minimizes static form information from the stimulus, but retains motion information. In these point-light displays, the movement figure, such as a body, is represented by a small number of illuminated dots positioned to highlight the motion of the body parts. We used Johansson’s model to explore the ability of children with ASD to understand social interactions based on human movement analysis. Three-second silent point-light displays were created by videotaping two actors. The two actors were either interacting together or moving side by side without interacting. A large range of social interaction displays were used to cover social scenes depicting social norms (conventional gestures and courteous attitudes), emotional situations (carrying positive or negative valences) and scenes from games (sports, dance, etc.). Children were asked to carefully watch the stimuli and to classify them according to the question « Are the two persons communicating or not? ». Four sessions of 3minutes were performed by each child. Children with ASD were compared with typically developing control children matched with either non verbal mental age or chronological age. Response and reaction time were recorded in this force-choice categorization task. RESULTS: The performance of children with ASD suggested that they were able to extract a social content from body motion. However, they were significantly less efficient than typically developing control children, either matched for non verbal mental age or chronological age. This was especially the case for the social interaction displays. Neither impaired global perceptual processing, nor cognitive development, nor emotional content could explain these lower performances. DISCUSSION AND CONCLUSION: The results are discussed in the context of an action representation deficit and a dysfunction of the mirror mechanism in ASD. In conclusion, this behavioural study highlights the potential of point-light displays as a rehabilitation tool in ASD.
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4. Duffy FH, Als H. {{A stable pattern of EEG spectral coherence distinguishes children with autism from neuro-typical controls – a large case control study}}. {BMC Med}. 2012; 10(1): 64.
ABSTRACT: BACKGROUND: The autism rate has recently increased to 1 in 100 children. Genetic studies demonstrate poorly understood complexity. Environmental factors apparently also play a role. Magnetic resonance imaging (MRI) studies demonstrate increased brain sizes and altered connectivity. EEG coherence studies confirm connectivity changes. However, genetic-, MRI-, and/or EEG-based diagnostic tests are not yet available. The varied study results likely reflect methodological and population differences, small samples, and for EEG, lack of attention to group-specific artifact. METHODS: Of the 1304 subjects with ages ranging from 1 to 18 years old and assessed with comparable EEG studies who participated in this study, 463 children were diagnosed with autism spectrum disorder (ASD); 571 children were neuro-typical controls (C). After artifact management, principal components analysis (PCA) identified EEG spectral coherence factors with corresponding loading patterns. The 2-12 year old subsample consisted of 430 ASD- and 554 C-group subjects (n=984). Discriminant function analysis (DFA) determined the spectral coherence factors’ discrimination success for the two groups. Loading patterns on the DFA-selected coherence factors described ASD-specific coherence differences when compared to controls. RESULTS: Total sample PCA of coherence data identified 40 factors which explained 50.8% of the total population variance. For the 2-12 year olds the 40 factors showed highly significant group differences (p<0.0001). Ten randomly generated split half replications demonstrated high-average classification success (C, 88.5%; ASD, 86.0%). Still higher success was obtained in the more restricted age sub-samples using the jackknifing technique: 2-4 year olds (C, 90.6%; ASD, 98.1%); 4-6 year olds (C, 90.9%; ASD 99.1%); and 6-12 year-olds (C, 98.7%; ASD, 93.9%). Coherence loadings demonstrated reduced short-distance and reduced as well as increased long-distance coherences for the ASD-groups, when compared to the controls. Average spectral loading per factor was wide (10.1 Hz). CONCLUSIONS: Classification success suggests a stable coherence loading pattern that differentiates ASD- from C-group subjects. This might constitute an EEG coherence-based phenotype of childhood autism. The predominantly reduced short-distance- coherences may indicate poor local network function. The increased long-distance- coherences may represent compensatory processes or reduced neural pruning. The wide average spectral range of factor loadings may suggest over-damped neural networks.
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5. Enticott PG, Kennedy HA, Rinehart NJ, Tonge BJ, Bradshaw JL, Fitzgerald PB. {{GABAergic activity in autism spectrum disorders: An investigation of cortical inhibition via transcranial magnetic stimulation}}. {Neuropharmacology}. 2012.
Mounting evidence suggests a possible role for gamma-aminobutyric acid (GABA) in the neuropathophysiology of autism spectrum disorders (ASD), but the extent of this impairment is unclear. A non-invasive, in vivo measure of GABA involves transcranial magnetic stimulation (TMS) of the primary motor cortex to probe cortical inhibition. Individuals diagnosed with ASD (high-functioning autism or Asperger’s disorder) (n = 36 [28 male]; mean age: 26.00 years) and a group of healthy individuals (n = 34 [23 male]; mean age: 26.21 years) (matched for age, gender, and cognitive function) were administered motor cortical TMS paradigms putatively measuring activity at GABA(A) and GABA(B) receptors (i.e., short and long interval paired pulse TMS, cortical silent period). All cortical inhibition paradigms yielded no difference between ASD and control groups. There was, however, evidence for short interval cortical inhibition (SICI) deficits among those ASD participants who had experienced early language delay, suggesting that GABA may be implicated in an ASD subtype. The current findings do not support a broad role for GABA in the neuropathophysiology of ASD, but provide further indication that GABA(A) could be involved in ASD where there is a delay in language acquisition. This article is part of a Special Issue entitled ‘Neurodevelopment Disorder’.
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6. Gandal MJ, Anderson RL, Billingslea EN, Carlson GC, Roberts TP, Siegel SJ. {{Mice with reduced NMDA receptor expression: more consistent with autism than schizophrenia?}}. {Genes Brain Behav}. 2012; 9999(999A).
Reduced NMDA-receptor (NMDAR) function has beenimplicated in the pathophysiology of neuropsychiatric disease, most strongly in schizophrenia but also recently in autism spectrum disorders (ASD). To determinethe direct contribution of NMDAR dysfunction to disease phenotypes, a mouse model with constitutively reduced expression of the obligatory NR1 subunit has been developed and extensively investigated. Adult NR1(neo) (-/-) mice show multiple abnormal behaviors, including reduced social interactions, locomotor hyperactivity, self-injury, deficits in prepulse inhibition, and sensory hypersensitivity, among others. Whereas such phenotypes have largely been interpreted in the context of schizophrenia, these behavioral abnormalities are rather non-specific and are frequently present across models of diseases characterized by negative symptom domains. This study investigated auditory electrophysiological and behavioral paradigms relevant to autism, to determine whether NMDAR hypofunctionmay bemore consistent with adult ASD-like phenotypes. Indeed, transgenic mice demonstrated behavioral deficits relevant to all core ASD symptoms, including decreased social interactions, altered ultrasonic vocalizations, and increased repetitive behaviors.NMDAR disruption recapitulated clinical endophenotypes including reduced prepulse inhibition, auditory-evoked response N1 latency delay, and reduced gamma synchrony. Auditory electrophysiological abnormalities more closely resembled those seen in clinical studies of autism than schizophrenia. These results suggest that NMDA-receptor hypofunction may be associated with a continuum of neuropsychiatric diseases, includingschizophrenia and autism. Neural synchrony abnormalities suggest an imbalance of glutamatergic and GABAergic coupling and may provide a target, along with behavioral phenotypes,for preclinical screening of novel therapeutics. (c) 2012 The Authors. Genes, Brain and Behavior (c) 2012 Blackwell Publishing Ltd and International Behavioural and Neural Genetics Society.
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7. Hus V, Lord C. {{Effects of Child Characteristics on the Autism Diagnostic Interview-Revised: Implications for Use of Scores as a Measure of ASD Severity}}. {J Autism Dev Disord}. 2012.
The Autism Diagnostic Interview-Revised (ADI-R) is commonly used to inform diagnoses of autism spectrum disorders (ASD). Considering the time dedicated to using the ADI-R, it is of interest to expand the ways in which information obtained from this interview is used. The current study examines how algorithm totals reflecting past (ADI-Diagnostic) and current (ADI-Current) behaviors are influenced by child characteristics, such as demographics, behavioral problems and developmental level. Children with less language at the time of the interview had higher ADI-Diagnostic and ADI-Current. ADI-Diagnostic totals were also associated with age; parents of older children reported more severe past behaviors. Recommendations are provided regarding the use of the ADI-R as a measure of ASD severity, taking language and age into account.
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8. Kuusikko-Gauffin S, Pollock-Wurman R, Mattila ML, Jussila K, Ebeling H, Pauls D, Moilanen I. {{Social Anxiety in Parents of High-Functioning Children with Autism and Asperger Syndrome}}. {J Autism Dev Disord}. 2012.
We evaluated social anxiety (SA) symptoms in parents of children with autism spectrum disorders (ASDs; N = 131) and community parents (N = 597) using the Social Phobia and Anxiety Inventory (SPAI). SA was significantly more common in ASD than control mothers (15.6 vs. 6.7 %) and more equal between the ASD and control fathers (3.3 vs. 4.8 %). The ASD mothers scored significantly higher than control mothers on all SPAI scales. ASD fathers scored significantly higher than control fathers on the somatic, cognitive, avoidance and agoraphobic symptoms of SA. It is of clinical import to support ASD parents’ well-being as their psychiatric features may contribute greatly to their children’s emotional development and the well-being of the whole family.
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9. Li Y, Jin P. {{RNA-mediated neurodegeneration in fragile X-associated tremor/ataxia syndrome}}. {Brain Res}. 2012; 1462: 112-7.
Carriers of fragile X syndrome (FXS) have FMR1 alleles, called premutations, with a number of 5′-untranslated-CGG repeats somewhere between patients, who have over 200 repeats, and normal individuals, with fewer than 60 repeats. Fragile X-associated tremor/ataxia syndrome (FXTAS), a late-onset neurodegenerative disorder, has been recognized in older male fragile X premutation carriers, and FXTAS is uncoupled from the neurodevelopmental disorder, FXS. Several lines of evidence have led to the proposal of an RNA (fragile X premutation rCGG repeat)-mediated gain-of-function toxicity model for FXTAS, in which rCGG repeat-binding proteins (RBPs) could become functionally limited by their sequestration to lengthy rCGG repeats. In this review, we will discuss the recent progress towards understanding the molecular basis of RNA-mediated neurodegeneration in FXTAS. This article is part of a Special Issue entitled: RNA-Binding Proteins.
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10. Luo R, Sanders SJ, Tian Y, Voineagu I, Huang N, Chu SH, Klei L, Cai C, Ou J, Lowe JK, Hurles ME, Devlin B, State MW, Geschwind DH. {{Genome-wide Transcriptome Profiling Reveals the Functional Impact of Rare De Novo and Recurrent CNVs in Autism Spectrum Disorders}}. {Am J Hum Genet}. 2012.
Copy-number variants (CNVs) are a major contributor to the pathophysiology of autism spectrum disorders (ASDs), but the functional impact of CNVs remains largely unexplored. Because brain tissue is not available from most samples, we interrogated gene expression in lymphoblasts from 244 families with discordant siblings in the Simons Simplex Collection in order to identify potentially pathogenic variation. Our results reveal that the overall frequency of significantly misexpressed genes (which we refer to here as outliers) identified in probands and unaffected siblings does not differ. However, in probands, but not their unaffected siblings, the group of outlier genes is significantly enriched in neural-related pathways, including neuropeptide signaling, synaptogenesis, and cell adhesion. We demonstrate that outlier genes cluster within the most pathogenic CNVs (rare de novo CNVs) and can be used for the prioritization of rare CNVs of potentially unknown significance. Several nonrecurrent CNVs with significant gene-expression alterations are identified (these include deletions in chromosomal regions 3q27, 3p13, and 3p26 and duplications at 2p15), suggesting that these are potential candidate ASD loci. In addition, we identify distinct expression changes in 16p11.2 microdeletions, 16p11.2 microduplications, and 7q11.23 duplications, and we show that specific genes within the 16p CNV interval correlate with differences in head circumference, an ASD-relevant phenotype. This study provides evidence that pathogenic structural variants have a functional impact via transcriptome alterations in ASDs at a genome-wide level and demonstrates the utility of integrating gene expression with mutation data for the prioritization of genes disrupted by potentially pathogenic mutations.
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11. Matson JL, Hattier MA, Williams LW. {{How Does Relaxing the Algorithm for Autism Affect DSM-V Prevalence Rates?}}. {J Autism Dev Disord}. 2012.
Although it is still unclear what causes autism spectrum disorders (ASDs), over time researchers and clinicians have become more precise with detecting and diagnosing ASD. Many diagnoses, however, are based on the criteria established within the Diagnostic and Statistical Manual of Mental Disorders (DSM); thus, any change in these diagnostic criteria can have a great effect upon children with ASD and their families. It is predicted that the prevalence of ASD diagnoses will dramatically decrease with the adoption of the proposed DSM-5 criteria in 2013. The aim of this current study was to inspect the changes in prevalence first using a diagnostic criteria set which was modified slightly from the DSM-5 criteria (Modified-1 criteria) and again using a set of criteria which was relaxed even a bit more (Modified-2 criteria). Modified-1 resulted in 33.77 % fewer toddlers being diagnosed with ASD compared to the DSM-IV, while Modified-2 resulted in only a 17.98 % decrease in ASD diagnoses. Children diagnosed with the DSM-5 criteria exhibited the greatest levels of autism symptomatology, but the Mod-1, Mod-2, and DSM-IV groups still demonstrated significant impairments. Implications of these findings are discussed.
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12. Nicholas JS, Carpenter LA, King LB, Jenner W, Wahlquist A, Logan S, Charles JM. {{Completeness of case ascertainment for surveillance of autism spectrum disorders using the autism developmental disabilities monitoring network methodology}}. {Disabil Health J}. 2012; 5(3): 185-9.
BACKGROUND: The Autism and Developmental Disabilities Monitoring Network (ADDM), sponsored by the Centers for Disease Control and Prevention, is the largest-scale project ever undertaken to identify the prevalence of Autism Spectrum Disorders (ASD) in the United States. OBJECTIVE: The objective of the present study was to examine the accuracy of the ADDM methodology in terms of completeness of case ascertainment; that is, to assess the success of the ADDM Network in identifying and accurately classifying all existing cases of ASD among 8-year-old children in the target study areas. METHODS: To accomplish this objective, the ADDM methodology was applied to a selected region of South Carolina for 8-year olds in 2000 (birth year 1992) and again seven years later for the same region and birth year. RESULTS: For this region and birth year, completeness of case ascertainment was high, with prevalence estimates of 7.6 per 1000 at both ages 8- and 15-years. For children common to both surveillance years, concordance in case status was also high (82%). CONCLUSIONS: Given that prevalence did not change within this region and birth year, continued research is needed to better understand the changes in prevalence estimates being found by the ADDM network across surveillance groups.
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13. Paul R, Campbell D, Gilbert K, Tsiouri I. {{Comparing Spoken Language Treatments for Minimally Verbal Preschoolers with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2012.
Preschoolers with severe autism and minimal speech were assigned either a discrete trial or a naturalistic language treatment, and parents of all participants also received parent responsiveness training. After 12 weeks, both groups showed comparable improvement in number of spoken words produced, on average. Approximately half the children in each group achieved benchmarks for the first stage of functional spoken language development, as defined by Tager-Flusberg et al. (J Speech Lang Hear Res, 52: 643-652, 2009). Analyses of moderators of treatment suggest that joint attention moderates response to both treatments, and children with better receptive language pre-treatment do better with the naturalistic method, while those with lower receptive language show better response to the discrete trial treatment. The implications of these findings are discussed.
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14. Salcedo-Marin MD, Moreno-Granados JM, Ruiz-Veguilla M, Ferrin M. {{Evaluation of Planning Dysfunction in Attention Deficit Hyperactivity Disorder and Autistic Spectrum Disorders Using the Zoo Map Task}}. {Child Psychiatry Hum Dev}. 2012.
Attention-Deficit-Hyperactivity-Disorders (ADHD) and Autistic-Spectrum-Disorders (ASD) share overlapping clinical and cognitive features that may confuse the diagnosis. Evaluation of executive problems and planning dysfunction may aid the clinical diagnostic process and help disentangle the neurobiological process underlying these conditions. This study evaluates the planning function problems in 80 male children and adolescents diagnosed with ADHD and 23 male children and adolescents with ASD using the Zoo Map Task; both groups were comparable in terms of age and IQ. The relationship between planning function and other executive functions is also assessed. In comparison to the ADHD groups, ASD children presented more errors in the open-ended tasks; these planning function problems seem to be mediated by processing speed and motor coordination, however it does not seem to be mediated by other executive function problems, including attention, working memory or response inhibition. In the time for planning, an interaction between the specific subgroups and working memory components was observed. ADHD and ASD present with different patterns of planning function, even when other components of executive function are taken into account; clinical and educational implications are discussed.
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15. Sharma A, Shaw SR. {{Efficacy of risperidone in managing maladaptive behaviors for children with autistic spectrum disorder: a meta-analysis}}. {J Pediatr Health Care}. 2012; 26(4): 291-9.
INTRODUCTION: Atypical antipsychotic agents are widely used psychopharmacological interventions for autism spectrum disorders (ASDs). Among the atypical antipsychotic agents, risperidone has demonstrated considerable benefits in reducing several behavioral symptoms associated with ASDs. This meta-analysis examined research regarding the effectiveness of risperidone use among children with ASD using articles published since the year 2000. METHODS: The database for the analyses comprised 22 studies including 16 open-label and six placebo-controlled studies. Based on the quality, sample size, and study design of studies prior to 2000, the database was then restricted to articles published after the year 2000. Effect sizes were calculated for each reported measure within a study to calculate an average effect size per study. RESULTS: The mean effect size for the database was 1.047 and the sample weighted mean effect size was 1.108, with a variance of 0.18. CONCLUSIONS: Outcome measures demonstrated mean improvement in problematic behaviors equaling one standard deviation, and thus current evidence supports the effectiveness of risperidone in managing behavioral problems and symptoms for children with ASD. Although Risperdal has several adverse effects, most are manageable or extremely rare. An exception is rapid weight gain, which is common and can create significant health problems. Overall, for most children with autism and irritable and aggressive behavior, risperidone is an effective psychopharmacological treatment.
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16. Srivastava DP, Woolfrey KM, Jones KA, Anderson CT, Smith KR, Russell TA, Lee H, Yasvoina MV, Wokosin DL, Ozdinler PH, Shepherd GM, Penzes P. {{An autism-associated variant of epac2 reveals a role for ras/epac2 signaling in controlling Basal dendrite maintenance in mice}}. {PLoS Biol}. 2012; 10(6): e1001350.
The architecture of dendritic arbors determines circuit connectivity, receptive fields, and computational properties of neurons, and dendritic structure is impaired in several psychiatric disorders. While apical and basal dendritic compartments of pyramidal neurons are functionally specialized and differentially regulated, little is known about mechanisms that selectively maintain basal dendrites. Here we identified a role for the Ras/Epac2 pathway in maintaining basal dendrite complexity of cortical neurons. Epac2 is a guanine nucleotide exchange factor (GEF) for the Ras-like small GTPase Rap, and it is highly enriched in the adult mouse brain. We found that in vivo Epac2 knockdown in layer 2/3 cortical neurons via in utero electroporation reduced basal dendritic architecture, and that Epac2 knockdown in mature cortical neurons in vitro mimicked this effect. Overexpression of an Epac2 rare coding variant, found in human subjects diagnosed with autism, also impaired basal dendritic morphology. This mutation disrupted Epac2’s interaction with Ras, and inhibition of Ras selectively interfered with basal dendrite maintenance. Finally, we observed that components of the Ras/Epac2/Rap pathway exhibited differential abundance in the basal versus apical dendritic compartments. These findings define a role for Epac2 in enabling crosstalk between Ras and Rap signaling in maintaining basal dendrite complexity, and exemplify how rare coding variants, in addition to their disease relevance, can provide insight into cellular mechanisms relevant for brain connectivity.
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17. van Steensel FJ, Bogels SM, Wood JJ. {{Autism Spectrum Traits in Children with Anxiety Disorders}}. {J Autism Dev Disord}. 2012.
The aim of this study was to examine ASD traits in children with clinical anxiety in early development, as well as current manifestations. Parents of 42 children with an anxiety disorder (but no known diagnosis of ASD) and 42 typically developing children were interviewed using the Autism Diagnostic Interview (ADI-R). They also completed questionnaires that assessed child anxiety (SCARED-71) and children’s ASD symptoms. Results revealed that children with anxiety disorders had higher scores than typically developing children, for both ASD traits in early development as well as current ASD symptoms. A specific association was found between symptoms of Social Anxiety Disorder and ASD traits early in life. Findings are considered in terms of clinical implications, and limitations are discussed.
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18. Williams D, Payne H, Marshall C. {{Non-word Repetition Impairment in Autism and Specific Language Impairment: Evidence for Distinct Underlying Cognitive Causes}}. {J Autism Dev Disord}. 2012.
Language-impaired individuals with autism perform poorly on tests such as non-word repetition that are sensitive clinical markers of specific language impairment (SLI). This has fuelled the theory that language impairment in autism represents a co-morbid SLI. However, the underlying cause of these deficits may be different in each disorder. In a novel task, we manipulated non-word stimuli in three ways known to influence the repetition accuracy of children with SLI. Participants with SLI were affected differently by these manipulations to children with autism. Children with autism performed similarly to language-matched typical children in terms of levels and patterns of performance, and types of error made, suggesting that the underlying cognitive cause of non-word repetition deficits is different in each disorder.
