1. Ambridge B, Bannard C, Jackson GH. {{Is Grammar Spared in Autism Spectrum Disorder? Data from Judgments of Verb Argument Structure Overgeneralization Errors}}. {J Autism Dev Disord};2015 (Jun 6)
Children with Autism Spectrum Disorder (ASD) aged 11-13 (N = 16) and an IQ-matched typically developing (TD) group aged 7-12 (N = 16) completed a graded grammaticality judgment task, as well as a standardized test of cognitive function. In a departure from previous studies, the judgment task involved verb argument structure overgeneralization errors (e.g., *Lisa fell the cup off the shelf) of the type sometimes observed amongst typically developing children, as well as grammatical control sentences with the same verbs (e.g., The cup fell off the shelf). The ASD group showed a smaller dispreference for ungrammatical sentences (relative to the control sentences) than did the TD group. These findings are indicative of a subtle grammatical impairment in even relatively high-functioning children with ASD.
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2. Borreca A, Gironi K, Amadoro G, Ammassari-Teule M. {{Opposite Dysregulation of Fragile-X Mental Retardation Protein and Heteronuclear Ribonucleoprotein C Protein Associates with Enhanced APP Translation in Alzheimer Disease}}. {Mol Neurobiol};2015 (Jun 6)
Amyloid precursor protein (APP) is overexpressed in familiar and sporadic Alzheimer Disease (AD) patients suggesting that, in addition to abnormalities in APP cleavage, enhanced levels of APP full length might contribute to the pathology. Based on data showing that the two RNA binding proteins (RBPs), Fragile-X Mental Retardation Protein (FMRP) and heteronuclear Ribonucleoprotein C (hnRNP C), exert an opposite control on APP translation, we have analyzed whether expression and translation of these two RBPs vary in relation to changes in APP protein and mRNA levels in the AD brain at 1, 3, and 6 months of age. Here, we show that, as expected, human APP is overexpressed in hippocampal total extract from Tg2576 mice at all age points. APP overexpression, however, is not stable over time but reaches its maximal level in 1-month-old mutants in association with the stronger (i) reduction of FMRP and (ii) augmentation of hnRNP C. APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels. Consistent with the mouse data, expression of FMRP and hnRNP C are, respectively, decreased and increased in hippocampal synaptosomes from sporadic AD patients. Our findings identify two RBP targets that might be manipulated for reducing abnormally elevated levels of APP in the AD brain, with the hypothesis that acting upstream of amyloidogenic processing might contribute to attenuate the amyloid burden.
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3. Brewer R, Biotti F, Catmur C, Press C, Happe F, Cook R, Bird G. {{Can Neurotypical Individuals Read Autistic Facial Expressions? Atypical Production of Emotional Facial Expressions in Autism Spectrum Disorders}}. {Autism Res};2015 (Jun 6)
The difficulties encountered by individuals with autism spectrum disorder (ASD) when interacting with neurotypical (NT, i.e. nonautistic) individuals are usually attributed to failure to recognize the emotions and mental states of their NT interaction partner. It is also possible, however, that at least some of the difficulty is due to a failure of NT individuals to read the mental and emotional states of ASD interaction partners. Previous research has frequently observed deficits of typical facial emotion recognition in individuals with ASD, suggesting atypical representations of emotional expressions. Relatively little research, however, has investigated the ability of individuals with ASD to produce recognizable emotional expressions, and thus, whether NT individuals can recognize autistic emotional expressions. The few studies which have investigated this have used only NT observers, making it impossible to determine whether atypical representations are shared among individuals with ASD, or idiosyncratic. This study investigated NT and ASD participants’ ability to recognize emotional expressions produced by NT and ASD posers. Three posing conditions were included, to determine whether potential group differences are due to atypical cognitive representations of emotion, impaired understanding of the communicative value of expressions, or poor proprioceptive feedback. Results indicated that ASD expressions were recognized less well than NT expressions, and that this is likely due to a genuine deficit in the representation of typical emotional expressions in this population. Further, ASD expressions were equally poorly recognized by NT individuals and those with ASD, implicating idiosyncratic, rather than common, atypical representations of emotional expressions in ASD. Autism Res 2015. (c) 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research.
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4. Brosnan M, Mills E. {{The effect of diagnostic labels on the affective responses of college students towards peers with ‘Asperger’s Syndrome’ and ‘Autism Spectrum Disorder’}}. {Autism};2015 (Jun 4)
Given the removal of Asperger’s Syndrome label in Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition, the impact of clinical labels upon the affective responses of college students was explored. A total of 120 college students read two vignettes depicting social interactions typical of a person with autism spectrum disorder. In one vignette, they were informed that the character was a typical college student and in the other, the character had a clinical disorder (either autism spectrum disorder, Asperger’s Syndrome or Schizophrenia). Participants’ affective responses were measured on the Positive and Negative Affect Scale. No significant differences in positive and negative affective responses were found between the clinical labels. However, affective responses were significantly more positive and less negative towards behaviours associated with clinical groups compared to the typical college student. The implications for students disclosing their diagnosis at university are discussed.
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5. Buie T. {{Potential Etiologic Factors of Microbiome Disruption in Autism}}. {Clin Ther};2015 (May 1);37(5):976-983.
PURPOSE: The primary purpose of this article was to consider the candidate disruptors of the development of a healthy microbiome in patients with autism. The reported abnormalities in the microbiome of individuals with autism are discussed. METHODS: This selected review used data from published articles related to the assessment of microbiota in autism. Evidence-based support of factors known to affect the intestinal microbiome in individuals with autism are presented. Proposed interventions are evaluated and discussed. FINDINGS: Studies that have investigated the intestinal microbiome in patients with autism have reported significant differences versus unaffected controls. Increased clostridial species in autism have been reported in several studies. These differences may have resulted from a number of environmental factors. Microbiome alterations that might contribute to the development of autism include altered immune function and bacterial metabolites. IMPLICATIONS: Efforts to modify microbial imbalances through a variety of interventions are addressed. Focusing on mechanisms that drive imbalances in the microbiome may affect the development of disease. Altered intestinal health may contribute to the development of autistic behaviors or autism itself. Interventions aimed at improving intestinal health may favorably affect the microbiome and autism.
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6. Chi OZ, Wu CC, Liu X, Rah KH, Jacinto E, Weiss HR. {{Restoration of Normal Cerebral Oxygen Consumption with Rapamycin Treatment in a Rat Model of Autism-Tuberous Sclerosis}}. {Neuromolecular Med};2015 (Jun 6)
Tuberous sclerosis (TSC) is associated with autism spectrum disorders and has been linked to metabolic dysfunction and unrestrained signaling of the mammalian target of rapamycin (mTOR). Inhibition of mTOR by rapamycin can mitigate some of the phenotypic abnormalities associated with TSC and autism, but whether this is due to the mTOR-related function in energy metabolism remains to be elucidated. In young Eker rats, an animal model of TSC and autism, which harbors a germ line heterozygous Tsc2 mutation, we previously reported that cerebral oxygen consumption was pronouncedly elevated. Young (4 weeks) male control Long-Evans and Eker rats were divided into control and rapamycin-treated (20 mg/kg once daily for 2 days) animals. Cerebral regional blood flow (14C-iodoantipyrine) and O2 consumption (cryomicrospectrophotometry) were determined in isoflurane-anesthetized rats. We found significantly increased basal O2 consumption in the cortex (8.7 +/- 1.5 ml O2/min/100 g Eker vs. 2.7 +/- 0.2 control), hippocampus, pons and cerebellum. Regional cerebral blood flow and cerebral O2 extractions were also elevated in all brain regions. Rapamycin had no significant effect on O2 consumption in any brain region of the control rats, but significantly reduced consumption in the cortex (4.1 +/- 0.3) and all other examined regions of the Eker rats. Phosphorylation of mTOR and S6K1 was similar in the two groups and equally reduced by rapamycin. Thus, a rapamycin-sensitive, mTOR-dependent but S6K1-independent, signal led to enhanced oxidative metabolism in the Eker brain. We found decreased Akt phosphorylation in Eker but not Long-Evans rat brains, suggesting that this may be related to the increased cerebral O2 consumption in the Eker rat. Our findings suggest that rapamycin targeting of Akt to restore normal cerebral metabolism could have therapeutic potential in tuberous sclerosis and autism.
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7. Cochoy DM, Kolevzon A, Kajiwara Y, Schoen M, Pascual-Lucas M, Lurie S, Buxbaum JD, Boeckers TM, Schmeisser MJ. {{Phenotypic and functional analysis of SHANK3 stop mutations identified in individuals with ASD and/or ID}}. {Mol Autism};2015;6:23.
BACKGROUND: SHANK proteins are crucial for the formation and plasticity of excitatory synapses. Although mutations in all three SHANK genes are associated with autism spectrum disorder (ASD), SHANK3 appears to be the major ASD gene with a prevalence of approximately 0.5% for SHANK3 mutations in ASD, with higher rates in individuals with ASD and intellectual disability (ID). Interestingly, the most relevant mutations are typically de novo and often are frameshift or nonsense mutations resulting in a premature stop and a truncation of SHANK3 protein. METHODS: We analyzed three different SHANK3 stop mutations that we identified in individuals with ASD and/or ID, one novel (c.5008A > T) and two that we recently described (c.1527G > A, c.2497delG). The mutations were inserted into the human SHANK3a sequence and analyzed for effects on subcellular localization and neuronal morphology when overexpressed in rat primary hippocampal neurons. RESULTS: Clinically, all three individuals harboring these mutations had global developmental delays and ID. In our in vitro assay, c.1527G > A and c.2497delG both result in proteins that lack most of the SHANK3a C-terminus and accumulate in the nucleus of transfected cells. Cells expressing these mutants exhibit converging morphological phenotypes including reduced complexity of the dendritic tree, less spines, and less excitatory, but not inhibitory synapses. In contrast, the truncated protein based on c.5008A > T, which lacks only a short part of the sterile alpha motif (SAM) domain in the very SHANK3a C-terminus, does not accumulate in the nucleus and has minor effects on neuronal morphology. CONCLUSIONS: In spite of the prevalence of SHANK3 disruptions in ASD and ID, only a few human mutations have been functionally characterized; here we characterize three additional mutations. Considering the transcriptional and functional complexity of SHANK3 in healthy neurons, we propose that any heterozygous stop mutation in SHANK3 will lead to a dysequilibrium of SHANK3 isoform expression and alterations in the stoichiometry of SHANK3 protein complexes, resulting in a distinct perturbation of neuronal morphology. This could explain why the clinical phenotype in all three individuals included in this study remains quite severe – regardless of whether there are disruptions in one or more SHANK3 interaction domains.
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8. Gardner RM, Lee BK, Magnusson C, Rai D, Frisell T, Karlsson H, Idring S, Dalman C. {{Maternal body mass index during early pregnancy, gestational weight gain, and risk of autism spectrum disorders: Results from a Swedish total population and discordant sibling study}}. {Int J Epidemiol};2015 (Jun 4)
BACKGROUND: Prenatal environmental factors such as maternal adiposity may influence the risk of offspring autism spectrum disorders (ASD), though current evidence is inconsistent. The objective of this study was to assess the relationship of parental BMI and gestational weight gain (GWG) with risk of offspring ASD in a population-based cohort study using family-based study designs. METHODS: The cohort was based in Stockholm County, Sweden, including 333 057 individuals born 1984-2007, of whom 6420 were diagnosed with an ASD. We evaluated maternal body mass index (BMI) at first antenatal visit, GWG and paternal BMI at the time of conscription into the Swedish military as exposures using general estimating equation (GEE) models with logit link. RESULTS: At the population level, maternal overweight/obesity was associated with increased risk of offspring ASD [odds ratio (OR)25 </= BMI < 30 1.31, 95% confidence interval = 1.21-1.41; ORBMI >/= 30 1.94, 1.72-2.17], as was paternal underweight (ORBMI < 18.5, 1.19, 1.06-1.33) and obesity (ORBMI >/= 30 1.47, 1.12-1.92) in mutually adjusted models. However, in matched sibling analyses, the relationship between elevated maternal BMI and ASD risk was not apparent. GWG had a U-shaped association with offspring ASD at the population level (ORinsufficient 1.22, 1.07-1.40; ORexcessive 1.23, 1.08-1.40). Matched sibling analyses were suggestive of elevated risk with excessive GWG (ORinsufficient 1.12, 0.68-1.84; ORexcessive 1.48, 0.93-2.38). CONCLUSIONS: Whereas population-level results suggested that maternal BMI was associated with ASD, sibling analyses and paternal BMI analyses indicate that maternal BMI may also be a proxy marker for other familial risk factors. Evidence is stronger for a direct link between GWG and ASD risk.
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9. Kanduri C, Kantojarvi K, Salo PM, Vanhala R, Buck G, Blancher C, Lahdesmaki H, Jarvela I. {{The landscape of copy number variations in Finnish families with autism spectrum disorders}}. {Autism Res};2015 (Jun 6)
Rare de novo and inherited copy number variations (CNVs) have been implicated in autism spectrum disorder (ASD) risk. However, the genetic underpinnings of ASD remain unknown in more than 80% of cases. Therefore, identification of novel candidate genes and corroboration of known candidate genes may broaden the horizons of determining genetic risk alleles, and subsequent development of diagnostic testing. Here, using genotyping arrays, we characterized the genetic architecture of rare CNVs (<1% frequency) in a Finnish case-control dataset. Unsurprisingly, ASD cases harbored a significant excess of rare, large (>1 Mb) CNVs and rare, exonic CNVs. The exonic rare de novo CNV rate ( approximately 22.5%) seemed higher compared to previous reports. We identified several CNVs in well-known ASD regions including GSTM1-5, DISC1, FHIT, RBFOX1, CHRNA7, 15q11.2, 15q13.2-q13.3, 17q12, and 22q11.21. Additionally, several novel candidate genes (BDKRB1, BDKRB2, AP2M1, SPTA1, PTH1R, CYP2E1, PLCD3, F2RL1, UQCRC2, LILRB3, RPS9, and COL11A2) were identified through gene prioritization. The majority of these genes belong to neuroactive ligand-receptor interaction pathways, and calcium signaling pathways, thus suggesting that a subset of these novel candidate genes may contribute to ASD risk. Furthermore, several metabolic pathways like caffeine metabolism, drug metabolism, retinol metabolism, and calcium-signaling pathway were found to be affected by the rare exonic ASD CNVs. Additionally, biological processes such as bradykinin receptor activity, endoderm formation and development, and oxidoreductase activity were enriched among the rare exonic ASD CNVs. Overall, our findings may add data about new genes and pathways that contribute to the genetic architecture of ASD. Autism Res 2015. (c) 2015 International Society for Autism Research, Wiley Periodicals, Inc.
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10. Keesler JM. {{Trauma-informed Day Services for Individuals with Intellectual/Developmental Disabilities: Exploring Staff Understanding and Perception within an Innovative Programme}}. {J Appl Res Intellect Disabil};2015 (Jun 3)
BACKGROUND: Trauma-informed care (TIC) is a systems-level philosophy of service delivery which integrates choice, collaboration, empowerment, safety and trust to create an organizational culture sensitive to trauma. This study explores staff understandings and perceptions within an innovative trauma-informed day program for individuals with Intellectual/developmental disabilities. METHODS: Semi-structured interviews queried staff members (n = 20) regarding trauma and TIC, the integration of the five principles of TIC, associated challenges and recommendations for improvement. RESULTS: Inductive analyses revealed reasonable understandings of trauma and TIC, highlighting factors critical to the five principles of TIC. Differences were associated with duration of employment and the presence of specialized training. Challenges with TIC emerged at different system levels: individuals, staff, management and interorganizational. CONCLUSIONS: This study presents preliminary insight for the innovative and formative process of integrating TIC with intellectual/developmental disabilities services.
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11. Kucharsky Hiess R, Alter R, Sojoudi S, Ardekani BA, Kuzniecky R, Pardoe HR. {{Corpus Callosum Area and Brain Volume in Autism Spectrum Disorder: Quantitative Analysis of Structural MRI from the ABIDE Database}}. {J Autism Dev Disord};2015 (Jun 5)
Reduced corpus callosum area and increased brain volume are two commonly reported findings in autism spectrum disorder (ASD). We investigated these two correlates in ASD and healthy controls using T1-weighted MRI scans from the Autism Brain Imaging Data Exchange (ABIDE). Automated methods were used to segment the corpus callosum and intracranial region. No difference in the corpus callosum area was found between ASD participants and healthy controls (ASD 598.53 +/- 109 mm2; control 596.82 +/- 102 mm2; p = 0.76). The ASD participants had increased intracranial volume (ASD 1,508,596 +/- 170,505 mm3; control 1,482,732 +/- 150,873.5 mm3; p = 0.042). No evidence was found for overall ASD differences in the corpus callosum subregions.
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12. LeClerc S, Easley D. {{Pharmacological therapies for autism spectrum disorder: a review}}. {P T};2015 (Jun);40(6):389-397.
Medications are often added to behavioral therapy to help patients with autism spectrum disorder function successfully. This review discusses approved and off-label pharmacotherapeutic options for the various symptoms of the disorder.
13. Lin HY, Ni HC, Lai MC, Tseng WY, Gau SS. {{Regional brain volume differences between males with and without autism spectrum disorder are highly age-dependent}}. {Mol Autism};2015;6:29.
BACKGROUND: Neuroanatomical differences between individuals with and without autism spectrum disorder (ASD) were inconsistent in the literature. Such heterogeneity may substantially originate from age-differential effects. METHODS: Voxel-based morphometry was applied in 86 males with ASD and 90 typically developing control (TDC) males (aged 7 to 29 years). Three steps of statistical modeling (model 1, multiple regression with age as a covariate; model 2, multiple regression further considering diagnosis-by-age interaction; model 3, age-stratified analyses) were performed to dissect the moderating effects of age on diagnostic group differences in neuroanatomy. RESULTS: Across ages, males with and without ASD did not differ significantly in total gray matter (GM) or white matter (WM) volumes. For both groups, total GM volumes decreased and WM volumes increased with age. For regional volume, comparing with the model only held the age constant (model 1), the main effect of group altered when diagnosis-by-age interaction effects were considered (model 2). Here, participants with ASD had significantly greater relative regional GM volumes than TDC in the right inferior orbitofrontal cortex and bilateral thalamus; for WM, participants with ASD were larger than TDC in the bilateral splenium of corpus callosum and right anterior corona radiata. Importantly, significant diagnosis-by-age interactions were identified at the bilateral anterior prefrontal cortex, bilateral cuneus, bilateral caudate, and the left cerebellum Crus I for GM and left forceps minor for WM. Finally, age-stratified analyses (model 3) showed distinct patterns in GM and WM volumetric alterations in ASD among subsamples of children, adolescents, and adults. CONCLUSIONS: Our findings suggest that the heterogeneous reports on the atypical neuroanatomy of ASD may substantially originate from age variation in the study samples. Age variation and its methodological and biological implications have to be carefully delineated in future studies of the neurobiology of ASD.
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14. Messinger DS, Young GS, Webb SJ, Ozonoff S, Bryson SE, Carter A, Carver L, Charman T, Chawarska K, Curtin S, Dobkins K, Hertz-Picciotto I, Hutman T, Iverson JM, Landa R, Nelson CA, Stone WL, Tager-Flusberg H, Zwaigenbaum L. {{Early sex differences are not autism-specific: A Baby Siblings Research Consortium (BSRC) study}}. {Mol Autism};2015;6:32.
BACKGROUND: The increased male prevalence of autism spectrum disorder (ASD) may be mirrored by the early emergence of sex differences in ASD symptoms and cognitive functioning. The female protective effect hypothesis posits that ASD recurrence and symptoms will be higher among relatives of female probands. This study examined sex differences and sex of proband differences in ASD outcome and in the development of ASD symptoms and cognitive functioning among the high-risk younger siblings of ASD probands and low-risk children. METHODS: Prior to 18 months of age, 1824 infants (1241 high-risk siblings, 583 low-risk) from 15 sites were recruited. Hierarchical generalized linear model (HGLM) analyses of younger sibling and proband sex differences in ASD recurrence among high-risk siblings were followed by HGLM analyses of sex differences and group differences (high-risk ASD, high-risk non-ASD, and low-risk) on the Mullen Scales of Early Learning (MSEL) subscales (Expressive and Receptive Language, Fine Motor, and Visual Reception) at 18, 24, and 36 months and Autism Diagnostic Observation Schedule (ADOS) domain scores (social affect (SA) and restricted and repetitive behaviors (RRB)) at 24 and 36 months. RESULTS: Of 1241 high-risk siblings, 252 had ASD outcomes. Male recurrence was 26.7 % and female recurrence 10.3 %, with a 3.18 odds ratio. The HR-ASD group had lower MSEL subscale scores and higher RRB and SA scores than the HR non-ASD group, which had lower MSEL subscale scores and higher RRB scores than the LR group. Regardless of group, males obtained lower MSEL subscale scores, and higher ADOS RRB scores, than females. There were, however, no significant interactions between sex and group on either the MSEL or ADOS. Proband sex did not affect ASD outcome, MSEL subscale, or ADOS domain scores. CONCLUSIONS: A 3.2:1 male:female odds ratio emerged among a large sample of prospectively followed high-risk siblings. Sex differences in cognitive performance and repetitive behaviors were apparent not only in high-risk children with ASD, but also in high-risk children without ASD and in low-risk children. Sex differences in young children with ASD do not appear to be ASD-specific but instead reflect typically occurring sex differences seen in children without ASD. Results did not support a female protective effect hypothesis.
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15. Mostert-Kerckhoffs MA, Staal WG, Houben RH, de Jonge MV. {{Stop and Change: Inhibition and Flexibility Skills Are Related to Repetitive Behavior in Children and Young Adults with Autism Spectrum Disorders}}. {J Autism Dev Disord};2015 (Jun 5)
Cognitive control dysfunctions, like inhibitory and attentional flexibility deficits are assumed to underlie repetitive behavior in individuals with autism spectrum disorders (ASD). In the present study, prepotent response inhibition and attentional flexibility were examined in 64 high-functioning individuals with ASD and 53 control participants. Performance under different task conditions were tested both in response to visual and auditory information, and requiring a motor or verbal response. Individuals with ASD showed significant more control dysfunctions than typically developing participants on the auditory computer task. Inhibitory control and attentional flexibility predicted RRB in everyday life. Specifically, response inhibition in reaction to visual information and task switching in reaction to auditory information predicted motor and sensory stereotyped behavior.
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16. Ohan JL, Ellefson SE, Corrigan PW. {{Brief Report: The Impact of Changing from DSM-IV ‘Asperger’s’ to DSM-5 ‘Autistic Spectrum Disorder’ Diagnostic Labels on Stigma and Treatment Attitudes}}. {J Autism Dev Disord};2015 (Jun 5)
In the DSM-5, ‘Asperger’s Disorder’ was incorporated into ‘Autistic Spectrum Disorder’ (ASD). One key concern in this change has been that the ASD label will increase negative attitudes relative to the Asperger’s label. To test this, we asked 465 American adults to read a vignette describing a child with autistic symptoms that included an ASD label, an Asperger’s label, or no label, and rate their stigma and treatment attitudes (help-seeking and perceived effectiveness). Contrary to predictions, label did not impact stigma. Label did impact treatment attitudes, with greater help-seeking and perceived treatment effectiveness for both Asperger’s and ASD labels. In sum, concern that the ASD label will increase negative perceptions, at least amongst the general public, is not supported.
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17. Patel S, Roncaglia P, Lovering RC. {{Using Gene Ontology to describe the role of the neurexin-neuroligin-SHANK complex in human, mouse and rat and its relevance to autism}}. {BMC Bioinformatics};2015;16(1):186.
BACKGROUND: People with an autistic spectrum disorder (ASD) display a variety of characteristic behavioral traits, including impaired social interaction, communication difficulties and repetitive behavior. This complex neurodevelopment disorder is known to be associated with a combination of genetic and environmental factors. Neurexins and neuroligins play a key role in synaptogenesis and neurexin-neuroligin adhesion is one of several processes that have been implicated in autism spectrum disorders. RESULTS: In this report we describe the manual annotation of a selection of gene products known to be associated with autism and/or the neurexin-neuroligin-SHANK complex and demonstrate how a focused annotation approach leads to the creation of more descriptive Gene Ontology (GO) terms, as well as an increase in both the number of gene product annotations and their granularity, thus improving the data available in the GO database. CONCLUSIONS: The manual annotations we describe will impact on the functional analysis of a variety of future autism-relevant datasets. Comprehensive gene annotation is an essential aspect of genomic and proteomic studies, as the quality of gene annotations incorporated into statistical analysis tools affects the effective interpretation of data obtained through genome wide association studies, next generation sequencing, proteomic and transcriptomic datasets.
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18. Spain D, Blainey SH. {{Group social skills interventions for adults with high-functioning autism spectrum disorders: A systematic review}}. {Autism};2015 (Jun 4)
Autism spectrum disorders are characterised by impairments in communication and social interaction. Social skills interventions have been found to ameliorate socio-communication deficits in children and adolescents with autism spectrum disorders. Little is known about the effectiveness of social skills interventions for adults with high-functioning autism spectrum disorders (hf-ASD) – a clinical population who can present with more subtle core deficits, but comparable levels of impairment and secondary difficulties. A systematic review was undertaken to investigate the effectiveness of social skills interventions for adults with high-functioning autism spectrum disorders. Five studies met the pre-specified review inclusion criteria: two quasi-experimental comparative trials and three single-arm interventions. There was a degree of variation in the structure, duration and content of the social skills interventions delivered, as well as several methodological limitations associated with included studies. Nevertheless, narrative analysis tentatively indicates that group social skills interventions may be effective for enhancing social knowledge and understanding, improving social functioning, reducing loneliness and potentially alleviating co-morbid psychiatric symptoms.
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19. Tillmann J, Olguin A, Tuomainen J, Swettenham J. {{The Effect of Visual Perceptual Load on Auditory Awareness in Autism Spectrum Disorder}}. {J Autism Dev Disord};2015 (Jun 5)
Recent work on visual selective attention has shown that individuals with Autism Spectrum Disorder (ASD) demonstrate an increased perceptual capacity. The current study examined whether increasing visual perceptual load also has less of an effect on auditory awareness in children with ASD. Participants performed either a high- or low load version of a line discrimination task. On a critical trial, an unexpected, task-irrelevant auditory stimulus was played concurrently with the visual stimulus. In contrast to typically developing (TD) children, children with ASD demonstrated similar detection rates across perceptual load conditions, and reported greater awareness than TD children in the high perceptual load condition. These findings suggest an increased perceptual capacity in children with ASD that operates across sensory modalities.
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20. van Bakel MM, Delobel-Ayoub M, Cans C, Assouline B, Jouk PS, Raynaud JP, Arnaud C. {{Low but Increasing Prevalence of Autism Spectrum Disorders in a French Area from Register-Based Data}}. {J Autism Dev Disord};2015 (Jun 6)
Register-based prevalence rates of childhood autism (CA), Asperger’s syndrome (AS) and other autism spectrum disorders (ASD) were calculated among children aged 7 years old of the 1997-2003 birth cohorts, living in four counties in France. The proportion of children presenting comorbidities was reported. 1123 children with ASD were recorded (M/F ratio: 4.1), representing an overall prevalence rate of 36.5/10,000 children (95 % CI 34.4-38.7): 8.8/10,000 for CA (95 % CI 7.8-9.9), 1.7/10,000 for AS (95 % CI 1.3-2.3) and 25.9/10,000 for other ASD (95 % CI 24.2-27.8). ASD prevalence significantly increased (p < 0.0001) during the period under study. The proportion of children with an intellectual disability was 47.3 %, all other comorbidities were present in less than 5 % of the cases.
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21. Veatch OJ, Maxwell-Horn AC, Malow BA. {{Sleep in Autism Spectrum Disorders}}. {Curr Sleep Med Rep};2015 (Jun);1(2):131-140.
Autism spectrum disorders (ASD) are common neurodevelopmental conditions, affecting 1 in 68 children. Sleep disturbance, particularly insomnia, is very common in children diagnosed with ASD, with evidence supporting overlapping neurobiological and genetic underpinnings. Disturbed sleep exacerbates core and related ASD symptoms and has a substantial negative impact on the entire family. Treatment of sleep disturbance holds promise for ameliorating many of the challenging behavioral symptoms that children with ASD and their families face. Behavioral and pharmacological studies indicate promising approaches to treating sleep disturbances in this population. Awareness of treatment options is particularly important as parents and clinicians may believe that sleep disturbance is part of autism and refractory to therapy. In addition, autism symptoms refractory to treatment with conventional psychiatric medications may improve when sleep is addressed. Additional evidence-based studies are needed, including those that address the underlying biology of this condition.
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22. Wiggins LD, Levy SE, Daniels J, Schieve L, Croen LA, DiGuiseppi C, Blaskey L, Giarelli E, Lee LC, Pinto-Martin J, Reynolds A, Rice C, Rosenberg CR, Thompson P, Yeargin-Allsopp M, Young L, Schendel D. {{Autism Spectrum Disorder Symptoms Among Children Enrolled in the Study to Explore Early Development (SEED)}}. {J Autism Dev Disord};2015 (Jun 6)
This study examined the phenotypic profiles of children aged 30-68 months in the Study to Explore Early Development (SEED). Children classified as autism spectrum disorder (ASD), developmental delay (DD) with ASD symptoms, DD without ASD symptoms, and population comparison (POP) differed significantly from each other on cognitive, adaptive, behavioral, and social functioning and the presence of parent-reported conditions. Children with ASD and DD with ASD symptoms had mild to severe ASD risk on several measures compared to children with other DD and POP who had little ASD risk across measures. We conclude that children in SEED have varying degrees of ASD impairment and associated deficits. SEED thus provides a valuable sample to explore ASD phenotypes and inform risk factor analyses.
