1. Alvarez-Fernandez S, Brown HR, Zhao Y, Raithel JA, Bishop SL, Kern SB, Lord C, Petkova E, Di Martino A. {{Perceived social support in adults with autism spectrum disorder and attention-deficit/hyperactivity disorder}}. {Autism Res};2017 (Mar 03)
Perceived social support (PSS) has been related to physical and mental well-being in typically developing individuals, but systematic characterizations of PSS in autism spectrum disorder (ASD) are limited. We compared self-report ratings of the multidimensional scale of PSS (MSPSS) among age- and IQ-matched groups of adults (18-58 years) with cognitively high-functioning ASD (N = 41), or attention-deficit/hyperactivity disorder (ADHD; N = 69), and neurotypical controls (NC; N = 69). Accompanying group comparisons, we used machine learning random forest (RF) analyses to explore predictors among a range of psychopathological and socio-emotional variables. Relative to both ADHD and NC, adults with ASD showed lower MSPSS ratings, specifically for the friends subscale (MSPSS-f). Across ASD and ADHD, interindividual differences in autism severity, affective empathy, symptoms of anxiety related to social interactions, hyperactivity/impulsivity, and somatization best predicted MSPSS-f. These relationships did not differ between clinical groups. While group comparisons demonstrated greater impairment in individuals with ASD, analyzing individuals’ characteristics revealed cross-diagnoses similarities in regard to their MSPSS-f relationships. This is consistent with the Research Domain Criteria framework, supporting a trans-diagnostic approach as on the path toward « precision medicine. » Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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2. Bishop SL, Farmer C, Bal V, Robinson EB, Willsey AJ, Werling DM, Havdahl KA, Sanders SJ, Thurm A. {{Identification of Developmental and Behavioral Markers Associated With Genetic Abnormalities in Autism Spectrum Disorder}}. {Am J Psychiatry};2017 (Mar 03):appiajp201716101115.
OBJECTIVE: Aside from features associated with risk of neurogenetic syndromes in general (e.g., cognitive impairment), limited progress has been made in identifying phenotype-genotype relationships in autism spectrum disorder (ASD). The objective of this study was to extend work in the Simons Simplex Collection by comparing the phenotypic profiles of ASD probands with or without identified de novo loss of function mutations or copy number variants in high-confidence ASD-associated genes or loci. METHOD: Analyses preemptively accounted for documented differences in sex and IQ in affected individuals with de novo mutations by matching probands with and without these genetic events on sex, IQ, and age before comparing them on multiple behavioral domains. RESULTS: Children with de novo mutations (N=112) had a greater likelihood of motor delay during early development (later age at walking), but they were less impaired on certain measures of ASD core symptoms (parent-rated social communication abnormalities and clinician-rated diagnostic certainty about ASD) in later childhood. These children also showed relative strengths in verbal and language abilities, including a smaller discrepancy between nonverbal and verbal IQ and a greater likelihood of having achieved fluent language (i.e., regular use of complex sentences). CONCLUSIONS: Children with ASD with de novo mutations may exhibit a « muted » symptom profile with respect to social communication and language deficits relative to those with ASD with no identified genetic abnormalities. Such findings suggest that examining early milestone differences and standardized testing results may be helpful in etiologic efforts, and potentially in clinical differentiation of various subtypes of ASD, but only if developmental and demographic variables are properly accounted for first.
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3. Cheng YK, Lin CS, Kwok YK, Chan YM, Lau TK, Leung TY, Choy KW. {{Identification of fragile X pre-mutation carriers in the Chinese obstetric population using a robust FMR1 polymerase chain reaction assay: implications for screening and prenatal diagnosis}}. {Hong Kong Med J};2017 (Mar 03)
INTRODUCTION: There is significant morbidity associated with fragile X syndrome. Unfortunately, most maternal carriers are clinically silent during their reproductive years. Because of this, many experts have put forward the notion of preconception or prenatal fragile X carrier screening for females. This study aimed to determine the prevalence of fragile X syndrome pre-mutation and asymptomatic full-mutation carriers in a Chinese pregnant population, and the distribution of cytosine-guanine-guanine (CGG) repeat numbers using a robust fragile X mental retardation 1 (FMR1) polymerase chain reaction assay. METHODS: This was a cross-sectional survey in prospectively recruited pregnant women from a university hospital in Hong Kong. Chinese pregnant women without a family history of fragile X syndrome were recruited between April 2013 and May 2015. A specific FMR1 polymerase chain reaction assay was performed on peripheral blood to determine the CGG repeat number of the FMR1 gene. Prenatal counselling was offered to full-mutation and pre-mutation carriers. RESULTS: In 2650 Chinese pregnant women, two individuals with pre-mutation alleles (0.08%, one in 1325) and one asymptomatic woman with full-mutation (0.04%, one in 2650) alleles were identified. The overall prevalence of pre-mutation and full-mutation alleles was 0.11% (1 in 883). Furthermore, 30 (1.1%) individuals with intermediate alleles were detected. In the 2617 women with normal CGG repeats, the most common CGG repeat allele was 30. CONCLUSIONS: The overall prevalence of pre-mutation and asymptomatic full-mutation carriers in the Chinese pregnant population was one in 883, detected by a new FMR1 polymerase chain reaction assay.
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4. Choueiri RN, Zimmerman AW. {{New Assessments and Treatments in ASD}}. {Curr Treat Options Neurol};2017 (Feb);19(2):6.
OPINION STATEMENT: The assessment of autism spectrum disorder (ASD) is complex and remains clinical, despite advances in basic research. In this chapter, we review new and updated clinical tools, such as screening and diagnostic tests, and discuss the DSM-5 criteria introduced in 2013. We provide an algorithm to guide clinical evaluation and referrals. We also review non-behavioral treatments and summarize recent research. Current conventional treatment of ASD in children includes intensive behavioral interventions (known as applied behavioral analysis or ABA), rehabilitative services such as speech therapy, occupational therapy, physical therapy, social skills training, and counseling. We present new validated information and provide clinical guidance for the evaluation and treatment of young children and youth with ASD.
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5. Garofoli F, Lombardi G, Orcesi S, Pisoni C, Mazzucchelli I, Angelini M, Balottin U, Stronati M. {{An Italian Prospective Experience on the Association Between Congenital Cytomegalovirus Infection and Autistic Spectrum Disorder}}. {J Autism Dev Disord};2017 (Mar 03)
The aim of this retrospective study, with prospective data collection, was to correlate congenital cytomegalovirus (CMV) infection with autism spectrum disorder (ASD) and to define its prevalence. Seventy proven congenitally-infected infants, born between 2007 and 2012, were referred to our centre for CMV diagnosis and follow-up, which consisted of a consolidated protocol allowing an early evaluation of autism. We considered four children 2-year old, two of whom, at the age of 3, were diagnosed with ASD demonstrating a 2-3 fold higher prevalence (2.86%), than that in general Italian population (0.66-1.36%).Our protocol enabled us to make the earliest diagnosis and highlight the role of the virus among other causes of autism, which may be a long term sequela of congenital CMV.
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6. Hagglund AC, Jones I, Carlsson L. {{A novel mouse model of anterior segment dysgenesis (ASD): conditional deletion of Tsc1 disrupts ciliary body and iris development}}. {Dis Model Mech};2017 (Mar 01);10(3):245-257.
Development of the cornea, lens, ciliary body and iris within the anterior segment of the eye involves coordinated interaction between cells originating from the ciliary margin of the optic cup, the overlying periocular mesenchyme and the lens epithelium. Anterior segment dysgenesis (ASD) encompasses a spectrum of developmental syndromes that affect these anterior segment tissues. ASD conditions arise as a result of dominantly inherited genetic mutations and result in both ocular-specific and systemic forms of dysgenesis that are best exemplified by aniridia and Axenfeld-Rieger syndrome, respectively. Extensive clinical overlap in disease presentation amongst ASD syndromes creates challenges for correct diagnosis and classification. The use of animal models has therefore proved to be a robust approach for unravelling this complex genotypic and phenotypic heterogeneity. However, despite these successes, it is clear that additional genes that underlie several ASD syndromes remain unidentified. Here, we report the characterisation of a novel mouse model of ASD. Conditional deletion of Tsc1 during eye development leads to a premature upregulation of mTORC1 activity within the ciliary margin, periocular mesenchyme and lens epithelium. This aberrant mTORC1 signalling within the ciliary margin in particular leads to a reduction in the number of cells that express Pax6, Bmp4 and Msx1 Sustained mTORC1 signalling also induces a decrease in ciliary margin progenitor cell proliferation and a consequent failure of ciliary body and iris development in postnatal animals. Our study therefore identifies Tsc1 as a novel candidate ASD gene. Furthermore, the Tsc1-ablated mouse model also provides a valuable resource for future studies concerning the molecular mechanisms underlying ASD and acts as a platform for evaluating therapeutic approaches for the treatment of visual disorders.
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7. Kaartinen M, Puura K, Helminen M, Salmelin R, Pelkonen E, Juujarvi P. {{Erratum to: Reactive aggression among children with and without autism spectrum disorder}}. {J Autism Dev Disord};2017 (Mar 03)
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8. Lim KK, Chong WH. {{Moderating Effect of Child’s Autism Spectrum Disorder (ASD) Diagnosis on Benefit Finding and Negative Affect of Parents}}. {Am J Orthopsychiatry};2017 (Mar 02)
Substantial empirical evidence has highlighted the psychological stress and negative well-being of parents whose children are diagnosed with autism spectrum disorder (ASD). It also indicated a need for understanding the mechanisms through which parents come to successfully meet the challenges of caregiving for these children whose condition are often characterized by persistent behavioral, social, and communication problems. This study seeks to explore the relationships between benefit finding and parental well-being and aims to bridge the research gaps in 3 ways. First, it seeks to examine the nature of relationships between benefit finding and parent positive and negative affect among parents whose children have ASD or other special needs. Second, we posit that this relationship would be moderated by the presence of ASD in the child. Third, we hypothesize that this moderation may vary with the children’s age. Three hundred and 2 parents responded to a self-report questionnaire. Specifically, for parents of children who are non-ASD, higher levels of perceived benefit finding were found to be associated with lower levels of negative affect, and this holds for those with young children below 7 years of age. For parents having a child with ASD, perceiving high or low levels of benefit did not mitigate their negative feelings regardless of the child’s age. The latter findings on the moderating effect of ASD diagnosis were unexpected and inconsistent with current research indications. These were discussed in the light of the literature, with potential implications for future research and practice. (PsycINFO Database Record
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9. Mahic M, Mjaaland S, Bovelstad HM, Gunnes N, Susser E, Bresnahan M, Oyen AS, Levin B, Che X, Hirtz D, Reichborn-Kjennerud T, Schjolberg S, Roth C, Magnus P, Stoltenberg C, Suren P, Hornig M, Lipkin WI. {{Maternal Immunoreactivity to Herpes Simplex Virus 2 and Risk of Autism Spectrum Disorder in Male Offspring}}. {mSphere};2017 (Jan-Feb);2(1)
Maternal infections during pregnancy are associated with risk of neurodevelopmental disorders, including autism spectrum disorders (ASDs). Proposed pathogenetic mechanisms include fetal infection, placental inflammation, and maternal cytokines or antibodies that cross the placenta. The Autism Birth Cohort comprises mothers, fathers, and offspring recruited in Norway in 1999 to 2008. Through questionnaire screening, referrals, and linkages to a national patient registry, 442 mothers of children with ASD were identified, and 464 frequency-matched controls were selected. Immunoglobulin G (IgG) antibodies to Toxoplasma gondii, rubella virus, cytomegalovirus (CMV), herpes simplex virus 1 (HSV-1), and HSV-2 in plasma collected at midpregnancy and after delivery were measured by multiplexed immunoassays. High levels of HSV-2 IgG antibodies in maternal midpregnancy plasma were associated with increased risk of ASD in male offspring (an increase in HSV-2 IgG levels from 240 to 640 arbitrary units/ml was associated with an odds ratio of 2.07; 95% confidence interval, 1.06 to 4.06; P = 0.03) when adjusted for parity and child’s birth year. No association was found between ASD and the presence of IgG antibodies to Toxoplasma gondii, rubella virus, CMV, or HSV-1. Additional studies are needed to test for replicability of risk and specificity of the sex effect and to examine risk associated with other infections. IMPORTANCE The cause (or causes) of most cases of autism spectrum disorder is unknown. Evidence from epidemiological studies and work in animal models of neurodevelopmental disorders suggest that both genetic and environmental factors may be implicated. The latter include gestational infection and immune activation. In our cohort, high levels of antibodies to herpes simplex virus 2 at midpregnancy were associated with an elevated risk of autism spectrum disorder in male offspring. These findings provide support for the hypothesis that gestational infection may contribute to the pathogenesis of autism spectrum disorder and have the potential to drive new efforts to monitor women more closely for cryptic gestational infection and to implement suppressive therapy during pregnancy.
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10. McDaniel J, Yoder P, Watson LR. {{A Path Model of Expressive Vocabulary Skills in Initially Preverbal Preschool Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2017 (Mar 01)
We examined direct and indirect paths involving receptive vocabulary and diversity of key consonants used in communication (DKCC) to improve understanding of why previously identified value-added predictors are associated with later expressive vocabulary for initially preverbal children with autism spectrum disorder (ASD; n = 87). Intentional communication, DKCC, and parent linguistic responses accounted for unique variance in later expressive vocabulary when controlling for mid-point receptive vocabulary, but responding to joint attention did not. We did not confirm any indirect paths through mid-point receptive vocabulary. DKCC mediated the association between intentional communication and expressive vocabulary. Further research is needed to replicate the findings, test potentially causal relations, and provide a specific sequence of intervention targets for preverbal children with ASD.
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11. Paquet A, Golse B, Girard M, Olliac B, Vaivre-Douret L. {{Laterality and Lateralization in Autism Spectrum Disorder, Using a Standardized Neuro-Psychomotor Assessment}}. {Dev Neuropsychol};2017 (Jan);42(1):39-54.
A detailed assessment of laterality in children with Autism Spectrum Disorder (ASD) was realized, including handedness and other measures (muscle tone, manual performance, dominant eye), using a standardized battery for the developmental assessment of neuro-psychomotor functions. The results of the laterality tests relating to cerebral hemisphere organization (spontaneous gestural laterality and tonic laterality) were different in ASD children, and indicate that the cerebral organization could be disrupted. These assessments, added to the observations of usual laterality most often reported in the literature, provide better understanding of the developmental organization from the pathophysiological point of view in children with ASD.
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12. Saskin A, Fulginiti V, Birch AH, Trakadis Y. {{Prevalence of four Mendelian disorders associated with autism in 2392 affected families}}. {J Hum Genet};2017 (Mar 02)
Autism spectrum disorder (ASD) is a neurobehavioral disorder with a heterogeneous genetic etiology. Based on the literature, several single-gene disorders, including Rett syndrome, Smith-Lemli-Opitz syndrome, PTEN hamartoma tumor syndrome and tuberous sclerosis, are associated with a high prevalence of ASD. We estimated the prevalence of these four conditions in a large cohort of patients using whole-exome sequencing data from 2392 families (1800 quads and 592 trios) with ASD from the National Database for Autism Research. Seven patients carried a pathogenic or likely pathogenic variant in either TSC1, TSC2, PTEN, DHCR7 or MECP2, with 6 out of 7 reportable variants occurring in PTEN (1 in 399).Journal of Human Genetics advance online publication, 2 March 2017; doi:10.1038/jhg.2017.16.
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13. Shawahna R, Fahed B, Qadri D, Sharawi L, Soroghli M, Dweik M. {{Awareness and Knowledge of Autism Spectrum Disorders Among Pharmacists: A Cross-Sectional Study in Palestinian Pharmacy Practice}}. {J Autism Dev Disord};2017 (Mar 01)
Pharmacists are trusted and easily accessible healthcare providers. We assessed awareness and knowledge of symptoms, etiology, and treatment of autism spectrum disorders (ASDs) among pharmacists practicing in Palestine. The pharmacists reported low familiarity with ASDs. The median score on the 12-item knowledge section was 50.0% with an interquartile range of 16.7%. Having course(s) or lecture(s) on ASDs during pharmacy degree program was significantly associated with familiarity (p value <0.001), knowledge (p value <0.001), and confidence (p value <0.05) scores. Nearly 62% of the pharmacists reported as not feeling confident enough in their ability to counsel parents about medications used for their children with ASDs and their side effects. This study revealed gaps in awareness and knowledge of ASDs among pharmacists. Lien vers le texte intégral (Open Access ou abonnement)
14. Shou XJ, Xu XJ, Zeng XZ, Liu Y, Yuan HS, Xing Y, Jia MX, Wei QY, Han SP, Zhang R, Han JS. {{A Volumetric and Functional Connectivity MRI Study of Brain Arginine-Vasopressin Pathways in Autistic Children}}. {Neurosci Bull};2017 (Mar 03)
Dysfunction of brain-derived arginine-vasopressin (AVP) systems may be involved in the etiology of autism spectrum disorder (ASD). Certain regions such as the hypothalamus, amygdala, and hippocampus are known to contain either AVP neurons or terminals and may play an important role in regulating complex social behaviors. The present study was designed to investigate the concomitant changes in autistic behaviors, circulating AVP levels, and the structure and functional connectivity (FC) of specific brain regions in autistic children compared with typically developing children (TDC) aged from 3 to 5 years. The results showed: (1) children with ASD had a significantly increased volume in the left amygdala and left hippocampus, and a significantly decreased volume in the bilateral hypothalamus compared to TDC, and these were positively correlated with plasma AVP level. (2) Autistic children had a negative FC between the left amygdala and the bilateral supramarginal gyri compared to TDC. The degree of the negative FC between amygdala and supramarginal gyrus was associated with a higher score on the clinical autism behavior checklist. (3) The degree of negative FC between left amygdala and left supramarginal gyrus was associated with a lowering of the circulating AVP concentration in boys with ASD. (4) Autistic children showed a higher FC between left hippocampus and right subcortical area compared to TDC. (5) The circulating AVP was negatively correlated with the visual and listening response score of the childhood autism rating scale. These results strongly suggest that changes in structure and FC in brain regions containing AVP may be involved in the etiology of autism.
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15. Stickley A, Tachibana Y, Hashimoto K, Haraguchi H, Miyake A, Morokuma S, Nitta H, Oda M, Ohya Y, Senju A, Takahashi H, Yamagata T, Kamio Y. {{Assessment of Autistic Traits in Children Aged 2 to 4(1/2) Years With the Preschool Version of the Social Responsiveness Scale (SRS-P): Findings from Japan}}. {Autism Res};2017 (Mar 03)
The recent development and use of autism measures for the general population has led to a growing body of evidence which suggests that autistic traits are distributed along a continuum. However, as most existing autism measures were designed for use in children older than age 4, to date, little is known about the autistic continuum in children younger than age 4. As autistic symptoms are evident in the first few years, to address this research gap, the current study tested the preschool version of the Social Responsiveness Scale (SRS-P) in children aged 2 to 4(1/2) years in clinical (N = 74, average age 40 months, 26-51 months) and community settings (N = 357, average age 39 months, 25-50 months) in Japan. Using information obtained from different raters (mothers, other caregivers, and teachers) it was found that the scale demonstrated a good degree of internal consistency, inter-rater reliability and test-retest reliability, and a satisfactory degree of convergent validity for the clinical sample when compared with scores from diagnostic « gold standard » autism measures. Receiver operating characteristic analyses and the group comparisons also showed that the SRS-P total score discriminated well between children with autism spectrum disorder (ASD) and those without ASD. Importantly, this scale could identify autistic symptoms or traits distributed continually across the child population at this age irrespective of the presence of an ASD diagnosis. These findings suggest that the SRS-P might be a sensitive instrument for case identification including subthreshold ASD, as well as a potentially useful research tool for exploring ASD endophenotypes. Autism Res 2016. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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16. Wang M, Li H, Takumi T, Qiu Z, Xu X, Yu X, Bian WJ. {{Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism}}. {Neurosci Bull};2017 (Mar 03)
Autism spectrum disorder (ASD) encompasses a complex set of developmental neurological disorders, characterized by deficits in social communication and excessive repetitive behaviors. In recent years, ASD is increasingly being considered as a disease of the synapse. One main type of genetic aberration leading to ASD is gene duplication, and several mouse models have been generated mimicking these mutations. Here, we studied the effects of MECP2 duplication and human chromosome 15q11-13 duplication on synaptic development and neural circuit wiring in the mouse sensory cortices. We showed that mice carrying MECP2 duplication had specific defects in spine pruning, while the 15q11-13 duplication mouse model had impaired spine formation. Our results demonstrate that spine pathology varies significantly between autism models and that distinct aspects of neural circuit development may be targeted in different ASD mutations. Our results further underscore the importance of gene dosage in normal development and function of the brain.
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17. Zhang J, Gambin T, Yuan B, Szafranski P, Rosenfeld JA, Balwi MA, Alswaid A, Al-Gazali L, Shamsi AM, Komara M, Ali BR, Roeder E, McAuley L, Roy DS, Manchester DK, Magoulas P, King LE, Hannig V, Bonneau D, Denomme-Pichon AS, Charif M, Besnard T, Bezieau S, Cogne B, Andrieux J, Zhu W, He W, Vetrini F, Ward PA, Cheung SW, Bi W, Eng CM, Lupski JR, Yang Y, Patel A, Lalani SR, Xia F, Stankiewicz P. {{Haploinsufficiency of the E3 ubiquitin-protein ligase gene TRIP12 causes intellectual disability with or without autism spectrum disorders, speech delay, and dysmorphic features}}. {Hum Genet};2017 (Mar 01)
Impairment of ubiquitin-proteasome system activity involving ubiquitin ligase genes UBE3A, UBE3B, and HUWE1 and deubiquitinating enzyme genes USP7 and USP9X has been reported in patients with neurodevelopmental delays. To date, only a handful of single-nucleotide variants (SNVs) and copy-number variants (CNVs) involving TRIP12, encoding a member of the HECT domain E3 ubiquitin ligases family on chromosome 2q36.3 have been reported. Using chromosomal microarray analysis and whole-exome sequencing (WES), we have identified, respectively, five deletion CNVs and four inactivating SNVs (two frameshifts, one missense, and one splicing) in TRIP12. Seven of these variants were found to be de novo; parental studies could not be completed in two families. Quantitative PCR analyses of the splicing mutation showed a dramatically decreased level of TRIP12 mRNA in the proband compared to the family controls, indicating a loss-of-function mechanism. The shared clinical features include intellectual disability with or without autistic spectrum disorders, speech delay, and facial dysmorphism. Our findings demonstrate that E3 ubiquitin ligase TRIP12 plays an important role in nervous system development and function. The nine presented pathogenic variants further document that TRIP12 haploinsufficiency causes a childhood-onset neurodevelopmental disorder. Finally, our data enable expansion of the phenotypic spectrum of ubiquitin-proteasome dependent disorders.
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18. Zhou B, Zhou H, Wu L, Zou X, Luo X, Fombonne E, Wang Y, Yan W, Xu X. {{Assessing the Accuracy of the Modified Chinese Autism Spectrum Rating Scale and Social Responsiveness Scale for Screening Autism Spectrum Disorder in Chinese Children}}. {Neurosci Bull};2017 (Mar 03)
The reported prevalence of autism spectrum disorder (ASD) has been increasing rapidly in many parts of the world. However, data on its prevalence in China are largely missing. Here, we assessed the suitability of the modified Chinese version of a newly-developed ASD screening tool, the Modified Chinese Autism Spectrum Rating Scales (MC-ASRS) in screening for ASD in Chinese children aged 6-12 years, through comparison with the Social Responsiveness Scale (SRS) that has been widely used for ASD screening. We recruited the parents/caregivers of 1588 typically-developing children and 190 children with ASD aged 6-12 years to complete the MC-ASRS and SRS, and evaluated the validity of both scales in discriminating children with ASD from those developing typically. The results showed that MC-ASRS performed as well as SRS in sensitivity, specificity, and area-under-the-curve (both >0.95) in receiver operating characteristic analysis, with a fair false-negative rate. These results suggest that MC-ASRS is a promising tool for screening for children with ASD in the general Chinese population.
