1. Carbone PS, Murphy NA, Norlin C, Azor V, Sheng X, Young PC. {{Parent and Pediatrician Perspectives Regarding the Primary Care of Children with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2012.
Parents of children with autism spectrum disorders (ASD) (n = 144) and primary care providers (PCPs) (n = 144) completed similar surveys assessing the ability of the PCP to address ASD-specific needs. Parents also rated their PCP’s ability to deliver family-centered care. A majority of parents rated their PCP’s ability as « not good » in addressing 14 of 17 ASD-specific needs, while a majority of PCPs rated themselves as « good » in addressing 10 of 17 areas. On 7 of 17 items, parents rated their PCPs lower than PCPs rated themselves. Parents who reported receiving family-centered care were more likely to rate the PCP’s ability to meet ASD specific needs as « good ». Both parents and PCPs identified areas for improvement in caring for children with ASD.
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2. Fabricius T. {{On neural systems for speech and song in autism}}. {Brain}. 2012.
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3. Georgiades S, Szatmari P, Zwaigenbaum L, Bryson S, Brian J, Roberts W, Smith I, Vaillancourt T, Roncadin C, Garon N. {{A Prospective Study of Autistic-Like Traits in Unaffected Siblings of Probands With Autism Spectrum Disorder}}. {Arch Gen Psychiatry}. 2012: 1-7.
CONTEXT The presence of autistic-like traits in relatives of individuals with autism spectrum disorder (ASD) is well recognized, but, to our knowledge, the emergence of these traits early in development has not been studied. OBJECTIVE To prospectively investigate the emergence of autistic-like traits in unaffected (no ASD diagnosis) infant siblings of probands diagnosed as having ASD. DESIGN Two groups of children unaffected with ASD were assessed prospectively-siblings of probands diagnosed as having ASD (high risk [HR]) and control subjects with no family history of ASD (low risk [LR]). Scores on a measure of autistic-like traits at 12 months of age were used in a cluster analysis of the entire sample. SETTING A prospective study of infant siblings of probands with ASD from 3 diagnostic centers in Canada. PARTICIPANTS The study included 170 HR and 90 LR children, none of whom was diagnosed as having ASD at age 3 years. MAIN OUTCOME MEASURES The Autism Observation Scale for Infants was used to measure autistic-like traits and derive clusters at 12 months of age. Clusters were compared on ASD symptoms, cognitive abilities, and social-emotional difficulties at age 3 years. RESULTS Two clusters were identified. Cluster 1 (n = 37; 14.2% of total sample) had significantly higher levels of autistic-like traits compared with cluster 2. Within cluster 1, 33 children came from the siblings (19.4% of HR group) and only 4 came from the control subjects (4.5% of LR group). At age 3 years, children from cluster 1 had more social-communication impairment (effect size > 0.70; P < .001), lower cognitive abilities (effect size = -0.59; P < .005), and more internalizing problems (effect size = 0.55; P = .01). Compared with control subjects, HR siblings had a relative risk of 4.3 (95% CI,1.6-11.9) for membership in cluster 1. CONCLUSIONS Study findings suggest the emergence of autistic-like traits resembling a broader autism phenotype by 12 months of age in approximately 19% of HR siblings who did not meet ASD diagnostic criteria at age 3 years.
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4. Leventhal-Belfer L. {{Potential Ramifications of DSM-5 Classification of Autistic Disorders: Comments from a Clinician’s Perspective}}. {J Autism Dev Disord}. 2012.
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5. Sterzing PR, Shattuck PT, Narendorf SC, Wagner M, Cooper BP. {{Bullying Involvement and Autism Spectrum Disorders: Prevalence and Correlates of Bullying Involvement Among Adolescents With an Autism Spectrum Disorder}}. {Arch Pediatr Adolesc Med}. 2012: 1-7.
OBJECTIVES To produce nationally representative estimates for rates of bullying involvement among adolescents with an autism spectrum disorder (ASD), to compare population estimates with adolescents who have other developmental disabilities, and to identify social ecological correlates of bullying involvement. DESIGN Nationally representative surveys from 2001. SETTING United States. PARTICIPANTS Parents of adolescents with an ASD, principals of the schools they attended, and staff members most familiar with their school programs. MAIN EXPOSURE Autism spectrum disorders. MAIN OUTCOME MEASURES Parent report of victimization, perpetration, and victimization/perpetration within the past school year. RESULTS The prevalence rates of bullying involvement for adolescents with an ASD were 46.3% for victimization, 14.8% for perpetration, and 8.9% for victimization/perpetration. Victimization was related to having a non-Hispanic ethnicity, attention-deficit/hyperactivity disorder, lower social skills, some form of conversational ability, and more classes in general education. Correlates of perpetration included being white, having attention-deficit/hyperactivity disorder, and getting together with friends at least once a week. Victimization/perpetration was associated with being white non-Hispanic, having attention-deficit/hyperactivity disorder, and getting together with friends at least once a week. CONCLUSIONS School-based bullying interventions need to target the core deficits of ASD (conversational ability and social skills) and comorbid conditions (eg, attention-deficit/hyperactivity disorder). Future bullying interventions also need to address the higher rates of victimization that occur in general education settings by increasing social integration into protective peer groups and increasing the empathy and social skills of typically developing students toward their peers with an ASD.
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6. Ziats MN, Rennert OM. {{Aberrant Expression of Long Noncoding RNAs in Autistic Brain}}. {J Mol Neurosci}. 2012.
The autism spectrum disorders (ASD) have a significant hereditary component, but the implicated genetic loci are heterogeneous and complex. Consequently, there is a gap in understanding how diverse genomic aberrations all result in one clinical ASD phenotype. Gene expression studies from autism brain tissue have demonstrated that aberrantly expressed protein-coding genes may converge onto common molecular pathways, potentially reconciling the strong heritability and shared clinical phenotypes with the genomic heterogeneity of the disorder. However, the regulation of gene expression is extremely complex and governed by many mechanisms, including noncoding RNAs. Yet no study in ASD brain tissue has assessed for changes in regulatory long noncoding RNAs (lncRNAs), which represent a large proportion of the human transcriptome, and actively modulate mRNA expression. To assess if aberrant expression of lncRNAs may play a role in the molecular pathogenesis of ASD, we profiled over 33,000 annotated lncRNAs and 30,000 mRNA transcripts from postmortem brain tissue of autistic and control prefrontal cortex and cerebellum by microarray. We detected over 200 differentially expressed lncRNAs in ASD, which were enriched for genomic regions containing genes related to neurodevelopment and psychiatric disease. Additionally, comparison of differences in expression of mRNAs between prefrontal cortex and cerebellum within individual donors showed ASD brains had more transcriptional homogeneity. Moreover, this was also true of the lncRNA transcriptome. Our results suggest that further investigation of lncRNA expression in autistic brain may further elucidate the molecular pathogenesis of this disorder.
