1. Brenner RA, Taneja GS, Schroeder TJ, Trumble AC, Moyer PM, Louis GM. {{Unintentional injuries among youth with developmental disabilities in the United States, 2006-2007}}. {Int J Inj Contr Saf Promot}. 2012.
We examined unintentional injury among youth with and without developmental disabilities. Our nationally representative sample included 6369 injured youth, aged 0-17 years, who were seen in one of the 63 US hospital emergency rooms that participated in the National Electronic Injury Surveillance System – All Injury Program (NEISS-AIP) in 2006-2007. Parents or guardians of injured youth were interviewed by telephone after the hospital visit to ascertain disability status. Denominator data were obtained from the National Health Interview Survey. Leading causes of injury were comparable for youth with and without disability. Injury rates (per 100 youth per year) were also comparable [10.4; 95% confidence interval (CI) 7.8, 13.0 and 10.5; 95% CI 8.2, 12.9, for youth with and without disability, respectively]. When examined by specific disability, the rate ratio for youth with learning disabilities versus youth without learning disability was 1.57 (95% CI 1.04, 2.10), which may represent a subgroup for targeted interventions.
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2. Buon M, Dupoux E, Jacob P, Chaste P, Leboyer M, Zalla T. {{The Role of Causal and Intentional Judgments in Moral Reasoning in Individuals with High Functioning Autism}}. {J Autism Dev Disord}. 2012.
In the present study, we investigated the ability to assign moral responsibility and punishment in adults with high functioning autism or Asperger Syndrome (HFA/AS), using non-verbal cartoons depicting an aggression, an accidental harm or a mere coincidence. Participants were asked to evaluate the agent’s causal and intentional roles, his responsibility and the punishment he deserves for his action. Adults with HFA/AS did not differ in judgments of suffering and causality from adults with typical development. However, subtle difficulties with judgments of intentional action and moral judgments were observed in participants with HFA/AS. These results are discussed in the light of emerging studies that deal with integrity of moral reasoning in individuals with autism spectrum disorders.
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3. De Felice C, Signorini C, Leoncini S, Pecorelli A, Durand T, Valacchi G, Ciccoli L, Hayek J. {{The role of oxidative stress in Rett syndrome: an overview}}. {Ann N Y Acad Sci}. 2012; 1259(1): 121-35.
The main cause of Rett syndrome (RTT), a pervasive development disorder almost exclusively affecting females, is a mutation in the methyl-CpG binding protein 2 (MeCP2) gene. To date, no cure for RTT exists, although disease reversibility has been demonstrated in animal models. Emerging evidence from our and other laboratories indicates a potential role of oxidative stress (OS) in RTT. This review examines the current state of the knowledge on the role of OS in explaining the natural history, genotype-phenotype correlation, and clinical heterogeneity of the human disease. Biochemical evidence of OS appears to be related to neurological symptom severity, mutation type, and clinical presentation. These findings pave the way for potential new genetic downstream therapeutic strategies aimed at improving patient quality of life. Further efforts in the near future are needed for investigating the yet unexplored « black box » between the MeCP2 gene mutation and subsequent OS derangement.
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4. Lewis S. {{Neurological disorders: SHANK2 misbehaves in autism}}. {Nat Rev Neurosci}. 2012.
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5. Needleman LA, McAllister AK. {{The major histocompatibility complex and autism spectrum disorder}}. {Dev Neurobiol}. 2012.
Autism spectrum disorder (ASD) is a complex disorder that appears to be caused by interactions between genetic changes and environmental insults during early development. A wide range of factors have been linked to the onset of ASD, but recently both genetic associations and environmental factors point to a central role for immune-related genes and immune responses to environmental stimuli. Specifically, many of the proteins encoded by the major histocompatibility complex (MHC) play a vital role in the formation, refinement, maintenance, and plasticity of the brain. Manipulations of levels of MHC molecules have illustrated how disrupted MHC signaling can significantly alter brain connectivity and function. Thus, an emerging hypothesis in our field is that disruptions in MHC expression in the developing brain caused by mutations and/or immune dysregulation may contribute to the altered brain connectivity and function characteristic of ASD. This review provides an overview of the structure and function of the three classes of MHC molecules in the immune system, healthy brain, and their possible involvement in ASD. (c) 2012 Wiley Periodicals, Inc. Develop Neurobiol, 2012.
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6. Pfeifer JH, Merchant JS, Colich NL, Hernandez LM, Rudie JD, Dapretto M. {{Neural and Behavioral Responses During Self-Evaluative Processes Differ in Youth With and Without Autism}}. {J Autism Dev Disord}. 2012.
This fMRI study investigated neural responses while making appraisals of self and other, across the social and academic domains, in children and adolescents with and without autism spectrum disorders (ASD). Compared to neurotypical youth, those with ASD exhibited hypoactivation of ventromedial prefrontal cortex during self-appraisals. Responses in middle cingulate cortex (MCC) and anterior insula (AI) also distinguished between groups. Stronger activity in MCC and AI during self-appraisals was associated with better social functioning in the ASD group. Although self-appraisals were significantly more positive in the neurotypical group, positivity was unrelated to brain activity in these regions. Together, these results suggest that multiple brain regions support making self-appraisals in neurotypical development, and function atypically in youth with ASD.
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7. Takeda A. {{[Parkinson’s disease with dementia (PDD)]}}. {Nihon Rinsho}. 2011; 69 Suppl 10(Pt 2): 350-5.
8. Tillett T. {{A Sensitive Approach to Studying ASDs: Teasing Out Relationships between Autism and Maternal Smoking}}. {Environ Health Perspect}. 2012; 120(7): a285.
