1. Coury DL. {{Review: little evidence of clear benefit for most medical treatments for children with autism spectrum disorders}}. {Evid Based Ment Health};2011 (Sep 30)
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2. Gadow KD, Guttmann-Steinmetz S, Rieffe C, Devincent CJ. {{Depression Symptoms in Boys with Autism Spectrum Disorder and Comparison Samples}}. {J Autism Dev Disord};2011 (Sep 30)
This study compares severity of specific depression symptoms in boys with autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), or chronic multiple tic disorder (CMTD) and typically developing boys (Controls). Children were evaluated with parent and teacher versions of the Child Symptom Inventory-4 (CSI-4) and a demographic questionnaire. Mothers’ and teachers’ ratings generally indicated the most severe symptoms in boys with ASD +/- ADHD. Associations of depression with ASD severity and IQ varied considerably for specific symptoms of depression, ASD functional domain, and informant. Findings provide additional support for the differential influence of neurobehavioral syndromes on co-occurring symptom severity and illustrate how more fine-grained analyses of clinical phenotypes may contribute to a better understanding of etiology and current nosology.
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3. Lord C. {{Unweaving the autism spectrum}}. {Cell};2011 (Sep 30);147(1):24-25.
Although genes associated with human autism spectrum disorders have been identified, bridging the gap between genetics and the patchwork of behavioral deficits associated with the disease remains an enormous challenge. Penagarikano et al. (2011) now show that mice lacking CNTNAP2, a gene that causes a rare form of epilepsy associated with autistic features and language impairment, display similar phenotypes to their human counterparts, raising hopes that such models may speed the identification of neuronal circuitries underlying the core features of autism.
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4. Patricia H. {{Review: possible benefits from early intensive behavioural and developmental interventions in children with autism spectrum disorders, but more research needed}}. {Evid Based Ment Health};2011 (Sep 30)
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5. Penagarikano O, Abrahams BS, Herman EI, Winden KD, Gdalyahu A, Dong H, Sonnenblick LI, Gruver R, Almajano J, Bragin A, Golshani P, Trachtenberg JT, Peles E, Geschwind DH. {{Absence of CNTNAP2 Leads to Epilepsy, Neuronal Migration Abnormalities, and Core Autism-Related Deficits}}. {Cell};2011 (Sep 30);147(1):235-246.
Although many genes predisposing to autism spectrum disorders (ASD) have been identified, the biological mechanism(s) remain unclear. Mouse models based on human disease-causing mutations provide the potential for understanding gene function and novel treatment development. Here, we characterize a mouse knockout of the Cntnap2 gene, which is strongly associated with ASD and allied neurodevelopmental disorders. Cntnap2(-/-) mice show deficits in the three core ASD behavioral domains, as well as hyperactivity and epileptic seizures, as have been reported in humans with CNTNAP2 mutations. Neuropathological and physiological analyses of these mice before the onset of seizures reveal neuronal migration abnormalities, reduced number of interneurons, and abnormal neuronal network activity. In addition, treatment with the FDA-approved drug risperidone ameliorates the targeted repetitive behaviors in the mutant mice. These data demonstrate a functional role for CNTNAP2 in brain development and provide a new tool for mechanistic and therapeutic research in ASD. PAPERFLICK:
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6. Sgado P, Dunleavy M, Genovesi S, Provenzano G, Bozzi Y. {{The role of GABAergic system in neurodevelopmental disorders: a focus on autism and epilepsy}}. {Int J Physiol Pathophysiol Pharmacol};2011 (Sep 30);3(3):223-235.
Autism spectrum disorders (ASD) and epilepsy are very common neurological disorders of childhood, with an estimated incidence of about 0.5 – 1 % in worldwide population. ASD and epilepsy are often associated, suggesting that common neurodevelopmental bases may exist for these two disorders. The neurodevelopmental bases of both ASD and epilepsy have been clearly showed by a number of genetic, neuroimaging and neuropathological studies. In recent years, dysfunction of inhibitory GABAergic circuits has been proposed as a cause for both disorders. Several studies performed on both animal models and postmortem human samples indicate that GABAergic neurons and circuits are altered in both ASD and epilepsy, suggesting that the excitation/inhibition imbalance resulting from neurodevelopmental defects in GABAergic circuitry might represent a common pathogenetic mechanism for these disorders. Here, we will review the most significant studies supporting this hypothesis.
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7. Shulman C, Guberman A, Shiling N, Bauminger N. {{Moral and Social Reasoning in Autism Spectrum Disorders}}. {J Autism Dev Disord};2011 (Sep 30)
This study compared moral and social reasoning in individuals with and without autism spectrum disorders (ASD). Ten familiar schoolyard transgressions were shown to 18 participants with and 18 participants without ASD. They judged the appropriateness of the behavior and explained their judgments. Analysis of the rationales revealed that participants with typical development used significantly more abstract rules than participants with ASD, who provided more nonspecific condemnations of the behaviors. Both groups judged social conventional transgressions to be more context-bound than moral transgressions, with this distinction more pronounced in typically developing individuals, who also provided significantly more examples of situations in which the depicted behaviors would be acceptable. The educational implications of these findings for individuals with ASD are discussed.
