1. Gantman A, Kapp SK, Orenski K, Laugeson EA. {{Social Skills Training for Young Adults with High-Functioning Autism Spectrum Disorders: A Randomized Controlled Pilot Study}}. J Autism Dev Disord. 2011.
Despite the psychosocial difficulties common among young adults with autism spectrum disorders (ASD), little to no evidence-based social skills interventions exist for this population. Using a randomized controlled trial (RCT) design, the current study tested the effectiveness of an evidence-based, caregiver-assisted social skills intervention known as PEERS for Young Adults with high-functioning young adults with ASD (ages 18-23) using self- and caregiver-report measures. Results revealed that treated young adults reported significantly less loneliness and improved social skills knowledge, while caregivers reported significant improvements in young adults’ overall social skills, social responsiveness, empathy, and frequency of get-togethers. Results support the effectiveness of using this caregiver-assisted, manualized intervention for young adults with ASD.
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2. Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela-Olech H, Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M. {{A potential pathogenic role of oxalate in autism}}. Eur J Paediatr Neurol. 2011.
BACKGROUND: Although autistic spectrum disorders (ASD) are a strongly genetic condition certain metabolic disturbances may contribute to clinical features. Metabolism of oxalate in children with ASD has not yet been studied. AIM: The objective was to determine oxalate levels in plasma and urine in autistic children in relation to other urinary parameters. METHOD: In this cross-sectional study, plasma oxalate (using enzymatic method with oxalate oxidase) and spontaneous urinary calcium oxalate (CaOx) crystallization (based on the Bonn-Risk-Index, BRI) were determined in 36 children and adolescents with ASD (26 boys, 10 girls) aged 2-18 years and compared with 60 healthy non-autistic children matched by age, gender and anthropometric traits. RESULTS: Children with ASD demonstrated 3-fold greater plasma oxalate levels [5.60 (5th-95th percentile: 3.47-7.51)] compared with reference [(1.84 (5th-95th percentile: 0.50-4.70) mumol/L (p < 0.05)] and 2.5-fold greater urinary oxalate concentrations (p < 0.05). No differences between the two groups were found in urinary pH, citraturia, calciuria or adjusted CaOx crystallization rates based on BRI. Despite significant hyperoxaluria no evidence of kidney stone disease or lithogenic risk was observed in these individuals. CONCLUSIONS: Hyperoxalemia and hyperoxaluria may be involved in the pathogenesis of ASD in children. Whether this is a result of impaired renal excretion or an extensive intestinal absorption, or both, or whether Ox may cross the blood brain barrier and disturb CNS function in the autistic children remains unclear. This appears to be the first report of plasma and urinary oxalate in childhood autism.
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3. Rousseau F, Labelle Y, Bussieres J, Lindsay C. {{The fragile x mental retardation syndrome 20 years after the FMR1 gene discovery: an expanding universe of knowledge}}. Clin Biochem Rev. 2011; 32(3): 135-62.
The fragile X mental retardation (FXMR) syndrome is one of the most frequent causes of mental retardation. Affected individuals display a wide range of additional characteristic features including behavioural and physical phenotypes, and the extent to which individuals are affected is highly variable. For these reasons, elucidation of the pathophysiology of this disease has been an important challenge to the scientific community. 1991 marks the year of the discovery of both the FMR1 gene mutations involved in this disease, and of their dynamic nature. Although a mouse model for the disease has been available for 16 years and extensive research has been performed on the FMR1 protein (FMRP), we still understand little about how the disease develops, and no treatment has yet been shown to be effective. In this review, we summarise current knowledge on FXMR with an emphasis on the technical challenges of molecular diagnostics, on its prevalence and dynamics among populations, and on the potential of screening for FMR1 mutations.
4. Schiff M, Benoist JF, Aissaoui S, Boepsflug-Tanguy O, Mouren MC, de Baulny HO, Delorme R. {{Correction: should metabolic diseases be systematically screened in nonsyndromic autism spectrum disorders?}}. PLoS One. 2011; 6(8).
[This corrects the article on p. e21932 in vol. 6.].
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5. Young GS, Rogers SJ, Hutman T, Rozga A, Sigman M, Ozonoff S. {{Imitation from 12 to 24 months in autism and typical development: A longitudinal Rasch analysis}}. Dev Psychol. 2011.
The development of imitation during the second year of life plays an important role in domains of sociocognitive development such as language and social learning. Deficits in imitation ability in persons with autism spectrum disorder (ASD) from toddlerhood into adulthood have also been repeatedly documented, raising the possibility that early disruptions in imitation contribute to the onset of ASD and the deficits in language and social interaction that define the disorder. This study prospectively examined the development of imitation between 12 and 24 months of age in 154 infants at familial risk for ASD and 78 typically developing infants who were all later assessed at 36 months for ASD or other developmental delays. The study established a developmental measure of imitation ability and examined group differences over time, using an analytic Rasch measurement model. Results revealed a unidimensional latent construct of imitation and verified a reliable sequence of imitation skills that was invariant over time for all outcome groups. Results also showed that all groups displayed similar significant linear increases in imitation ability between 12 and 24 months and that these increases were related to individual growth in both expressive language and ratings of social engagement but not in fine motor development. The group of children who developed ASD by age 3 years exhibited delayed imitation development compared with the low-risk typical outcome group across all time-points, but were indistinguishable from other high-risk infants who showed other cognitive delays not related to ASD. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
