1. Besag FM. {{The relationship between epilepsy and autism: a continuing debate}}. {Acta Paediatr};2009 (Apr);98(4):618-620.
2. Hoffman L. {{Asperger’s syndrome and Autistic disorder: clearly differentiating the diagnostic criteria}}. {Am J Psychiatry};2009 (Feb);166(2):235; author reply 235-236.
3. Kanne SM, Abbacchi AM, Constantino JN. {{Multi-informant ratings of psychiatric symptom severity in children with autism spectrum disorders: the importance of environmental context}}. {J Autism Dev Disord};2009 (Jun);39(6):856-864.
The present study examines co-occurring psychiatric syndromes in a well-characterized sample of youths with autism spectrum disorders (ASD; n = 177) and their siblings (n = 148), reported independently by parents and teachers. In ASD, parents reported substantial comorbidity with affective (26%), anxiety (25%), attentional (25%), conduct (16%), oppositional (15%), and somatic problems (6%). Teachers reported a much lower prevalence. Autistic severity scores for children with ASD exhibited moderate correlations with general psychopathology within- but not across-informants, whereas, sibling correlations were significant both within- and across-informants. Results support the role of environmental context in psychiatric symptom expression in children affected by autism and suggest that informant discrepancies may more provide critical cues for these children via specific environmental modifications.
4. Ming X, Johnson WG, Stenroos ES, Mars A, Lambert GH, Buyske S. {{Genetic variant of glutathione peroxidase 1 in autism}}. {Brain Dev} (Feb);32(2):105-109.
Genetic factors can contribute to autistic disorder (AD). Abnormal genes of oxidative stress pathways and increased oxidative stress have been reported in autism spectrum disorders. Polymorphisms of genes involved in glutathione metabolism, e.g. GSTP1 and GSTM1 are reportedly associated with autistic disorder. We investigated a GCG repeat polymorphism of a human glutathione peroxidase (GPX1) polyalanine repeat (ALA5, ALA6 and ALA7) in 103 trios of AD (probands and parents) using the transmission disequilibrium test. Significant transmission disequilibrium (p=0.044) was found in the overall transmission of the three alleles. The ALA6 allele was under transmitted (p=0.017). These results suggest that possessing this ALA6 allele may be protective for AD. Future study of interaction of the GPX1 GCG repeat and other gene polymorphisms such as the MnSOD ALA16 or the GPX1 Pro198Leu polymorphism in this cohort of AD families may shed light in whether the combination of the ALA6 allele with another polymorphism of antioxidant allele contributes to the increased oxidative stress in autism.
5. Nakashima N, Yamagata T, Mori M, Kuwajima M, Suwa K, Momoi MY. {{Expression analysis and mutation detection of DLX5 and DLX6 in autism}}. {Brain Dev} (Feb);32(2):98-104.
Linkage analysis has reported the chromosomal region 7q21 to be related with autism. This region contains an imprinting region with MECP2-binding sites, and DLX5 is reported to be modulated by MECP2. DLX5 and adjacent DLX6 are homeobox genes working in neurogenesis. From these points, DLX5 and DLX6 are candidate genes for autism. Therefore, we analyzed the expression of DLX5 and DLX6, and also PEG10 as a control in the lymphoblasts of autistic spectrum disorder (ASD) patients by real-time PCR to identify potential abnormality of expression. And we also analyzed DLX5 and DLX6 on ASD patients for mutation by direct sequence. The expression level of DLX5 was not different between ASD and controls but was higher in four ASD patients compared to controls. Clinical features of these four patients were variable. DLX5 expression was biallelic in two ASD patients and two controls, indicating that DLX5 was not imprinted. There was no mutation in DLX5 in ASD. Although DLX5 was not likely to play major role in ASD, genes relating to DLX5 expression and downstream of DLX5 are considered to be candidate genes for some of the ASD patients. In DLX6, we detected a G656A base change (R219H) in two ASD patients who were male siblings. DLX6 may contribute to the pathogenesis of ASD.
6. Stichter JP, Randolph JK, Kay D, Gage N. {{The use of structural analysis to develop antecedent-based interventions for students with autism}}. {J Autism Dev Disord};2009 (Jun);39(6):883-896.
Evidence continues to maintain that the use of antecedent variables (i.e., instructional practices, and environmental characteristics) increase prosocial and adaptive behaviors of students with disabilities (e.g., Kern et al. in J Appl Behav Anal 27(1):7-19, 1994; Stichter et al. in Behav Disord 30:401-418, 2005). This study extends the literature by systematically utilizing practitioner-implemented structural analyzes within school settings to determine antecedent variables affecting the prosocial behavior of students with autism. Optimal antecedents were combined into intervention packages and assessed utilizing a multiple baseline design across settings. All three students demonstrated improvement across all three settings. Rates of engagement and social interaction were obtained from classroom peers to serve as benchmark data. Findings indicate that practitioners can implement structural analyzes and design corresponding interventions for students with ASD within educational settings.
