1. Bhatara AK, Quintin EM, Heaton P, Fombonne E, Levitin DJ. {{The Effect of Music on Social Attribution in Adolescents with Autism Spectrum Disorders}}. {Child Neuropsychol};2009 (Jan 13):1-22.
High-functioning adolescents with ASD and matched controls were presented with animations that depicted varying levels of social interaction and were either accompanied by music or silent. Participants described the events of the animation, and we scored responses for intentionality, appropriateness, and length of description. Adolescents with ASD were less likely to make social attributions, especially for those animations with the most complex social interactions. When stimuli were accompanied by music, both groups were equally impaired in appropriateness and intentionality. We conclude that adolescents with ASD perceive and integrate musical soundtracks with visual displays equivalent to typically developing individuals.
2. Buttenschon HN, Lauritsen MB, El Daoud A, Hollegaard M, Jorgensen M, Tvedegaard K, Hougaard D, Borglum A, Thorsen P, Mors O. {{A population-based association study of glutamate decarboxylase 1 as a candidate gene for autism}}. {J Neural Transm};2009 (Mar);116(3):381-388.
Linkage studies, genome-wide scans and screening of possible candidate genes suggest that chromosome 2q31 may harbour one or more susceptibility genes for autism. The glutamate decarboxylase gene 1 (GAD1) located within chromosome 2q31 encodes the enzyme, GAD67, catalyzing the production of gamma-aminobutyric acid (GABA) from glutamate. Numerous independent findings have suggested the GABAergic system to be involved in autism. The present study investigates a Danish population-based, case-control sample of 444 subjects with childhood autism and 444 controls. Nine single nucleotide polymorphisms (SNPs) comprising the GAD1 gene and the microsatellite marker D2S2381 were examined for association with autism. We found no association between childhood autism and any single marker or 2-5 marker haplotypes. However, a rare nine-marker haplotype was associated with childhood autism. We cannot exclude neither GAD1 as a susceptibility gene nor the possibility of another susceptibility gene for autism to be located on chromosome 2q31.
3. Geurts HM, Corbett B, Solomon M. {{The paradox of cognitive flexibility in autism}}. {Trends Cogn Sci};2009 (Feb);13(2):74-82.
We present an overview of current literature addressing cognitive flexibility in autism spectrum disorders. Based on recent studies at multiple sites, using diverse methods and participants of different autism subtypes, ages and cognitive levels, no consistent evidence for cognitive flexibility deficits was found. Researchers and clinicians assume that inflexible everyday behaviors in autism are directly related to cognitive flexibility deficits as assessed by clinical and experimental measures. However, there is a large gap between the day-to-day behavioral flexibility and that measured with these cognitive flexibility tasks. To advance the field, experimental measures must evolve to reflect mechanistic models of flexibility deficits. Moreover, ecologically valid measures are required to be able to resolve the paradox between cognitive and behavioral inflexibility.
4. Thiessen C, Fazzio D, Arnal L, Martin GL, Yu CT, Keilback L. {{Evaluation of a self-instructional manual for conducting discrete-trials teaching with children with autism}}. {Behav Modif};2009 (May);33(3):360-373.
Discrete-trials teaching (DTT) is commonly used to implement applied behavior analysis treatment for children with autism. The authors investigated a revised self-instructional manual for teaching university students to implement a 21-component DTT procedure to teach three tasks to confederates role-playing children with autism. Also, as a motivational contingency, for each DTT session in which a student scored at or above 90% accuracy, they received US$10. After an average of 4.5 hr to master the training manual, students’ average DTT performance improved from 52% in baseline to 88% while teaching a confederate. Students averaged 77% DTT performance during subsequent generalization sessions with a child with autism.
5. Zhang A, Shen CH, Ma SY, Ke Y, El Idrissi A. {{Altered expression of Autism-associated genes in the brain of Fragile X mouse model}}. {Biochem Biophys Res Commun};2009 (Feb 20);379(4):920-923.
Autism is a severe neurodevelopmental disorder, which typically emerges in early childhood. Most cases of autism have not been linked to mutations in a specific gene, and the etioloty of the disorder remains to be established [S.S. Moy, J.J. Nadler, T.R. Magnuson, J.N. Crawley, Mouse models of autism spectrum disorders: the challenge for behavioral genetics, Am. J. Med. Genet. 142 (2006) 40-51]. Fragile X syndrome is caused by mutation in the FMR1 gene and is characterized by mental retardation, physical abnormalities, and, in most case, autistic-like behavior [R.J. Hagerman, A.W. Jackson, A. Levitas, B. Rimland, M. Braden, An analysis of autism in fifty males with the Fragile X syndrome, Am. J. Med. Genet. 23 (1986) 359-374, C.E. Bakker, C. Verheij, R. Willemsen, R. van der Helm, F. Oerlemans, M. Vermeij, A. Bygrave, A.T. Hoogeveen, B.A. Oostra, E. Reyniers, K. De Boulle, R. D’Hooge, P. Cras, D. van Velzen, G. Nagels, J.J. Marti, P. De Deyn, J.K. Darby, P.J. Willems, Fmr1 knockout mice: a model to study Fragile X mental retardation, Cell 78 (1994) 23-33]. The FMR1 knockout (KO) mouse is one of the best characterized animal models for human disorders associated with autism [S.S. Moy, J.J. Nadler, T.R. Magnuson, J.N. Crawley, Mouse models of autism spectrum disorders: the challenge for behavioral genetics, Am. J. Med. Genet. 142 (2006) 40-51]. We have used real-time PCR to investigate changes in expression levels of three genes: WNT2, MECP2, and FMR1 in different brain regions of Fagile X mice and litter mate controls. We found major changes in the expression pattern for the three genes examined. FMR1, MECP2, and WNT2 expression were drastically down regulated in the Fragile X mouse brain.
