1. Chan AS, Cheung MC, Han YM, Sze SL, Leung WW, Man HS, To CY. {{Executive function deficits and neural discordance in children with Autism Spectrum Disorders}}. {Clin Neurophysiol};2009 (May 11)
OBJECTIVE: This study examined neurophysiologic activities, executive dysfunctions, and their association in children with Autism Spectrum Disorders (ASD). METHODS: Thirty-eight normal and 16 children with ASD participated with parental consent. Executive functions were measured using neuropsychological tests and parent ratings, and neurophysiologic activities were measured using EEG to yield cordance values, an indirect measure of brain perfusion. RESULTS: Children with ASD made significantly more intrusion errors and False Alarms on the Hong Kong List Learning Test (HKLLT) and Object Recognition Test (OR) than normal children, but were comparable to normal children on the Rey-Osterrieth Complex Figure Test and Continuous Performance Test. They also showed significantly poorer executive functions in everyday activities as shown on the Behavior Rating Inventory of Executive Function (BRIEF), and had lower frontal perfusion patterns than normal children as shown in the neurophysiologic cordance measures. Frontal cordance values were found to be significantly associated with executive dysfunctions in HKLLT Delayed Intrusions, OR False Alarms and BRIEF. CONCLUSIONS: Children with ASD were impaired in everyday executive functioning and response inhibition. The cordance value, which has been shown to correlate with brain perfusion in a number of studies, was significantly correlated with executive dysfunctions. SIGNIFICANCE: Exploration of this measure as an index for response to intervention is warranted.
2. Chapleau CA, Calfa GD, Lane MC, Albertson AJ, Larimore JL, Kudo S, Armstrong DL, Percy AK, Pozzo-Miller L. {{Dendritic Spine Pathologies in Hippocampal Pyramidal Neurons from Rett Syndrome Brain and after Expression of Rett-Associated MECP2 Mutations}}. {Neurobiol Dis};2009 (May 11)
Rett syndrome (RTT) is an X chromosome-linked neurodevelopmental disorder associated with the characteristic neuropathology of dendritic spines common in diseases presenting with mental retardation (MR). Here, we present the first quantitative analyses of dendritic spine density in postmortem brain tissue from female RTT individuals, which revealed that hippocampal CA1 pyramidal neurons have lower spine density than age-matched non-MR female control individuals. The majority of RTT individuals carry mutations in MECP2, the gene coding for a methylated DNA-binding transcriptional regulator. While altered synaptic transmission and plasticity has been demonstrated in Mecp2-deficient mouse models of RTT, observations regarding dendritic spine density and morphology have produced varied results. We investigated the consequences of MeCP2 dysfunction on dendritic spine structure by overexpressing ( approximately twofold) MeCP2-GFP constructs encoding either the wildtype (WT) protein, or missense mutations commonly found in RTT individuals. Pyramidal neurons within hippocampal slice cultures transfected with either WT or mutant MECP2 (either R106W or T158M) showed a significant reduction in total spine density after 48hrs of expression. Interestingly, spine density in neurons expressing WT MECP2 for 96hrs was comparable to that in control neurons, while neurons expressing mutant MECP2 continued to have lower spines density than controls after 96hrs of expression. Knockdown of endogenous Mecp2 with a specific small hairpin interference RNA (shRNA) also reduced dendritic spine density, but only after 96hrs of expression. On the other hand, the consequences of manipulating MeCP2 levels for dendritic complexity in CA3 pyramidal neurons were only minor. Together, these results demonstrate reduced dendritic spine density in hippocampal pyramidal neurons from RTT patients, a distinct dendritic phenotype also found in neurons expressing RTT-associated MECP2 mutations or after shRNA-mediated endogenous Mecp2 knockdown, suggesting that this phenotype represent a cell-autonomous consequence of MeCP2 dysfunction.
3. Desoto MC. {{Ockham’s Razor and autism: The case for developmental neurotoxins contributing to a disease of neurodevelopment}}. {Neurotoxicology};2009 (May);30(3):331-337.
Much professional awareness regarding environmental triggers for ASD has been narrowly focused on a single possible exposure pathway (vaccines). Meanwhile, empirical support for environmental toxins as a broad class has been quietly accumulating. Recent research has shown that persons with ASD have comparatively higher levels of various toxins and are more likely to have reduced detoxifying ability, and, that rates of ASD may be higher in areas with greater pollution. This report documents that within the state with the highest rate of ASD, the rate is higher for schools near EPA Superfund sites, t (332)=3.84, p=.0001. The reasons for the rise in diagnoses likely involve genetically predisposed individuals being exposed to various environmental triggers at higher rates than in past generations.
4. Finke EH, McNaughton DB, Drager KD. {{« All Children Can and Should Have the Opportunity to Learn »: General Education Teachers’ Perspectives on Including Children with Autism Spectrum Disorder who Require AAC}}. {Augment Altern Commun};2009 (Jun);25(2):110-122.
A qualitative online focus group methodology was used to investigate the experiences of five elementary school teachers (grades K-5) who had included in their general education classrooms children with autism spectrum disorders (ASD) who required augmentative and alternative communication (AAC). Information was obtained from the participants in the following areas: (a) the benefits of educational inclusion, (b) the negative impacts of educational inclusion, (c) the challenges of educational inclusion, (d) the supports for educational inclusion, and (e) recommendations for other teachers and individuals involved in the inclusion process. Participants primarily chose to focus on inclusion as a beneficial practice for all involved, but did describe a few barriers and challenges of inclusion. The results are discussed as they relate to these themes and with reference to published literature. Recommendations for future directions are also presented.
5. Johnston SS, Buchanan S, Davenport L. {{Comparison of Fixed and Gradual Array When Teaching Sound-Letter Correspondence to Two Children with Autism who Use AAC}}. {Augment Altern Commun};2009 (Jun);25(2):136-144.
The purpose of this study was to compare two conditions for teaching two children with autism (ages 4;10 and 5;4) who used Augmentative and Alternative Communication (AAC) to point to the printed letter that corresponded to the spoken letter sounds of /t/ and /m/. In one condition (gradual array), the printed letter was first presented in isolation and then distracter letters were gradually introduced. In the other condition (fixed array), the printed letter was immediately presented in combination with seven distracter letters. Using an alternating treatment design, results revealed that the fixed array condition resulted in a faster rate of acquisition of target skills for both participants. Implications and directions for future research are discussed.
