(1-9)1. Bayliss AP, Kritikos A. {{Brief Report: Perceptual Load and the Autism Spectrum in Typically Developed Individuals}}. {J Autism Dev Disord}. 2010 Dec 28.
A fundamental task of the cognitive system is to prioritize behaviourally relevant sensory inputs for processing at the expense of irrelevant inputs. In a study of neurotypical participants (n = 179), we utilized a brief flanker interference task while varying the perceptual load of the visual display. Typically, increasing perceptual load (i.e., with greater numbers of search items) reduces interference from a competing peripheral distractor. We show that individuals who score above average on the Autism Spectrum Quotient (AQ) show stronger interference at high perceptual load than individuals with below-average AQ scores. This is consistent with recent findings in individuals with autism spectrum conditions, and supports the idea that the cognitive style of the autistic brain is reflected in a broader phenotype across the population.
2. Bowler D. {{Autism. Editorial}}. {Autism}. 2010 Nov;14(6):555-7.
3. Catarino A, Luke L, Waldman S, Andrade A, Fletcher PC, Ring H. {{An fMRI investigation of detection of semantic incongruities in autistic spectrum conditions}}. {Eur J Neurosci}. 2010 Dec 29.
The aim of this study was to investigate differences in the brain’s haemodynamic response to semantically incongruent and congruent sentences in adults with an autistic spectrum condition (ASC) and a typically developing Control group. We used functional magnetic resonance imaging to measure regional variations in neural activity during detection of semantic incongruities within written sentences. Whilst the 12 controls showed a pattern of activity extending from posterior cingulate cortices bilaterally and the left occipitotemporal region to the left superior and inferior temporal lobes, right anterior cingulate and right inferior frontal gyrus, the 12 participants with an ASC presented a more spatially restricted activation pattern, including the left inferior frontal gyrus, left anterior cingulate cortex and right middle frontal gyrus. These results are coherent with the hypothesis that impaired integration of multiple neural networks in people with an ASC is related to previous observations that this group have difficulties in the use of context to predict the final word of sentences.
4. Dufour-Rainfray D, Vourc’h P, Tourlet S, Guilloteau D, Chalon S, Andres CR. {{Fetal exposure to teratogens: evidence of genes involved in autism?}}. {Neurosci Biobehav Rev}. 2010 Dec 29.
Dufour-Rainfray, D., Vourc’h, P., Tourlet, S., Guilloteau, D., Chalon, S. and Andres, C.R. Fetal exposure to teratogens: evidence of genes involved in autism? NEUROSCI BIOBEHAV REV XX(X) XXX-XXX, 2010.-Environmental challenges during the prenatal period can result in behavioral abnormalities and cognitive deficits that appear later in life such as autism. Prenatal exposure to valproic acid, ethanol, thalidomide and misoprostol has been shown to be associated with an increased incidence of autism. In addition, rodents exposed in utero to some of these drugs show autism-like abnormalities, including brain changes and lifelong behavior dysfunction. Our aim is to summarize current understanding of the relationship between in utero exposure to these drugs and autism in humans and in autism-like animal model phenotypes. It also highlights the importance of these models to understanding the neurobiology of autism, particularly in the identification of susceptibility genes. These drugs are able to modulate the expression of many genes involved in processes such as proliferation, apoptosis, neuronal differentiation and migration, synaptogenesis and synaptic activity. It seems essential to focus research on genes expressed during early neurodevelopment which may be the target of mutations or affected by drugs such as those included in this review.
5. Granana N, Taddeo P, Espoueys P, Nazer C. {{[Pubertal behavioral decompensation in patients with pervasive developmental disorders.]}}. {Vertex}. 2010 May;XXI(91):245-9.
Objectives: To describe behavioral descompensation in adolescents with autistic spectrum disorders (ASD). Methods: We analyzed in a prospective study the stories of 11 children and adolescents with ASD, their demographic characteristics, initial symptoms of descompensation at pubertal or adolescence stages, interventions developed and evolution with them. Results: We studied the clinical stories of eleven patients, 8 men and 3 women, who consulted with behavioral descompensation periods at a mean age of 13 years (range 10- 16 years). They presented with hyperactivity/agitation (6), injuries and aggression against others or themselves (6), irritability/ emotional labiality (6), inappropriate shouting (6), inflexibility/ rituals (4) and catatonia (2). Almost all patients had received psychiatric medication before descompensation, except patients with catatonia. Four of 11 presented two episodes and seven patients only one episode during a period of 2.7 years of follow-up (range 1- 6 years). Eight of 11 patients recovered with psychological and pharmacological (a medium of 2 drugs) interventions in a mean time of 4 months. Both patients with catatonia didn’t recovered, and one more patient didn’t improved with pharmacological treatment. Conclusions: Behavioral descompensations are very frequent complications in patients with autism at puberty or adolescence stages. Most of them recover with very close combined interventions and familial support.
6. Hoekstra PJ, Troost PW, Lahuis BE, Mulder H, Mulder EJ, Franke B, et al. {{Risperidone-Induced Weight Gain in Referred Children with Autism Spectrum Disorders Is Associated with a Common Polymorphism in the 5-Hydroxytryptamine 2C Receptor Gene}}. {J Child Adolesc Psychopharmacol}. 2010 Dec;20(6):473-7.
Abstract Weight gain is an important adverse effect of risperidone, but predictors of significant weight gain have yet to be identified in pediatric patients. Here, we investigated differences between age- and gender-normed body mass index-standardized z scores at baseline and after 8 weeks of open-label, flexible-dose risperidone treatment (mean dose: 1.70 mg/day) in 32 youths with pervasive developmental disorder (mean age = 8.74, range = 5-16 years) in relation to -759C/T 5-hydroxytryptamine 2C receptor (HTR2C) promoter and rs1414334 HTR2C intragenic C/G alleles, along with gender, age, and risperidone dose, using repeated measures analyses of variance. Carriers of the HTR2C promoter T allele gained an average of 0.043 +/- 0.017 body mass index-standardized z scores (1.84 +/- 1.51 kg) versus 0.64 +/- 0.35 z (3.23 +/- 1.47 kg) for non-T-allele carriers (p < 0.001). Presence of the rs1414334 C allele played no significant role. Further, weight gain appeared to be associated with younger age and higher doses of risperidone. The current preliminary findings suggest that the variant T allele of the -759C/T HTR2C promoter polymorphism is protective against risperidone-induced weight gain. Younger children and those treated with higher doses of risperidone may be at higher risk for weight gain.
7. Kim KC, Kim P, Go HS, Choi CS, Yang SI, Cheong JH, et al. {{The critical period of valproate exposure to induce autistic symptoms in Sprague-Dawley rats}}. {Toxicol Lett}. 2010 Dec 29.
Prenatal exposure to valproic acid (VPA) induces neural tube defects and impairment in social behaviors related to autistic spectrum disorder in newborns, which make it a useful animal model of autism. In this study, we compared the effects of different time window of prenatal valproic acid exposure for inducing the altered social behaviors relevant to autism from embryonic day 7 to embryonic day 15 in Sprague-Dawley rats to determine the critical periods for the impairment. Compared to E7, E9.5 and E15 exposure, VPA exposure at E12 showed most significant changes in behaviors over control animals with reduced sociability and social preference. E9.5 exposure to valproic acid showed strong reproductive toxicity including decrease in the number of live birth. In general, exposure at E15 showed only marginal effects on reproduction and social behaviors. Finally, VPA-exposed rats at E12 were more sensitive to electric shock than VPA-exposed rats at any other periods. These results suggested that E12 is the critical period in rats when valproate exposure has prominent effects for inducing the altered social behavior similar to human autistic behavior.
8. Shipman DL, Sheldrick RC, Perrin EC. {{Quality of Life in Adolescents With Autism Spectrum Disorders: Reliability and Validity of Self-Reports}}. {J Dev Behav Pediatr}. 2010 Dec 23.
PURPOSE:: This study examined the reliability and validity of self-reported quality of life (QoL) among adolescents with autism spectrum disorders (ASDs) but without mental retardation (IQ >70) using a validated QoL measure, Pediatric Quality of Life Inventory. Secondarily, the self-reported QoL of adolescents with ASDs was compared with published normative data. METHODS:: Thirty-nine adolescents with ASDs and their parents completed a QoL instrument and brief measures of psychosocial distress and self-esteem. A screening test of cognitive abilities was administered to adolescents; parents completed an assessment of behavioral and emotional symptoms and an assessment of the presence and extent of autistic social impairments. RESULTS:: Adolescent self-reports of QoL demonstrated internal reliability and concurrent validity. Self-reports on the Pediatric Quality of Life Inventory demonstrated moderate to large positive correlations with a measure of self-esteem and moderate to large negative correlations with measures of anxiety and mood. Concurrent validity with parent proxy reports fell within the range of expected values based on past studies of inter-rater reliability for QoL, with parents of adolescents reporting lower QoL when compared with adolescent reports. Adolescents reported QoL below the population mean for all domains. CONCLUSIONS:: Results of this study provide preliminary evidence that adolescents with ASDs are able to report on their own QoL in a valid and reliable manner. Based on our findings, the measurement of QoL may be useful for clinical care and research about adolescents with ASDs.
9. Silverman JL, Yang M, Turner SM, Katz AM, Bell DB, Koenig JI, et al. {{Low stress reactivity and neuroendocrine factors in the BTBR T+tf/J mouse model of autism}}. {Neuroscience}. 2010 Dec 29;171(4):1197-208.
Autism is a neurodevelopmental disorder characterized by abnormal reciprocal social interactions, communication deficits, and repetitive behaviors with restricted interests. BTBR T+tf/J (BTBR) is an inbred mouse strain that displays robust behavioral phenotypes with analogies to all three of the diagnostic symptoms of autism, including low social interactions, reduced vocalizations in social settings, and high levels of repetitive self-grooming. Autism-relevant phenotypes in BTBR offer translational tools to discover neurochemical mechanisms underlying unusual mouse behaviors relevant to symptoms of autism. Because repetitive self-grooming in mice may be a displacement behavior elevated by stressors, we investigated neuroendocrine markers of stress and behavioral reactivity to stressors in BTBR mice, as compared to C57BL/6J (B6), a standard inbred strain with high sociability. Radioimmunoassays replicated previous findings that circulating corticosterone is higher in BTBR than in B6. Higher basal glucocorticoid receptor mRNA and higher oxytocin peptide levels were detected in the brains of BTBR as compared to B6. No significant differences were detected in corticotrophin releasing factor (CRF) peptide or CRF mRNA. In response to behavioral stressors, BTBR and B6 were generally similar on behavioral tasks including stress-induced hyperthermia, elevated plus-maze, light <–> dark exploration, tail flick, acoustic startle and prepulse inhibition. BTBR displayed less reactivity than B6 to a noxious thermal stimulus in the hot plate, and less immobility than B6 in both the forced swim and tail suspension depression-related tasks. BTBR, therefore, exhibited lower depression-like scores than B6 on two standard tests sensitive to antidepressants, did not differ from B6 on two well-validated anxiety-like behaviors, and did not exhibit unusual stress reactivity to sensory stimuli. Our findings support the interpretation that autism-relevant social deficits, vocalizations, and repetitive behaviors are not the result of abnormal stress reactivity in the BTBR mouse model of autism.
