1. Alderson-Day B, McGonigle-Chalmers M. {{Is It a Bird? Is It a Plane? Category Use in Problem-solving in Children with Autism Spectrum Disorders}}. {J Autism Dev Disord};2011 (May);41(5):555-565.

Fourteen children with autism spectrum disorders (ASD) and fourteen age-matched typically-developing (TD) controls were tested on an adapted version of the Twenty Questions Task (Mosher and Hornsby in Studies in cognitive growth. Wiley, New York, pp 86-102, 1966) to examine effects of content, executive and verbal IQ factors on category use in problem-solving (age range 8-17). Across conditions participants with ASD asked questions that focussed on smaller categories than controls. Specific group differences were observed in the handling of abstract content and response to additional working memory demands. In addition, post hoc regression analysis indicated that VIQ predicted performance in ASD but not TD participants. The implications for theories of category processing in autism are discussed.

2. Allen ML, Haywood S, Rajendran G, Branigan H. {{Evidence for syntactic alignment in children with autism}}. {Dev Sci};2011 (May);14(3):540-548.

We report an experiment that examined whether children with Autistic Spectrum Disorder (ASD) spontaneously converge, or align, syntactic structure with a conversational partner. Children with ASD were more likely to produce a passive structure to describe a picture after hearing their interlocutor use a passive structure to describe an unrelated picture when playing a card game. Furthermore, they converged syntactic structure with their interlocutor to the same extent as did both chronological and verbal age-matched controls. These results suggest that the linguistic impairment that is characteristic of children with ASD, and in particular their difficulty with interactive language usage, cannot be explained in terms of a general deficit in linguistic imitation.

3. Altieri L, Neri C, Sacco R, Curatolo P, Benvenuto A, Muratori F, Santocchi E, Bravaccio C, Lenti C, Saccani M, Rigardetto R, Gandione M, Urbani A, Persico AM. {{Urinary p-cresol is elevated in small children with severe autism spectrum disorder}}. {Biomarkers};2011 (May);16(3):252-260.

Several studies have described in autistic patients an overgrowth of unusual gut bacterial strains, able to push the fermentation of tyrosine up to the formation of p-cresol. We compared levels of urinary p-cresol, measured by high-performance liquid chromatography-ultraviolet, in 59 matched case-control pairs. Urinary p-cresol was significantly elevated in autistic children smaller than 8 years of age (p < 0.01), typically females (p < 0.05), and more severely affected regardless of sex (p < 0.05). Urinary cotinine measurements excluded smoking-related hydrocarbon contaminations as contributors to these differences. Hence, elevated urinary p-cresol may serve as a biomarker of autism liability in small children, especially females and more severely affected males. 4. Anderson JS, Druzgal TJ, Froehlich A, Dubray MB, Lange N, Alexander AL, Abildskov T, Nielsen JA, Cariello AN, Cooperrider JR, Bigler ED, Lainhart JE. {{Decreased interhemispheric functional connectivity in autism}}. {Cereb Cortex};2011 (May);21(5):1134-1146. The cortical underconnectivity theory asserts that reduced long-range functional connectivity might contribute to a neural mechanism for autism. We examined resting-state blood oxygen level-dependent interhemispheric correlation in 53 males with high-functioning autism and 39 typically developing males from late childhood through early adulthood. By constructing spatial maps of correlation between homologous voxels in each hemisphere, we found significantly reduced interhemispheric correlation specific to regions with functional relevance to autism: sensorimotor cortex, anterior insula, fusiform gyrus, superior temporal gyrus, and superior parietal lobule. Observed interhemispheric connectivity differences were better explained by diagnosis of autism than by potentially confounding neuropsychological metrics of language, IQ, or handedness. Although both corpus callosal volume and gray matter interhemispheric connectivity were significantly reduced in autism, no direct relationship was observed between them, suggesting that structural and functional metrics measure different aspects of interhemispheric connectivity. In the control but not the autism sample, there was decreasing interhemispheric correlation with subject age. Greater differences in interhemispheric correlation were seen for more lateral regions in the brain. These findings suggest that long-range connectivity abnormalities in autism are spatially heterogeneous and that transcallosal connectivity is decreased most in regions with functions associated with behavioral abnormalities in autism. Autism subjects continue to show developmental differences in interhemispheric connectivity into early adulthood. 5. Bastiaansen JA, Thioux M, Nanetti L, van der Gaag C, Ketelaars C, Minderaa R, Keysers C. {{Age-related increase in inferior frontal gyrus activity and social functioning in autism spectrum disorder}}. {Biol Psychiatry};2011 (May 1);69(9):832-838. BACKGROUND: Hypoactivation of the inferior frontal gyrus during the perception of facial expressions has been interpreted as evidence for a deficit of the mirror neuron system in children with autism. We examined whether this dysfunction persists in adulthood, and how brain activity in the mirror neuron system relates to social functioning outside the laboratory. METHODS: Twenty-one adult males with autism spectrum disorders and 21 typically developing subjects matched for age, sex, and IQ were scanned in three conditions: observing short movies showing facial expressions, performing a facial movement, and experiencing a disgusting taste. Symptom severity and level of social adjustment were measured with the Autism Diagnostic Observation Schedule and the Social Functioning Scale. RESULTS: Inferior frontal gyrus activity during the observation of facial expressions increased with age in subjects with autism, but not in control subjects. The age-related increase in activity was associated with changes in gaze behavior and improvements in social functioning. These age-related neurocognitive improvements were not found in a group of individuals with schizophrenia, who had comparable levels of social functioning. CONCLUSIONS: The results of this cross-sectional study suggest that mirror neuron system activity augments with age in autism and that this is accompanied by changes in gaze behavior and improved social functioning. It is the first demonstration of an age-related neurocognitive improvement in autism. Increased motor simulation may contribute to the amelioration in social functioning documented in adolescence and adulthood. This finding should encourage the development of new therapeutic interventions directed at emotion simulation. 6. Bent S, Bertoglio K, Ashwood P, Bostrom A, Hendren RL. {{A pilot randomized controlled trial of omega-3 Fatty acids for autism spectrum disorder}}. {J Autism Dev Disord};2011 (May);41(5):545-554. We conducted a pilot randomized controlled trial to determine the feasibility and initial safety and efficacy of omega-3 fatty acids (1.3 g/day) for the treatment of hyperactivity in 27 children ages 3-8 with autism spectrum disorder (ASD). After 12 weeks, hyperactivity, as measured by the Aberrant Behavior Checklist, improved 2.7 (+/-4.8) points in the omega-3 group compared to 0.3 (+/-7.2) points in the placebo group (p = 0.40; effect size = 0.38). Correlations were found between decreases in five fatty acid levels and decreases in hyperactivity, and the treatment was well tolerated. Although this pilot study did not find a statistically significant benefit from omega-3 fatty acids, the small sample size does not rule out small to moderate beneficial effects. 7. Cardon TA, Wilcox MJ. {{Promoting imitation in young children with autism: a comparison of reciprocal imitation training and video modeling}}. {J Autism Dev Disord};2011 (May);41(5):654-666. The inability to imitate is a salient diagnostic marker for autism. It has been suggested that for children with autism, imitation may be a prerequisite skill that can assist in the development of various skills. Using a multiple baseline design across subjects, the purpose of this research was to determine if two interventions, reciprocal imitation training and video modeling were effective in promoting imitation acquisition in young children with autism. Six boys were matched across various features (i.e., age, language, autism severity) and randomly placed in a treatment condition. Results indicated that all six participants increased their imitation skills to varying degrees in both conditions, and imitation maintained and generalized at higher than baseline levels post treatment. 8. Chen R, Jiao Y, Herskovits EH. {{Structural MRI in autism spectrum disorder}}. {Pediatr Res};2011 (May);69(5 Pt 2):63R-68R. Magnetic resonance (MR) examination provides a powerful tool for investigating brain structural changes in children with autism spectrum disorder (ASD). We review recent advances in the understanding of structural MR correlates of ASD. We summarize findings from studies based on voxel-based morphometry, surface-based morphometry, tensor-based morphometry, and diffusion-tensor imaging. Finally, we discuss diagnostic models of ASD based on MR-derived features. ABBREVIATIONS:: 9. Constantino JN. {{The quantitative nature of autistic social impairment}}. {Pediatr Res};2011 (May);69(5 Pt 2):55R-62R. Autism, like intellectual disability, represents the severe end of a continuous distribution of developmental impairments that occur in nature, that are highly inherited, and that are orthogonally related to other parameters of development. A paradigm shift in understanding the core social abnormality of autism as a quantitative trait rather than as a categorically defined condition has key implications for diagnostic classification, the measurement of change over time, the search for underlying genetic and neurobiologic mechanisms, and public health efforts to identify and support affected children. Here, a recent body of research in genetics and epidemiology is presented to examine a dimensional reconceptualization of autistic social impairment-as manifested in clinical autistic syndromes, the broader autism phenotype, and normal variation in the general population. It illustrates how traditional categorical approaches to diagnosis may lead to misclassification of subjects (especially girls and mildly affected boys in multiple-incidence autism families), which can be particularly damaging to biological studies and proposes continued efforts to derive a standardized quantitative system by which to characterize this family of conditions. ABBREVIATIONS:: 10. Dardennes RM, Al Anbar NN, Prado-Netto A, Kaye K, Contejean Y. {{Treating the cause of illness rather than the symptoms: parental causal beliefs and treatment choices in autism spectrum disorder}}. {Res Dev Disabil};2011 (May-Jun);32(3):1137-1146. OBJECTIVES: To explore the relationship between causal beliefs on autism (CBA) and treatment choices. DESIGN AND METHODS: A cross-sectional design was employed. Parents of a child with autism spectrum disorder (ASD) were asked to complete the Lay-Beliefs about Autism Questionnaire (LBA-Q) and answer questions about treatments used. Only items inquiring about a cause of autism were retained for analysis. Series of forward stepwise logistic regressions were performed with each treatment as dependent variable and the scores given to each of the CBA items as independent variables. RESULTS: 78 parents were included. The most strongly held causal beliefs were brain abnormalities and genetic factors. Parents who had more beliefs in the causal role of very early traumatic experiences were less likely to use behavior therapy and PECS. Higher beliefs in illness during pregnancy increased the odds of medication use. Stronger beliefs on the role of food allergy were associated with higher use of detoxification treatments, special diets, and vitamins. On the contrary, these beliefs reduced the odds of drug use. CONCLUSIONS: Causal beliefs are associated with treatment choices. Such preliminary results highlight the value of continued studies, not only to establish the causal nature of these associations, but also to demonstrate the utility of modifying such beliefs for both parents' and child's benefits. Identifying parents' beliefs about their child's illness may be an important step in formulating interventions facilitating appropriate care. 11. Dealberto MJ. {{Prevalence of autism according to maternal immigrant status and ethnic origin}}. {Acta Psychiatr Scand};2011 (May);123(5):339-348. Dealberto M.-J. Prevalence of autism according to maternal immigrant status and ethnic origin. Objective: To examine the rates of autism separately according to maternal immigrant status and ethnic origin in respect to the vitamin D insufficiency hypothesis. Method: Articles were identified by electronic searches. Studies were selected when they analysed autism rates according to maternal immigrant status and/or ethnic origin using multivariate techniques. Results: This review gave further support to the association between maternal immigrant status and an increased risk of autism. The relationship with ethnic origin was more complex. Although the crude rates did not differ, multivariate analyses taking into account confounding factors found that black ethnicity was associated with an increased risk for autism. The risk was highly significant when considering the strict definition of autistic disorders as opposed to the large definition of other pervasive developmental disorders. The risk was also very significant for autism associated with mental retardation. Conclusion: These results are consistent with the maternal vitamin D insufficiency hypothesis. Neurobiological studies are warranted to document the effect of maternal vitamin D insufficiency during pregnancy on the foetal brain and the window of vulnerability. This review stresses the importance of monitoring vitamin D levels in pregnant women, especially those who are immigrant, dark-skinned or veiled, and the urgency of randomized controlled trials. 12. Delbroek H, Steyaert J, Legius E. {{An 8.9 year old girl with autism and Gorlin syndrome}}. {Eur J Paediatr Neurol};2011 (May);15(3):268-270. We present an 8.9 year old girl diagnosed with autism and macrocrania. Because of macrocrania, hypertelorism and epidermal punctiform lesions in the palm of the hand, Gorlin syndrome was clinically suspected and molecularly confirmed by finding a deletion of 22 base pairs in the PTCH1 gene. The possibility of an association between autism and Gorlin syndrome is discussed. 13. Di Martino A, Kelly C, Grzadzinski R, Zuo XN, Mennes M, Mairena MA, Lord C, Castellanos FX, Milham MP. {{Aberrant striatal functional connectivity in children with autism}}. {Biol Psychiatry};2011 (May 1);69(9):847-856. BACKGROUND: Models of autism spectrum disorders (ASD) as neural disconnection syndromes have been predominantly supported by examinations of abnormalities in corticocortical networks in adults with autism. A broader body of research implicates subcortical structures, particularly the striatum, in the physiopathology of autism. Resting state functional magnetic resonance imaging has revealed detailed maps of striatal circuitry in healthy and psychiatric populations and vividly captured maturational changes in striatal circuitry during typical development. METHODS: Using resting state functional magnetic resonance imaging, we examined striatal functional connectivity (FC) in 20 children with ASD and 20 typically developing children between the ages of 7.6 and 13.5 years. Whole-brain voxelwise statistical maps quantified within-group striatal FC and between-group differences for three caudate and three putamen seeds for each hemisphere. RESULTS: Children with ASD mostly exhibited prominent patterns of ectopic striatal FC (i.e., functional connectivity present in ASD but not in typically developing children), with increased functional connectivity between nearly all striatal subregions and heteromodal associative and limbic cortex previously implicated in the physiopathology of ASD (e.g., insular and right superior temporal gyrus). Additionally, we found striatal functional hyperconnectivity with the pons, thus expanding the scope of functional alterations implicated in ASD. Secondary analyses revealed ASD-related hyperconnectivity between the pons and insula cortex. CONCLUSIONS: Examination of FC of striatal networks in children with ASD revealed abnormalities in circuits involving early developing areas, such as the brainstem and insula, with a pattern of increased FC in ectopic circuits that likely reflects developmental derangement rather than immaturity of functional circuits. 14. Dingfelder HE, Mandell DS. {{Bridging the Research-to-Practice Gap in Autism Intervention: An Application of Diffusion of Innovation Theory}}. {J Autism Dev Disord};2011 (May);41(5):597-609. There is growing evidence that efficacious interventions for autism are rarely adopted or successfully implemented in public mental health and education systems. We propose applying diffusion of innovation theory to further our understanding of why this is the case. We pose a practical set of questions that administrators face as they decide about the use of interventions. Using literature from autism intervention and dissemination science, we describe reasons why efficacious interventions for autism are rarely adopted, implemented, and maintained in community settings, all revolving around the perceived fit between the intervention and the needs and capacities of the setting. Finally, we suggest strategies for intervention development that may increase the probability that these interventions will be used in real-world settings. 15. Doyen C, Mighiu D, Kaye K, Colineaux C, Beaumanoir C, Mouraeff Y, Rieu C, Paubel P, Contejean Y. {{Melatonin in children with autistic spectrum disorders: recent and practical data}}. {Eur Child Adolesc Psychiatry};2011 (May);20(5):231-239. Over the last 20 years, melatonin, a pineal hormone synthesized from serotonin, has been implicated in various studies on the autism spectrum disorder (ASD) and altered melatonin levels were detected in subgroups of subjects with ASD. Its effect on sleep disturbances got the attention of clinicians and several investigations were carried out to determine the usefulness and safety of melatonin administration in this disorder. Hypotheses were also raised regarding the possibility that the dysfunctional synthesis and secretion of melatonin detected in subgroups of subjects with ASD may increase the risk as well the severity of ASD. The purpose of this paper is to review our pharmacokinetic knowledge on melatonin and present results from recent studies on sleep disorders in autism, their treatment with melatonin and the impact of melatonin prescription in children with ASD evaluated in a Diagnostic Center for Autism Spectrum Disorder in Paris, France. 16. Eapen V. {{Genetic basis of autism: is there a way forward?}}. {Curr Opin Psychiatry};2011 (May);24(3):226-236. PURPOSE OF REVIEW: This paper outlines some of the key findings from genetic research carried out in the last 12-18 months, which indicate that autism spectrum disorder (ASD) is a complex disorder involving interactions between genetic, epigenetic and environmental factors. RECENT FINDINGS: The current literature highlights the presence of genetic and phenotypic heterogeneity in ASD with a number of underlying pathogenetic mechanisms. In this regard, there are at least three phenotypic presentations with distinct genetic underpinnings: autism plus phenotype characterized by syndromic ASD caused by rare, single-gene disorders; broad autism phenotype caused by genetic variations in single or multiple genes, each of these variations being common and distributed continually in the general population, but resulting in varying clinical phenotypes when it reaches a certain threshold through complex gene-gene and gene-environment interactions; and severe and specific phenotype caused by 'de-novo' mutations in the patient or transmitted through asymptomatic carriers of such mutation. SUMMARY: Understanding the neurobiological processes by which genotypes become phenotypes, along with the advances in developmental neuroscience and neuronal networks at the cellular and molecular level, is paving the way for translational research involving targeted interventions of affected molecular pathways and early intervention programs that promote normal brain responses to stimuli and alter the developmental trajectory. 17. Edens AC, Lyons MJ, Duron RM, Dupont BR, Holden KR. {{Autism in two females with duplications involving Xp11.22-p11.23}}. {Dev Med Child Neurol};2011 (May);53(5):463-466. We present two phenotypically similar females with Xp duplication who have autism and epilepsy. Case 1 is a 14-year-old Honduran female with autism and medically refractory complex partial, secondarily generalized epilepsy. Case 2 is a 3-year-old Austrian female with autism and medically refractory complex partial epilepsy. Both patients also share features of severe intellectual disability (case 1 has a developmental quotient of 23, case 2 has a developmental quotient of 42) and dysmorphic facial features. Autism was confirmed by thorough clinical evaluations and testing. Case 1 has a karyotype of 46,X,dup(X)(p11.2-p22.33) and a highly skewed X-inactivation pattern (94:6). Brain magnetic resonance imaging (MRI) and electroencephalogram (EEG) were abnormal. Case 2 has a 5-megabase duplication of Xp11.22-p11.23 on chromosome microarray analysis. The patient has a random X-inactivation pattern (77:23). Brain MRI was normal, but EEG was abnormal. Both patients have duplications involving the Xp11.22-p11.23 region, indicating that this is an area of interest for future translational autism research. 18. Esposito G, Venuti P, Apicella F, Muratori F. {{Analysis of unsupported gait in toddlers with autism}}. {Brain Dev};2011 (May);33(5):367-373. Aims: A number of studies have suggested the importance of motor development in autism. Motor development has been considered a possible bio-marker of autism since it does not depend on either social or linguistic development. In this study, using retrospective video analysis we investigated the first unsupported gait in toddlers with autism. Methods: Fifty-five toddlers, belonging to three groups were recruited: toddlers with autistic disorder (AD, n=20, age 14.2mo, sd 1.4mo) and as comparison groups: typically developing toddlers (TD, n=20, age 12.9mo, sd 1.1mo) and toddlers with non-autistic developmental delays of mixed aetiology (DD, n=15, age 13.1mo, sd 0.8mo). The Walking Observation Scale (WOS) and the Positional Pattern for Symmetry during Walking (PPSW) were used to gather data on the first unsupported gait. The WOS includes 11 items that analyze gait through three axes: foot movements; arm movements; general movements while the PPSW analyses static and dynamical symmetry during gait. Results: Our results have identified significant differences in gait patterns among the group of toddlers with AD as opposed to the control groups. Significant differences between AD and the two control groups were found for both WOS (p<.001) and PPSW (p<.001). Conclusion: The specificity of motor disturbances we have identified in autism (postural asymmetry) is consistent with previous findings that implicated cerebellar involvement in the motor symptoms of autism. 19. Frankel FD, Gorospe CM, Chang YC, Sugar CA. {{Mothers' reports of play dates and observation of school playground behavior of children having high-functioning autism spectrum disorders}}. {J Child Psychol Psychiatry};2011 (May);52(5):571-579. Background: Children with high-functioning autism spectrum disorders (ASD) are generally included with typically developing peers at school. They have difficulties interacting with peers on the school playground. Previous literature suggests that having play dates in the home may be related to better peer acceptance at school. Methods: This study examines the relationship between mother-reported play date frequency and amount of conflict, and peer interaction observed on the school playground for a sample of 27 boys and 4 girls meeting structured interview and observation criteria for ASD. Measures of intellectual functioning, adaptive behavior, and social skills were included in a stepwise regression analysis to account for their impact on relationships between maternal play date reports, general peer acceptance at school (as rated by the child's teacher) and observations of school playground behavior. Results: Results revealed that children with autism spectrum disorders who had more play dates in their home tended to spend a greater amount of time engaged in behaviors such as mutual offering of objects, conversing and other turn-taking activities with peers on the school playground. They also received more positive responses to their overtures from peers. These relationships remained highly significant even after accounting for other demographic, general social, and cognitive variables. Conclusions: The present results suggest that play date frequency is strongly related to school playground behavior. Owing to the design of this study, future research must assess whether play dates in the home promote better peer relationships on the playground or the reverse. In either case, the assessment of play dates, as well as observation of spontaneous unsupervised social interactions, are important outcome measures to consider in social skills interventions for children with high-functioning ASD. 20. Fraser R, Angus B, Cotton S, Gentle E, Allott K, Thompson A. {{Prevalence of autism spectrum conditions in a youth mental health service}}. {Aust N Z J Psychiatry};2011 (May);45(5):426. 21. Frye RE, Rossignol DA. {{Mitochondrial dysfunction can connect the diverse medical symptoms associated with autism spectrum disorders}}. {Pediatr Res};2011 (May);69(5 Pt 2):41R-47R. Autism spectrum disorder (ASD) is a devastating neurodevelopmental disorder. Over the past decade, evidence has emerged that some children with ASD suffer from undiagnosed comorbid medical conditions. One of the medical disorders that has been consistently associated with ASD is mitochondrial dysfunction. Individuals with mitochondrial disorders without concomitant ASD manifest dysfunction in multiple high-energy organ systems, such as the central nervous, muscular, and gastrointestinal (GI) systems. Interestingly, these are the identical organ systems affected in a significant number of children with ASD. This finding increases the possibility that mitochondrial dysfunction may be one of the keys that explains the many diverse symptoms observed in some children with ASD. This article will review the importance of mitochondria in human health and disease, the evidence for mitochondrial dysfunction in ASD, the potential role of mitochondrial dysfunction in the comorbid medical conditions associated with ASD, and how mitochondrial dysfunction can bridge the gap for understanding how these seemingly disparate medical conditions are related. We also review the limitations of this evidence and other possible explanations for these findings. This new understanding of ASD should provide researchers a pathway for understanding the etiopathogenesis of ASD and clinicians the potential to develop medical therapies. ABBREVIATION:: 22. Ghanizadeh A. {{Targeting of Glycine Site on NMDA Receptor as a Possible New Strategy for Autism Treatment}}. {Neurochem Res};2011 (May);36(5):922-923. The exact pathophysiology of the neurodevelopment disorder of autism is not clear and there is not any curative approach for it. There is only one FDA-approved medication for its management. Therefore, providing of novel treatments is highly required. The hypofunction of GABAergic system and glutamate toxicity are generally believed to have a causal role for autism. The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism. 23. Greene DJ, Colich N, Iacoboni M, Zaidel E, Bookheimer SY, Dapretto M. {{Atypical neural networks for social orienting in autism spectrum disorders}}. {Neuroimage};2011 (May 1);56(1):354-362. Autism spectrum disorders (ASD) are characterized by significant social impairments, including deficits in orienting attention following social cues. Behavioral studies investigating social orienting in ASD, however, have yielded mixed results, as the use of naturalistic paradigms typically reveals clear deficits whereas computerized laboratory experiments often report normative behavior. The present study is the first to examine the neural mechanisms underlying social orienting in ASD in order to provide new insight into the social attention impairments that characterize this disorder. Using fMRI, we examined the neural correlates of social orienting in children and adolescents with ASD and in a matched sample of typically developing (TD) controls while they performed a spatial cueing paradigm with social (eye gaze) and nonsocial (arrow) cues. Cues were either directional (indicating left or right) or neutral (indicating no direction), and directional cues were uninformative of the upcoming target location in order to engage automatic processes by minimizing expectations. Behavioral results demonstrated intact orienting effects for social and nonsocial cues, with no differences between groups. The imaging results, however, revealed clear group differences in brain activity. When attention was directed by social cues compared to nonsocial cues, the TD group showed increased activity in frontoparietal attention networks, visual processing regions, and the striatum, whereas the ASD group only showed increased activity in the superior parietal lobule. Significant groupxcue type interactions confirmed greater responsivity in task-relevant networks for social cues than nonsocial cues in TD as compared to ASD, despite similar behavioral performance. These results indicate that, in the autistic brain, social cues are not assigned the same privileged status as they are in the typically developing brain. These findings provide the first empirical evidence that the neural circuitry involved in social orienting is disrupted in ASD and highlight that normative behavioral performance in a laboratory setting may reflect compensatory mechanisms rather than intact social attention. 24. Hamdan FF, Daoud H, Piton A, Gauthier J, Dobrzeniecka S, Krebs MO, Joober R, Lacaille JC, Nadeau A, Milunsky JM, Wang Z, Carmant L, Mottron L, Beauchamp MH, Rouleau GA, Michaud JL. {{De Novo SYNGAP1 Mutations in Nonsyndromic Intellectual Disability and Autism}}. {Biol Psychiatry};2011 (May 1);69(9):898-901. BACKGROUND: Little is known about the genetics of nonsyndromic intellectual disability (NSID). Recently, we reported de novo truncating mutations in the SYNGAP1 gene of 3 of 94 NSID cases, suggesting that its disruption represents a common cause of autosomal dominant NSID. METHODS: To further explore the involvement of SYNGAP1 in NSID, we sequenced its exons and intronic boundaries in 60 additional sporadic cases of NSID, including 30 patients with autism spectrum disorders (ASD) and 9 with epilepsy, and in 380 control individuals. RESULTS: We identified de novo out-of-frame deletions in two patients with NSID and mild generalized epilepsy (c.2677delC/p.Q893RfsX184 and c.321_324delGAAG/p. K108VfsX25) and a de novo splicing mutation (c.2294 + 1G>A), which results in the creation of a premature stop codon, in a patient with NSID and autism. No splicing or truncating mutations were found in control subjects. CONCLUSIONS: We provide evidence that truncating mutations in SYNGAP1 are common in NSID and can be also associated with autism.

25. Hampson DR, Adusei DC, Pacey LK. {{The neurochemical basis for the treatment of autism spectrum disorders and Fragile X Syndrome}}. {Biochem Pharmacol};2011 (May 1);81(9):1078-1086.

Autism spectrum disorders (ASD) and Fragile X Syndrome (FXS) are neurodevelopmental disorders that share overlapping behavioral characteristics. While FXS is known to result from a specific genetic mutation, the causes of the majority of cases of ASD are unknown. Animal models of FXS have revealed new insight into the cellular and biochemical changes that occur in the central nervous system in this disorder, while human genetic studies on individuals with autism have identified sets of genes that may increase susceptibility to the disorder. Together these discoveries suggest overlapping biochemical characteristics and reveal new directions for the potential development of pharmacological therapies that might prove useful in the treatment of both FXS and ASD. In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD. Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.

26. Hoekstra RA, Vinkhuyzen AA, Wheelwright S, Bartels M, Boomsma DI, Baron-Cohen S, Posthuma D, van der Sluis S. {{The Construction and Validation of an Abridged Version of the Autism-Spectrum Quotient (AQ-Short)}}. {J Autism Dev Disord};2011 (May);41(5):589-596.

This study reports on the development and validation of an abridged version of the 50-item Autism-Spectrum Quotient (AQ), a self-report measure of autistic traits. We aimed to reduce the number of items whilst retaining high validity and a meaningful factor structure. The item reduction procedure was performed on data from 1,263 Dutch students and general population adults. The resulting 28-item AQ-Short was subsequently validated in 3 independent samples, both clinical and controls, from the Netherlands and the UK. The AQ-Short comprises two higher-order factors assessing ‘social behavioral difficulties’ and ‘a fascination for numbers/patterns’. The clear factor structure of the AQ-Short and its high sensitivity and specificity make the AQ-Short a useful alternative to the full 50-item version.

27. Jepson B, Granpeesheh D, Tarbox J, Olive ML, Stott C, Braud S, Yoo JH, Wakefield A, Allen MS. {{Controlled evaluation of the effects of hyperbaric oxygen therapy on the behavior of 16 children with autism spectrum disorders}}. {J Autism Dev Disord};2011 (May);41(5):575-588.

Hyperbaric oxygen therapy (HBOT) has been used to treat individuals with autism. However, few studies of its effectiveness have been completed. The current study examined the effects of 40 HBOT sessions at 24% oxygen at 1.3 ATA on 11 topographies of directly observed behavior. Five replications of multiple baselines were completed across a total of 16 participants with autism spectrum disorders. No consistent effects were observed across any group or within any individual participant, demonstrating that HBOT was not an effective treatment for the participants in this study. This study represents the first relatively large-scale controlled study evaluating the effects of HBOT at the level of the individual participant, on a wide array of behaviors.

28. Kikuchi Y, Senju A, Akechi H, Tojo Y, Osanai H, Hasegawa T. {{Atypical disengagement from faces and its modulation by the control of eye fixation in children with autism spectrum disorder}}. {J Autism Dev Disord};2011 (May);41(5):629-645.

By using the gap overlap task, we investigated disengagement from faces and objects in children (9-17 years old) with and without autism spectrum disorder (ASD) and its neurophysiological correlates. In typically developing (TD) children, faces elicited larger gap effect, an index of attentional engagement, and larger saccade-related event-related potentials (ERPs), compared to objects. In children with ASD, by contrast, neither gap effect nor ERPs differ between faces and objects. Follow-up experiments demonstrated that instructed fixation on the eyes induces larger gap effect for faces in children with ASD, whereas instructed fixation on the mouth can disrupt larger gap effect in TD children. These results suggest a critical role of eye fixation on attentional engagement to faces in both groups.

29. King CR. {{A novel embryological theory of autism causation involving endogenous biochemicals capable of initiating cellular gene transcription: A possible link between twelve autism risk factors and the autism ‘epidemic’}}. {Med Hypotheses};2011 (May);76(5):653-660.

Human alpha-fetoprotein is a pregnancy-associated protein with an undetermined physiological role. As human alpha-fetoprotein binds retinoids and inhibits estrogen-dependent cancer cell proliferation, and because retinoic acid (a retinol metabolite) and estradiol (an estrogen) can both initiate cellular gene transcription, it is hypothesized here that alpha-fetoprotein functions during critical gestational periods to prevent retinoic acid and maternal estradiol from inappropriately stimulating gene expression in developing brain regions which are sensitive to these chemicals. Prenatal/maternal factors linked to increased autism risk include valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism. It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol – whether by direct promotion or by reducing production of alpha-fetoprotein. It is thus hypothesized here that autism is not a genetic disorder, but is rather an epigenetic disruption in brain development caused by gestational exposure to chemicals and/or conditions which either inhibit alpha-fetoprotein production or directly promote retinoic acid-sensitive or estradiol-sensitive gene expression. This causation model leads to potential chemical explanations for autistic brain morphology, the distinct symptomatology of Asperger’s syndrome, and the differences between high-functioning and low-functioning autisms with regard to mental retardation, physical malformation, and sex ratio. It will be discussed how folic acid may cause autism under the retinoic acid/estradiol model, and the history of prenatal folic acid supplementation will be shown to coincide with the history of what is popularly known as the autism epidemic. It is thus hypothesized here that prenatal folic acid supplementation has contributed to the post-1980 increase in US autism diagnoses. In addition to explaining the epidemic within the wider retinoic acid/estradiol model of causation, this theory leads to potential explanations for certain genetic findings in autism, autistic regression, and changing trends in autism symptomatology with regard to mental retardation, wheat allergy, and gastrointestinal problems.

30. Lewis S. {{Autism: Grooming mice to model autism}}. {Nat Rev Neurosci};2011 (May);12(5):248-249.

31. Lyall K, Pauls DL, Santangelo S, Spiegelman D, Ascherio A. {{Maternal Early Life Factors Associated with Hormone Levels and the Risk of Having a Child with an Autism Spectrum Disorder in the Nurses Health Study II}}. {J Autism Dev Disord};2011 (May);41(5):618-627.

It is not known whether reproductive factors early in the mother’s life influence risk of autism spectrum disorders (ASD). We assessed maternal age at menarche, menstrual cycle characteristics during adolescence, oral contraceptive use prior to first birth, body shape, and body mass index (BMI) in association with ASD using binomial regression in a cohort study of 61,596 women, including 743 cases. Overall, early life factors were not associated with ASD, though early age at menarche (RR for age 10 or less = 1.54, 95% CI 1.18, 2.02, p = 0.0002) and BMI at age 18 of >/=30 (RR 2.03, 95% CI 1.34, 3.08, p = 0.0008) were significantly associated with increased risk of ASD. Further work should investigate the potential influence of these factors.

32. Lyall K, Pauls DL, Santangelo SL, Spiegelman D, Ascherio A. {{Erratum to: Maternal Early Life Factors Associated with Hormone Levels and the Risk of Having a Child with an Autism Spectrum Disorder in the Nurses Health Study II}}. {J Autism Dev Disord};2011 (May);41(5):628.

33. Marco EJ, Hinkley LB, Hill SS, Nagarajan SS. {{Sensory processing in autism: a review of neurophysiologic findings}}. {Pediatr Res};2011 (May);69(5 Pt 2):48R-54R.

Atypical sensory-based behaviors are a ubiquitous feature of autism spectrum disorders (ASDs). In this article, we review the neural underpinnings of sensory processing in autism by reviewing the literature on neurophysiological responses to auditory, tactile, and visual stimuli in autistic individuals. We review studies of unimodal sensory processing and multisensory integration that use a variety of neuroimaging techniques, including electroencephalography (EEG), magnetoencephalography (MEG), and functional MRI. We then explore the impact of covert and overt attention on sensory processing. With additional characterization, neurophysiologic profiles of sensory processing in ASD may serve as valuable biomarkers for diagnosis and monitoring of therapeutic interventions for autism and reveal potential strategies and target brain regions for therapeutic interventions. ABBREVIATIONS::

34. Meyer U, Feldon J, Dammann O. {{Schizophrenia and autism: both shared and disorder-specific pathogenesis via perinatal inflammation?}}. {Pediatr Res};2011 (May);69(5 Pt 2):26R-33R.

Prenatal exposure to infection and subsequent inflammatory responses have been implicated in the etiology of schizophrenia and autism. In this review, we summarize current evidence from human and animal studies supporting the hypothesis that the pathogenesis of these two disorders is linked via exposure to inflammation at early stages of development. Moreover, we propose a hypothetical model in which inflammatory mechanisms may account for multiple shared and disorder-specific pathological characteristics of both entities. In essence, our model suggests that acute neuroinflammation during early fetal development may be relevant for the induction of psychopathological and neuropathological features shared by schizophrenia and autism, whereas postacute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively. ABBREVIATIONS::

35. Mironov SL, Skorova EY, Kugler S. {{Epac-mediated cAMP-signalling in the mouse model of Rett Syndrome}}. {Neuropharmacology};2011 (May);60(6):869-877.

Rett Syndrome (RTT) is a neurodevelopmental disease thought to be caused by deficits in synaptogenesis and neuronal circuitry. cAMP is one of the key factors for neuronal outgrowth, plasticity and regeneration. We examined its homeostasis in RTT during early postnatal development of the essential part of the respiratory network, pre-Botzinger complex. Using targeted expression of Epac1-camps sensor in neurons we quantified cAMP levels and their fluctuations in MeCP2-/y mice, an established model of RTT. Resting cAMP levels in the mutant were smaller than in the wild-type. cAMP transients elicited by depolarisation and stimulation of adenylate cyclase had also smaller amplitudes and faster time-courses. The anomalies in MeCP2 -/y mice were removed after inhibition of phosphodiesterase PDE4 with rolipram. Brief cAMP elevations triggered elongation of neuronal processes that was significantly bigger in the wild-type. The effects were observed after inhibition of protein kinase A and mimicked by activation of a guanine nucleotide exchange factor, Epac, with 8-(4-Chlorophenylthio)-2′-O-methyladenosine-3′,5′-cyclic monophosphate (8-pCPT). The agonist reinforced bursting in preBotC neurons in the mutant and converted it to the wild-type. All actions of 8-pCPT were not reproduced by its non-active analogue and abolished by Epac signalling inhibitor Brefeldin A. We propose that disturbances in cAMP homeostasis in MeCP2 -/y mice can lead to inadequate Epac signalling. Concomitant defective development of respiratory circuits may be responsible for irregular breathing activity in RTT.

36. Mouridsen SE, Rich B, Isager T. {{A longitudinal study of epilepsy and other central nervous system diseases in individuals with and without a history of infantile autism}}. {Brain Dev};2011 (May);33(5):361-366.

Objective: To compare the prevalence and types of epilepsy and other central nervous system (CNS) diseases in a clinical sample of 118 individuals diagnosed as children with infantile autism (IA) with 336 matched controls from the general population. Methods: All participants were screened through the nationwide Danish National Hospital Register (DNHR). The average observation time was 30.3years (range 27-30years), and mean age at follow-up was 42.7years (range 27-57years). Results: Of the 118 individuals with IA, 29 (24.6%) were registered with at least one epilepsy diagnosis against 5 (1.5%) in the comparison group (p<0.0001; OR=21.6; 95% CI 8.1-57.3). Other CNS diseases occurred with low frequency in both groups and only cerebral palsy, unspecified (p=0.02) was significantly more frequent among participants with a history of IA. Conclusions: Our study lends further support to the notion that epilepsy, but not other CNS diseases, is a common comorbid condition in IA. Low intelligence, but not gender, was a risk factor for epilepsy in IA. 37. Nickl-Jockschat T, Michel TM. {{The role of neurotrophic factors in autism}}. {Mol Psychiatry};2011 (May);16(5):478-490. Autism spectrum disorders (ASDs) are pervasive developmental disorders that frequently involve a triad of deficits in social skills, communication and language. For the underlying neurobiology of these symptoms, disturbances in neuronal development and synaptic plasticity have been discussed. The physiological development, regulation and survival of specific neuronal populations shaping neuronal plasticity require the so-called 'neurotrophic factors' (NTFs). These regulate cellular proliferation, migration, differentiation and integrity, which are also affected in ASD. Therefore, NTFs have gained increasing attention in ASD research. This review provides an overview and explores the key role of NTFs in the aetiology of ASD. We have also included evidence derived from neurochemical investigations, gene association studies and animal models. By focussing on the role of NTFs in ASD, we intend to further elucidate the puzzling aetiology of these conditions. 38. Ooi YP, Tan ZJ, Lim CX, Goh TJ, Sung M. {{Prevalence of behavioural and emotional problems in children with high-functioning autism spectrum disorders}}. {Aust N Z J Psychiatry};2011 (May);45(5):370-375. Objective: The goal of the present study was to examine the prevalence of behavioural and emotional problems among children with high-functioning autism spectrum disorders (ASD). Method: Archival data from a total of 71 children (Mage = 10.24, SD = 2.91) diagnosed by their clinicians to have high-functioning ASD were obtained. Information on demographics and behavioural and emotional problems from the Child Behavioural Checklist (CBCL) were entered. Results: We found that between 72% and 86% of children with high-functioning ASD had at least one behavioural or emotional problem of clinical concerns as indicated by the CBCL syndromes and DSM-oriented scales. The most commonly reported problems were social problems (60.6%), thought problems (50.7%), attention problems (49.3%), and withdrawn/depressed (40.8%). Using the DSM-oriented scales, the most commonly reported problems were attention deficit/hyperactivity problems (35.2%), anxiety problems (33.8%) and affective problems (31%). Conclusions: Findings from the present study provide further evidence to support the high prevalence of behavioural and emotional problems, which could result in multiple psychiatric diagnoses among children with high-functioning ASD. 39. Palmer E, Ketteridge C, Parr JR, Baird G, Le Couteur A. {{Autism spectrum disorder diagnostic assessments: improvements since publication of the National Autism Plan for Children}}. {Arch Dis Child};2011 (May);96(5):473-475. Objectives To assess in the context of a publically funded healthcare system, change in UK autism spectrum disorder (ASD) clinical diagnostic practice following the recommendations of the National Autism Plan for Children (NAP-C 2003). Methods In 2007, a questionnaire based on standards from the NAP-C was sent to UK child development teams (CDTs); results were compared with 2001 data from the National Initiative for Autism Screening and Assessment. Main findings Responses were received from 149 of 243 UK CDTs (61%). Most teams used standardised autism diagnostic assessments. There was greater access to members of the multidisciplinary team than in 2001. Only one-third of teams had a defined timescale for completion of assessment; of those teams, about half met the recommended NAP-C target. Conclusions Since 2001, there has been an improvement in diagnostic services for children with ASD, however, inequalities remain. Providers should continue to improve services in order to deliver timely and comprehensive assessments for children with ASD. 40. Patterson PH. {{Modeling autistic features in animals}}. {Pediatr Res};2011 (May);69(5 Pt 2):34R-40R. A variety of features of autism can be simulated in rodents, including the core behavioral hallmarks of stereotyped and repetitive behaviors, and deficits in social interaction and communication. Other behaviors frequently found in autism spectrum disorders (ASDs) such as neophobia, enhanced anxiety, abnormal pain sensitivity and eye blink conditioning, disturbed sleep patterns, seizures, and deficits in sensorimotor gating are also present in some of the animal models. Neuropathology and some characteristic neurochemical changes that are frequently seen in autism, and alterations in the immune status in the brain and periphery are also found in some of the models. Several known environmental risk factors for autism have been successfully established in rodents, including maternal infection and maternal valproate administration. Also under investigation are a number of mouse models based on genetic variants associated with autism or on syndromic disorders with autistic features. This review briefly summarizes recent developments in this field, highlighting models with face and/or construct validity, and noting the potential for investigation of pathogenesis, and early progress toward clinical testing of potential therapeutics. Wherever possible, reference is made to reviews rather than to primary articles. ABBREVIATIONS:: 41. Ray-Subramanian CE, Huai N, Ellis Weismer S. {{Brief report: adaptive behavior and cognitive skills for toddlers on the autism spectrum}}. {J Autism Dev Disord};2011 (May);41(5):679-684. This study examined adaptive behavior and cognitive skills for 125 toddlers on the autism spectrum using the recently updated Vineland-II and Bayley-III. Delays in adaptive skills were apparent at 2 years of age. As a group, toddlers on the autism spectrum had a profile of Vineland-II standard scores in which Motor Skills > Daily Living Skills > Socialization > Communication. Vineland-II scores were significantly correlated with Bayley-III Cognitive scores. Performance on the ADOS was significantly negatively correlated with Bayley-III Cognitive standard scores and standard scores in the Daily Living Skills and Communication domains of the Vineland-II. However, calibrated ADOS scores did not contribute significant variance to Vineland-II scores beyond that predicted by age and Bayley-III scores.

42. Reed P, Clark C. {{Impact of intervening learning on resurgence in humans with Autism Spectrum Disorders}}. {Learn Behav};2011 (May);39(2):163-170.

In the present study, we investigated the degree to which responding would resurge in children diagnosed with Autism Spectrum Disorders (ASD) following an intervening training period comprising different schedules of reinforcement. Twenty-four children of the ages 7-15, with a diagnosis of an ASD, were taught a play a sequence on a variable ratio- (VR) 3 schedule of reinforcement, during a 30-min session. The play sequence was then extinguished before the participants were taught a second play sequence, using a VR-4 schedule for 30 min, a VR-4 schedule for 60 min, or a VR-2 schedule for 30 min. A 5-min extinction session was then conducted to determine the impact that the intervening schedules had on the resurgence of the original behavior. The original sequence resurged to a greater extent for Group VR-4 30 min than it did for the other two groups. The results provide evidence that the length of time between initial training and testing is not a prime determinant of the level of resurgence, but that the amount of conditioning may play a stronger role: The greater the number of reinforcers received, the smaller the resurgence effect.

43. Rommelse NN, Geurts HM, Franke B, Buitelaar JK, Hartman CA. {{A review on cognitive and brain endophenotypes that may be common in autism spectrum disorder and attention-deficit/hyperactivity disorder and facilitate the search for pleiotropic genes}}. {Neurosci Biobehav Rev};2011 (May);35(6):1363-1396.

We propose to bring together the hitherto rather separate research fields of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), and argue that by contrasting and combining findings of the endophenotypes of ASD and ADHD new insights can be gained into the etiology and pathophysiology of these two disorders. Given the highly heritable nature of both disorders, studies of the genes explaining the shared origins of the two neurodevelopmental disorders seem particularly called for. Instead of the clinical diagnosis, using neurocognitive measures as (endo)phenotypes that index genetic liability appears a powerful tool in gene finding. We, therefore, extensively reviewed the literature and not only included research wherein ASD and ADHD were compared within a single study, but extended our search also to the separate lines of cognitive neuroscience research. We discuss which cognitive and brain measures will be useful in future genetic studies targeting pleiotropic genes for ASD and ADHD. By specifying the most promising endophenotypic measures we chart the future course for endophenotypic research in ASD and ADHD. We also discuss the various models that may explain the frequent co-occurrence of ASD and ADHD.

44. Sala M, Braida D, Lentini D, Busnelli M, Bulgheroni E, Capurro V, Finardi A, Donzelli A, Pattini L, Rubino T, Parolaro D, Nishimori K, Parenti M, Chini B. {{Pharmacologic rescue of impaired cognitive flexibility, social deficits, increased aggression, and seizure susceptibility in oxytocin receptor null mice: a neurobehavioral model of autism}}. {Biol Psychiatry};2011 (May 1);69(9):875-882.

BACKGROUND: Oxytocin (OT) has been suggested as a treatment to improve social behavior in autistic patients. Accordingly, the OT (Oxt(-/-)) and the OT receptor null mice (Oxtr(-/-)) display autistic-like deficits in social behavior, increased aggression, and reduced ultrasonic vocalization. METHODS: Oxtr(-/-) mice were characterized for general health, sociability, social novelty, cognitive flexibility, aggression, and seizure susceptibility. Because vasopressin (AVP) and OT cooperate in controlling social behavior, learning, and aggression, they were tested for possible rescue of the impaired behaviors. Primary hyppocampal cultures from Oxtr(+/+) and Oxtr(-/-) mouse embryos were established to investigate the balance between gamma-aminobutyric acid (GABA) and glutamate synapses and the expression levels of OT and AVP (V1a) receptors were determined by autoradiography. RESULTS: Oxtr(-/-) mice display two additional, highly relevant, phenotypic characteristics: 1) a resistance to change in a learned pattern of behavior, comparable to restricted interests and repetitive behavior in autism, and 2) an increased susceptibility to seizures, a frequent and clinically relevant symptom of autism. We also show that intracerebral administration of both OT and AVP lowers aggression and fully reverts social and learning defects by acting on V1a receptors and that seizure susceptibility is antagonized by peripherally administered OT. Finally, we detect a decreased ratio of GABA-ergic versus total presynapses in hippocampal neurons of Oxtr(-/-) mice. CONCLUSIONS: Autistic-like symptoms are rescued on administration of AVP and OT to young Oxtr(-/-) adult animals. The Oxtr(-/-) mouse is thus instrumental to investigate the neurochemical and synaptic abnormalities underlying autistic-like disturbances and to test new strategies of pharmacologic intervention.

45. Taylor JL, Seltzer MM. {{Employment and post-secondary educational activities for young adults with autism spectrum disorders during the transition to adulthood}}. {J Autism Dev Disord};2011 (May);41(5):566-574.

This report describes the post-high school educational and occupational activities for 66 young adults with autism spectrum disorders who had recently exited the secondary school system. Analyses indicated low rates of employment in the community, with the majority of young adults (56%) spending time in sheltered workshops or day activity centers. Young adults with ASD without an intellectual disability were three times more likely to have no daytime activities compared to adults with ASD who had an intellectual disability. Differences in behavioral functioning were observed by employment/day activity group. Our findings suggest that the current service system may be inadequate to accommodate the needs of youths with ASD who do not have intellectual disabilities during the transition to adulthood.

46. Verity CM, Stellitano LS, Winstone AM. {{The PIND study found no association between vaccination and autism in mitochondrial disease – correction}}. {Dev Med Child Neurol};2011 (May);53(5):477.

47. Whitehouse AJ, Maybery M, Wray JA, Hickey M. {{No association between early gastrointestinal problems and autistic-like traits in the general population}}. {Dev Med Child Neurol};2011 (May);53(5):457-462.

Aim The aim of this study was to determine whether gastrointestinal problems in early childhood relate to autistic-like traits in a general population sample. Method The parents of 804 children (442 females; 362 males) reported at 1-, 2-, 3-, and 5-year follow-ups whether their child had been taken to a hospital, general practitioner, or health clinic for any of five gastrointestinal symptoms: (1) constipation; (2) diarrhoea; (3) abdominal bloating, discomfort, or irritability; (4) gastro-oesophageal reflux or vomiting; and (5) feeding issues or food selectivity. Parents also reported whether their child had received the measles, mumps, and rubella vaccination. Autistic-like traits were measured when the children had reached early adulthood (mean age 19y 7mo; SD 0.63y) using a self-report questionnaire, the Autism Spectrum Quotient (AQ). Results There was no statistically significant difference in AQ scores between those who had (n=133) and those who had not (n=671) experienced early gastrointestinal symptoms. chi(2) analyses revealed that the children with early gastrointestinal problems were no more likely to be represented in the upper quintile of scores on any of the AQ scales. The measles, mumps, and rubella vaccination was unrelated to gastrointestinal symptoms or AQ scores. Interpretation Parent-reported gastrointestinal problems in early childhood are unrelated to self-reported autistic-like traits in the general population.

48. Zhu H, Sun Y, Zeng J, Sun H. {{Mirror neural training induced by virtual reality in brain-computer interfaces may provide a promising approach for the autism therapy}}. {Med Hypotheses};2011 (May);76(5):646-647.

Previous studies have suggested that the dysfunction of the human mirror neuron system (hMNS) plays an important role in the autism spectrum disorder (ASD). In this work, we propose a novel training program from our interdisciplinary research to improve mirror neuron functions of autistic individuals by using a BCI system with virtual reality technology. It is a promising approach for the autism to learn and develop social communications in a VR environment. A test method for this hypothesis is also provided.

49. Zwaigenbaum L, Howarth B. {{For toddlers with autism spectrum disorders, supplementing a comprehensive intervention with interpersonal synchrony improves socially engaged imitation}}. {Evid Based Ment Health};2011 (May);14(2):54.