1. Banji D, Banji OJ, Abbagoni S, Hayath MS, Kambam S, Chiluka VL. {{Amelioration of behavioral aberrations and oxidative markers by green tea extract in valproate induced autism in animals}}. {Brain Res}. 2011 Sep 2;1410:141-51.
Exposure to toxicants prenatally and postnatally could have deleterious consequences on the offspring. Postnatal exposure to valproate in mice pups is capable of inducing experimental autism resulting in neurobehavioral aberrations. Consumption of green tea has been associated with neuronal protection against the impact of toxicants. We investigated the role of green tea extract in reversing cardinal behavioral changes and aberrations in oxidative stress induced by valproate exposure. Young mice of both genders received a single dose of valproate (400mg/kg subcutaneously) on postnatal day 14 followed by a daily dose of green tea extract (75 and 300mg/kg) orally up to postnatal day 40. Mice pups were subjected to behavioral testing to assess motor co-ordination, nociceptive response, locomotion, anxiety, exploratory activity and cognition on various postnatal days up to postnatal day 40. At the end of behavioral testing, blood was withdrawn from the retro orbital plexus for the estimation of lipid peroxides. Animals were sacrificed on postnatal day 41 and whole brain was subjected to histopathological examination. Our studies revealed a significant improvement in behavioral assessments particularly with 300mg/kg of green tea extract. Formation of markers of oxidative stress was reduced at both dose levels. Histological findings confirm the neuroprotective effect of green tea at a dose of 300mg/kg. In conclusion it can be stated that green tea exerts neuronal cytoprotective action possibly due to anti-oxidant action and could be efficacious in the management of autism.
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2. Bernhardt EB, Walsh KH, Posey DJ, McDougle CJ. {{Memantine for comorbid obsessive-compulsive disorder and asperger disorder suggests a link in glutamatergic dysregulation}}. {J Clin Psychopharmacol}. 2011 Oct;31(5):673-5.
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3. Bishop SL, Lahvis GP. {{The autism diagnosis in translation: shared affect in children and mouse models of ASD}}. {Autism Res}. 2011 Aug 31.
In the absence of molecular biomarkers that can be used to diagnose ASD, current diagnostic tools depend upon clinical assessments of behavior. Research efforts with human subjects have successfully utilized standardized diagnostic instruments, which include clinician interviews with parents and direct observation of the children themselves [Risi et al., 2006]. However, because clinical instruments are semi-structured and rely heavily on dynamic social processes and clinical skill, scores from these measures do not necessarily lend themselves directly to experimental investigations into the causes of ASD. Studies of the neurobiology of autism require experimental animal models. Mice are particularly useful for elucidating genetic and toxicological contributions to impairments in social function [Halladay et al., 2009]. Behavioral tests have been developed that are relevant to autism [Crawley, 2004, 2007], including measures of repetitive behaviors [Lewis, Tanimura, Lee, & Bodfish, 2007; Moy et al., 2008], social behavior [Brodkin, 2007; Lijam et al., 1997; Moretti, Bouwknecht, Teague, Paylor, & Zoghbi, 2005], and vocal communication [D’Amato et al., 2005; Panksepp et al., 2007; Scattoni et al., 2008]. Advances also include development of high-throughput measures of mouse sociability that can be used to reliably compare inbred mouse strains [Moy et al., 2008; Nadler et al., 2004], as well as measures of social reward [Panksepp & Lahvis, 2007] and empathy [Chen, Panksepp, & Lahvis, 2009; Langford et al., 2006]. With continued generation of mouse gene-targeted mice that are directly relevant to genetic linkages in ASD, there remains an urgent need to utilize a full suite of mouse behavioral tests that allows for a comprehensive assessment of the spectrum of social difficulties relevant to ASD. Using impairments in shared affect as an example, this paper explores potential avenues for collaboration between clinical and basic scientists, within an amply considered translational framework. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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4. David N, T RS, Vogeley K, Engel AK. {{Impairments in multisensory processing are not universal to the autism spectrum: no evidence for crossmodal priming deficits in Asperger syndrome}}. {Autism Res}. 2011 Aug 31.
Individuals suffering from autism spectrum disorders (ASD) often show a tendency for detail- or feature-based perception (also referred to as « local processing bias ») instead of more holistic stimulus processing typical for unaffected people. This local processing bias has been demonstrated for the visual and auditory domains and there is evidence that multisensory processing may also be affected in ASD. Most multisensory processing paradigms used social-communicative stimuli, such as human speech or faces, probing the processing of simultaneously occuring sensory signals. Multisensory processing, however, is not limited to simultaneous stimulation. In this study, we investigated whether multisensory processing deficits in ASD persist when semantically complex but nonsocial stimuli are presented in succession. Fifteen adult individuals with Asperger syndrome and 15 control persons participated in a visual-audio priming task, which required the classification of sounds that were either primed by semantically congruent or incongruent preceding pictures of objects. As expected, performance on congruent trials was faster and more accurate compared with incongruent trials (crossmodal priming effect). The Asperger group, however, did not differ significantly from the control group. Our results do not support a general multisensory processing deficit, which is universal to the entire autism spectrum. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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5. Demb H, Valicenti-McDermott M, Navarro A, Ayoob KT. {{The effect of long-term use of risperidone on body weight of children with an autism spectrum disorder}}. {J Clin Psychopharmacol}. 2011 Oct;31(5):669-70.
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6. Ellegood J, Lerch JP, Henkelman RM. {{Brain abnormalities in a Neuroligin3 R451C knockin mouse model associated with autism}}. {Autism Res}. 2011 Aug 31.
Magnetic resonance imaging (MRI) has been used quite extensively for examining morphological changes in human and animal brains. One of the many advantages to examining mouse models of human autism is that we are able to examine single gene targets, like that of Neuroligin3 R451C knockin (NL3 KI), which has been directly implicated in human autism. The NL3 KI mouse model has marked volume differences in many different structures in the brain: gray matter structures, such as the hippocampus, the striatum, and the thalamus, were all found to be smaller in the NL3 KI. Further, many white matter structures were found to be significantly smaller, such as the cerebral peduncle, corpus callosum, fornix/fimbria, and internal capsule. Fractional anisotropy measurements in these structures were also measured, and no differences were found. The volume changes in the white matter regions, therefore, are not due to a general breakdown in the microstructure of the tissue and seem to be caused by fewer axons or less mature axons. A larger radial diffusivity was also found in localized regions of the corpus callosum and cerebellum. The corpus callosal changes are particularly interesting as the thinning (or reduced volume) of the corpus callosum is a consistent finding in autism. This suggests that the NL3 KI model may be useful for examining white matter changes associated with autism. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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7. Flores CG, Valcante G, Guter S, Zaytoun A, Wray E, Bell L, et al. {{Repetitive behavior profiles: Consistency across autism spectrum disorder cohorts and divergence from Prader-Willi syndrome}}. {J Neurodev Disord}. 2011 Sep 1.
Restricted and repetitive behavior (RRB) is a group of heterogeneous maladaptive behaviors. RRB is one of the key diagnostic features of autism spectrum disorders (ASDs) and also commonly observed in Prader-Willi syndrome (PWS). In this study, we assessed RRB using the Repetitive Behavior Scale-Revised (RBS-R) in two ASD samples (University of Illinois at Chicago [UIC] and University of Florida [UF]) and one PWS sample. We compared the RBS-R item endorsements across three ASD cohorts (UIC, UF and an ASD sample from Lam, The Repetitive Behavior Scale-Revised: independent validation and the effect of subject variables, PhD thesis, 2004), and a PWS sample. We also compared the mean RBS-R subscale/sum scores across the UIC, UF and PWS samples; across the combined ASD (UIC + UF), PWS-deletion and PWS-disomy groups; and across the combined ASD sample, PWS subgroup with a Social Communication Questionnaire (SCQ) score >/=15, and PWS subgroup with a SCQ score <15. Despite the highly heterogeneous nature, the three ASD samples (UIC, UF and Lam’s) showed a similar pattern of the RBS-R endorsements, and the mean RBS-R scores were not different between the UIC and UF samples. However, higher RRB was noted in the ASD sample compared with the PWS sample, as well as in the PWS subgroup with a SCQ score >/=15 compared with the PWS subgroup with a SCQ score <15. Study limitations include a small sample size, a wide age range of our participants, and not controlling for potential covariates. A future replication study using a larger sample and further investigation into the genetic bases of overlapping ASD and RRB phenomenology are needed, given the higher RRB in the PWS subgroup with a SCQ score >/=15.
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8. Geluk CA, Jansen LM, Vermeiren R, Doreleijers TA, van Domburgh L, de Bildt A, et al. {{Autistic symptoms in childhood arrestees: longitudinal association with delinquent behavior}}. {J Child Psychol Psychiatry}. 2011 Sep 2.
Background: To compare childhood arrestees with matched comparison groups on levels of autistic symptoms and to assess the unique predictive value of autistic symptoms for future delinquent behavior in childhood arrestees. Methods: Childhood first-time arrestees (n = 308, baseline age 10.7 +/- 1.5 years) were followed up for 2 years. Autistic symptoms, externalizing disorders and delinquent behavior were assessed yearly. Childhood arrestees were compared on autistic symptoms with matched (age, gender) general population and clinical autism spectrum disorder samples. The predictive value of autistic symptoms for delinquent behavior was analyzed using generalized estimating equations. Results: At each assessment, levels of autistic symptoms in childhood arrestees were in between levels found in the general population and autism spectrum disorder samples. Autistic symptoms were positively associated with delinquent behavior in childhood arrestees, even after adjustment for externalizing disorders: IRR (incidence rate ratio) 1.23; 95% CI 1.11-1.36 and IRR 1.29; 95% CI 1.15-1.45 for core autistic symptoms and total symptom score, respectively. Conclusions: Autistic symptoms are more prevalent in childhood arrestees compared to the general population and are uniquely associated with future delinquent behavior. Attention should, therefore, be given to the possible presence of autism related symptomatology in these children. Implications for diagnostic assessment and intervention need further investigation.
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9. Higashida H, Yokoyama S, Munesue T, Kikuchi M, Minabe Y, Lopatina O. {{CD38 gene knockout juvenile mice: a model of oxytocin signal defects in autism}}. {Biol Pharm Bull}. 2011;34(9):1369-72.
Oxytocin (OXT) in the hypothalamus is the biological basis of social recognition, trust, and bonding. We showed that CD38, a leukaemia cell marker, plays an important role in the hypothalamus in the process of OXT release in adult mice. Disruption of Cd38 (Cd38(-/-)) produced impairment of maternal behavior and male social recognition in mice, similar to the behavior observed in Oxt and OXT receptor (Oxtr) gene knockout (Oxt(-/-) and Oxtr(-/-), respectively) mice. Locomotor activity induced by separation from the dam was higher and the number of ultrasonic vocalization (USV) calls was lower in Cd38(-/-) than Cd38(+/+) pups. These phenotypes seemed to be caused by the high plasma OXT levels during development from neonates to 3-week-old juvenile mice. ADP-ribosyl cyclase activity was markedly lower in the knockout mice from birth, suggesting that weaning for mice is a critical time window of differentiating plasma OXT. Contribution by breastfeeding was an important exogenous source for regulating plasma OXT before weaning by the presence of OXT in milk and the dam’s mammary glands. The dissimilarity of Cd38(-/-) infant behaviour to Oxt(-/-) or Oxtr(-/-) mice can be explained partly by this exogenous source of OXT. These results suggest that secretion of OXT into the brain in a CD38-dependent manner may play an important role in the development of social behavior, and mice with OXT signalling deficiency, including Cd38(-/-), Oxt(-/-) and Oxtr(-/-) mice are good animal models for developmental disorders, such as autism.
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10. Hoshiko S, Grether JK, Windham GC, Smith D, Fessel K. {{Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis?}}. {Autism Res}. 2011 Aug 31.
Thyroid hormones substantially influence central nervous system development during gestation. We hypothesized that perturbations of early thyroid profiles may contribute to the development of autism spectrum disorders (ASD). Thyroid pathways could provide a mechanism by which environmental factors that affect the thyroid system may impact autism occurrence or phenotypic expression. We investigated whether thyroxine (T4) levels at birth are associated with subsequent ASD, using two existing California study groups in multivariate analysis. One study group included children born in the San Francisco Bay Area in 1994, with cases identified through the California Department of Developmental Services (DDS) and/or the Kaiser Permanente Medical Care Program of Northern California (244 cases, 266 controls); the other included children born in California in 1995, with cases identified through DDS (310 cases, 518 controls). Matched controls were selected from birth certificate records. This exploratory analysis suggested that infants with very low T4 (<3rd percentile) may have higher ASD risk, although results reached statistical significance only for the 1995 study group (1995: OR = 2.74 (95% CI 1.30-5.75; 1994: OR = 1.71 (95% CI 0.57-5.19). A variety of alternate analyses were conducted with available data, without further resolution of the difference between the two study groups. The results of our study indicate that further studies are warranted to investigate whether thyroid hormone perturbations play a role in the development of ASD by evaluating additional potential confounders and genotype or phenotype in larger studies. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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11. Jacome LF, Burket JA, Herndon AL, Deutsch SI. {{Genetically inbred Balb/c mice differ from outbred Swiss Webster mice on discrete measures of sociability: relevance to a genetic mouse model of autism spectrum disorders}}. {Autism Res}. 2011 Aug 31.
The Balb/c mouse is proposed as a model of human disorders with prominent deficits of sociability, such as autism spectrum disorders (ASDs) that may involve pathophysiological disruption of NMDA receptor-mediated neurotransmission. A standard procedure was used to measure sociability in 8-week-old male genetically inbred Balb/c and outbred Swiss Webster mice. Moreover, because impaired sociability may influence the social behavior of stimulus mice, we also measured the proportion of total episodes of social approach made by the stimulus mouse while test and stimulus mice were allowed to interact freely. Three raters with good inter-rater agreement evaluated operationally defined measures of sociability chosen because of their descriptive similarity to deficits of social behavior reported in persons with ASDs. The data support previous reports that the Balb/c mouse is a genetic mouse model of impaired sociability. The data also show that the behavior of the social stimulus mouse is influenced by the impaired sociability of the Balb/c strain. Interestingly, operationally defined measures of sociability did not necessarily correlate with each other within mouse strain and the profile of correlated measures differed between strains. Finally, « stereotypic » behaviors (i.e. rearing, grooming and wall climbing) recorded during the session of free interaction between the test and social stimulus mice were more intensely displayed by Swiss Webster than Balb/c mice, suggesting that the domains of sociability and « restricted repetitive and stereotyped patterns of behavior » are independent of each other in the Balb/c strain. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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12. Matson ML, Matson JL, Beighley JS. {{Comorbidity of physical and motor problems in children with autism}}. {Res Dev Disabil}. 2011 Sep 2.
Autism and the related pervasive developmental disorders are a heavily researched group of neurodevelopmental conditions. In addition to core symptoms, there are a number of other physical and motor conditions that co-occur at high rates. This paper provides a review of factors and behaviors that correlate highly with disorders on the autism spectrum. Among these conditions are premature birth, birth defects, gross and fine motor skills, and obesity. Each of these topics is addressed, and what researchers have found are presented. These data have important implications for the types of collateral behaviors that should be assessed and treated, along with the core symptoms of autism.
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13. Meirsschaut M, Warreyn P, Roeyers H. {{What is the impact of autism on mother-child interactions within families with a child with autism spectrum disorder?}}. {Autism Res}. 2011 Aug 31.
This within-family study investigated whether mothers differentiate between children in their interactive behavior. Mothers were observed during a play and a task interaction separately with their child with autism spectrum disorder (ASD) (between 46 and 84 months old, M = 68) and with a younger sibling (between 29 and 67 months old, M = 48). Additionally, the social behavior of the children with ASD and their non-ASD siblings was compared. Results show that mothers differentiated in their responsiveness but not in their initiatives toward the children. Children with ASD and their non-ASD siblings were equally responsive but children with ASD were more imperative toward their caregiver. Several interpretations of these findings are discussed. Finally, it is concluded that family-based interventions will benefit from a better understanding of the effect of ASD on mother-child interactions within families with a child with ASD. Therefore, between-family studies should be complemented with within-family studies. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
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14. Tondo M, Poo P, Naudo M, Ferrando T, Genoves J, Molero M, et al. {{Predisposition to epilepsy in fragile X syndrome: Does the Val66Met polymorphism in the BDNF gene play a role?}}. {Epilepsy Behav}. 2011 Sep 2.
Epilepsy is detected in about 23% of patients with fragile X syndrome (FXS). Absence or reduced levels of the fragile X mental retardation protein (FMRP), a global regulator of translation in neurons and an important factor in synaptic plasticity, produce the observed epileptic patterns. The brain-derived neurotrophic factor (BDNF) gene is a specific regulator of synaptic plasticity, and disturbances in its function cause dendrite abnormalities similar to those observed in FXS. A putative reciprocal regulation of FMRP and BDNF has been hypothesized. The Val66Met polymorphism in the BDNF gene may be involved in the alteration of normal secretion of the mature peptide and may modulate the epileptic phenotype observed in some patients with FXS. We investigated the relationship of this Met66 allele to the prevalence of epilepsy in 77 patients with FXS. No association was observed between this polymorphism and epilepsy in our group of patients. Therefore, it should not be considered a biomarker for developing epilepsy in patients with FXS.
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15. Uddin LQ, Menon V, Young CB, Ryali S, Chen T, Khouzam A, et al. {{Multivariate Searchlight Classification of Structural Magnetic Resonance Imaging in Children and Adolescents with Autism}}. {Biol Psychiatry}. 2011 Sep 2.
BACKGROUND: Autism spectrum disorders (ASD) are neurodevelopmental disorders with a prevalence of nearly 1:100. Structural imaging studies point to disruptions in multiple brain areas, yet the precise neuroanatomical nature of these disruptions remains unclear. Characterization of brain structural differences in children with ASD is critical for development of biomarkers that may eventually be used to improve diagnosis and monitor response to treatment. METHODS: We use voxel-based morphometry along with a novel multivariate pattern analysis approach and searchlight algorithm to classify structural magnetic resonance imaging data acquired from 24 children and adolescents with autism and 24 age-, gender-, and IQ-matched neurotypical participants. RESULTS: Despite modest voxel-based morphometry differences, multivariate pattern analysis revealed that the groups could be distinguished with accuracies of approximately 90% based on gray matter in the posterior cingulate cortex, medial prefrontal cortex, and bilateral medial temporal lobes-regions within the default mode network. Abnormalities in the posterior cingulate cortex were associated with impaired Autism Diagnostic Interview communication scores. Gray matter in additional prefrontal, lateral temporal, and subcortical structures also discriminated between groups with accuracies between 81% and 90%. White matter in the inferior fronto-occipital and superior longitudinal fasciculi, and the genu and splenium of the corpus callosum, achieved up to 85% classification accuracy. CONCLUSIONS: Multiple brain regions, including those belonging to the default mode network, exhibit aberrant structural organization in children with autism. Brain-based biomarkers derived from structural magnetic resonance imaging data may contribute to identification of the neuroanatomical basis of symptom heterogeneity and to the development of targeted early interventions.
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16. Wang L, Li J, Jia M, Yue W, Ruan Y, Lu T, et al. {{No association of polymorphisms in the CDK5, NDEL1, and LIS1 with autism in Chinese Han population}}. {Psychiatry Res}. 2011 Sep 2.
Autism is a pervasive neurodevelopmental disorder. CDK5 (cyclin-dependent kinase 5) and its interacting molecules are involved in neurodevelopment. We performed a family-based association analysis between CDK5, NDEL1, and LIS1 polymorphisms and autism in Chinese Han population. Our study did not detect significant association. It indicated that common genetic variations in these genes might not play a role in the genetic predisposition to autism.
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17. Zaidman-Zait A, Mirenda P, Zumbo BD, Georgiades S, Szatmari P, Bryson S, et al. {{Factor analysis of the Parenting Stress Index-Short Form with parents of young children with autism spectrum disorders}}. {Autism Res}. 2011 Aug 31.
The primary purpose of this study was to examine the underlying factor structure of the Parenting Stress Index-Short Form (PSI-SF) in a large cohort of parents of young children with autism spectrum disorder (ASD). A secondary goal was to examine relationships between PSI-SF factors and autism severity, child behavior problems, and parental mental health variables that have been shown to be related to parental stress in previous research. A confirmatory factor analysis (CFA) was used to examine the three-factor structure described in the PSI-SF manual [Abidin, 1995]: parental distress, parent-child dysfunctional interaction, and difficult child. Results of the CFA indicated that the three-factor structure was unacceptable when applied to the study sample. Thus, an exploratory factor analysis was conducted and suggested a six-factor model as the best alternative for the PSI-SF index. Spearman’s correlations revealed significant positive correlations with moderate to large effect sizes between the revised PSI-SF factors and autism severity, externalizing and internalizing child behaviors, and an index of parent mental health. The revised factors represent more narrowly defined aspects of the three original subscales of the PSI-SF and might prove to be advantageous in both research and clinical applications. Autism Res 2011,4:xxx-xxx. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc.
