1. {{Monkey model of MECP2 duplication syndrome aids autism research: Monkeys genetically altered with extra copies of MECP2 are being used as a model for research into autism and MECP2 duplication syndrome}}. {Am J Med Genet A};2016 (May);170(5):1112-1113.
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2. Alrayes N, Mohamoud HS, Ahmed S, Almramhi MM, Shuaib TM, Wang J, Al-Aama JY, Everett K, Nasir J, Jelani M. {{The alkylglycerol monooxygenase (AGMO) gene previously involved in autism also causes a novel syndromic form of primary microcephaly in a consanguineous Saudi family}}. {J Neurol Sci};2016 (Apr 15);363:240-244.
Autosomal recessive primary microcephaly (MCPH) refers to a genetically heterogeneous group of neurodevelopmental disorders in which patients exhibit a marked decrease in occipitofrontal head circumference at birth and a variable degree of intellectual disability. To date, 18 genes have been reported for MCPH worldwide. We enrolled a consanguineous family from Saudi Arabia presenting with primary microcephaly, developmental delay, short stature and intellectual disability. Whole exome sequencing (WES) with 100x coverage was performed on two affected siblings after defining common regions of homozygosity through genome-wide single nucleotide polymorphism (SNP) microarray genotyping. WES data analysis, confirmed by subsequent Sanger sequence validation, identified a novel homozygous deletion mutation (c.967delA; p.Glu324Lysfs12*) in exon 10 of the alkylglycerol monooxygenase (AGMO) gene on chromosome 7p21.2. Population screening of 178 ethnically matched control chromosomes and consultation of the Exome Aggregation Consortium database, containing 60,706 individuals’ exomes worldwide, confirmed that this mutation was not present outside the family. To the best of our knowledge, this is the first evidence of an AGMO mutation underlying primary microcephaly and intellectual disability in humans. Our findings further expand the genetic heterogeneity of MCPH in familial cases.
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3. Been LE, Moore KM, Kennedy BC, Meisel RL. {{Metabotropic Glutamate Receptor and Fragile X Signaling in a Female Model of Escalated Aggression}}. {Biol Psychiatry};2016 (Apr 15);79(8):685-692.
BACKGROUND: Escalated aggression is a behavioral sign of numerous psychiatric disorders characterized by a loss of control. The neurobiology underlying escalated aggression is unknown and is particularly understudied in females. Research in our laboratory demonstrated that repeated aggressive experience in female hamsters resulted in an escalated response to future aggressive encounters and an increase in dendritic spine density on nucleus accumbens (NAc) neurons. We hypothesized that the activation of group I metabotropic glutamate receptor signaling though the fragile X mental retardation protein (FMRP) pathway may underlie synaptic plasticity associated with aggression escalation. METHODS: Female hamsters were given five daily aggression tests with or without prior treatment with the metabotropic glutamate receptor 5 (mGluR5) antagonist 2-methyl-6-(phenylethynyl)-pyridine. Following aggression testing, messenger RNA expression and protein levels were measured in the nucleus accumbens for postsynaptic density protein 95 (PSD-95) and SAP90/PSD-95-associated protein 3, as well as the levels of phosphorylated FMRP. RESULTS: Experience-dependent escalation of aggression in female hamsters depends on activation of mGluR5 receptors. Furthermore, aggressive experience decreases phosphorylation of FMRP in the NAc, which is coupled to a long-term increase in the expression of the synaptic scaffolding proteins PSD-95 and SAP90/PSD-95-associated protein 3. Finally, the experience-dependent increase in PSD-95 is prevented by antagonism of the mGluR5 receptor. CONCLUSIONS: Activation of the FMRP pathway by group I metabotropic glutamate receptors is involved in regulating synaptic plasticity following aggressive experience. The NAc is a novel target for preclinical studies of the treatment of escalated aggression, with the added benefit that emerging therapeutic approaches are likely to be effective in treating pathologic aggression in both female and male subjects.
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4. Bohland JW. {{Toward a Multimodal, Multiscale Understanding of White Matter Abnormalities in Autism Spectrum Disorder}}. {Biol Psychiatry};2016 (Apr 15);79(8):e47-48.
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5. Branigan HP, Tosi A, Gillespie-Smith K. {{Spontaneous Lexical Alignment in Children With an Autistic Spectrum Disorder and Their Typically Developing Peers}}. {J Exp Psychol Learn Mem Cogn};2016 (Apr 14)
It is well established that adults converge on common referring expressions in dialogue, and that such lexical alignment is important for successful and rewarding communication. The authors show that children with an autistic spectrum disorder (ASD) and chronological- and verbal-age-matched typically developing (TD) children also show spontaneous lexical alignment. In a card game, both groups tended to refer to an object using the same name as their partner had previously used for the same or a different token of the object. This tendency to align on a pragmatically conditioned aspect of language did not differ between ASD and TD groups, and was unaffected by verbal/chronological age, or (in the ASD group) Theory of Mind or social functioning. The authors suggest that lexical priming can lead to automatic lexical alignment in both ASD and TD children’s dialogue. Their results further suggest that ASD children’s conversational impairments do not involve an all-encompassing deficit in linguistic imitation. (PsycINFO Database Record
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6. Chong WH, Kua SM. {{Parenting Self-Efficacy Beliefs in Parents of Children With Autism: Perspectives From Singapore}}. {Am J Orthopsychiatry};2016 (Apr 14)
Substantial empirical evidence has highlighted the psychological stress and negative well-being of parents whose children are diagnosed with autism. It has further indicated a need for understanding the mechanisms through which these parents come to successfully meet the challenges of caregiving for these children whose condition are often characterized by persistent behavioral, social, and communication problems. This qualitative study aims to bridge the research gap in 3 ways. First, we sought to understand the ways in which mothers of children having autism foster their parenting self-efficacy (PSE) when caring for their child. Second, we sought to identify additional PSE sources. Third, we attempted to understand how these mothers successfully manage negative experiences that were often in the way of their parenting efforts. Ten mothers with children between 7 and 9 years of age were interviewed. Bandura’s social-cognitive framework guided the analyses of the sources of PSE (Bandura, 1997). Mastery experiences were identified as the most critical PSE source, and the physiological and affective states of the mothers were second most important in shaping their PSE. Vicarious experiences and verbal persuasion did not emerge as salient sources. « Support in parenting » was also found to be significant in fostering the mothers’ perceived capability. Furthermore, we noted that while multiple negative experiences were encountered, these mothers tended to frame their experiences in adaptive ways to allow them to use these as feedback for subsequent parenting endeavors to booster their perceived capability. Implications for future research were discussed in the light of these findings. (PsycINFO Database Record
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7. Firouzabadi N, Ghazanfari N, Alavi Shoushtari A, Erfani N, Fathi F, Bazrafkan M, Bahramali E. {{Genetic Variants of Angiotensin-Converting Enzyme Are Linked to Autism: A Case-Control Study}}. {PLoS One};2016;11(4):e0153667.
BACKGROUND: Autism is a disease of complex nature with a significant genetic component. The importance of renin-angiotensin system (RAS) elements in cognition and behavior besides the interaction of angiotensin II (Ang II), the main product of angiotensin-converting enzyme (ACE), with neurotransmitters in CNS, especially dopamine, proposes the involvement of RAS in autism. Since the genetic architecture of autism has remained elusive, here we postulated that genetic variations in RAS are associated with autism. METHODS: Considering the relation between the three polymorphisms of ACE (I/D, rs4343 and rs4291) with the level of ACE activity, we have investigated this association with autism, in a case-control study. Genotype and allele frequencies of polymorphisms were determined in DNAs extracted from venous blood of 120 autistic patients and their age and sex-matched healthy controls, using polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) methods. RESULTS: There were strong associations between both DD genotype of ACE I/D and the D allele, with autism (P = 0.006, OR = 2.9, 95% CI = 1.64-5.13 and P = 0.006, OR = 2.18, 95% CI = 1.37-3.48 respectively). Furthermore, a significant association between the G allele of rs4343 and autism was observed (P = 0.006, OR = 1.84, 95%CI = 1.26-2.67). Moreover, haplotype analysis revealed an association between DTG haplotype and autism (P = 0.008). CONCLUSION: Our data suggests the involvement of RAS genetic diversity in increasing the risk of autism.
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8. Geretsegger M, Holck U, Bieleninik L, Gold C. {{Feasibility of a Trial on Improvisational Music Therapy for Children with Autism Spectrum Disorder}}. {J Music Ther};2016 (Apr 15)
BACKGROUND: To conduct generalizable, rigorously designed, adequately powered trials investigating music therapy and other complex interventions, it is essential that study procedures are feasible and acceptable for participants. To date, only limited evidence on feasibility of trial designs and strategies to facilitate study implementation is available in the music therapy literature. OBJECTIVE: Using data from a subsample of a multi-center RCT on improvisational music therapy (IMT) for autism spectrum disorder (ASD), this study aims to evaluate feasibility of study procedures, evaluate safety, document concomitant treatment, and report consistency of individuals’ trends over time in chosen outcome measures. METHODS: Children with ASD aged between 4 years, 0 months, and 6 years, 11 months, were randomly assigned to one of three conditions: one (low intensity) vs. three weekly IMT sessions (high intensity) for five months vs. standard care. Feasibility was evaluated by examining recruitment, implementation of study conditions, assessment procedures, blinding, and retention; we also evaluated safety, concomitant treatment, and consistency of changes in standardized scales completed by blinded assessors and parents before and 5 months after randomization. RESULTS: Within this subsample (n = 15), recruitment rates, session attendance in the high-intensity condition, and consistency between outcome measures were lower than expected. Session attendance in the low-intensity and control conditions, treatment fidelity, measurement completion, blinding, retention, and safety met a priori thresholds for feasibility. CONCLUSIONS: By discussing strategies to improve recruitment and to minimize potential burden on study participants, referrers, and researchers, this study helps build knowledge about designing and implementing trials successfully.
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9. Kaluzna-Czaplinska J, Jozwik-Pruska J. {{Chromatographic and mass spectrometric techniques in studies on oxidative stress in autism}}. {J Chromatogr B Analyt Technol Biomed Life Sci};2016 (Apr 15);1019:4-14.
Healthy body is characterized by the presence of a dynamic and balanced equilibrium between the production of reactive oxygen species (ROS) and the antioxidant capacity. In oxidative stress this balance is switched to reactions of oxidation leading to increased production of ROS, exceeding the capacity of physiological antioxidant systems. Oxidative stress is known to be linked to many disturbances, disorders and diseases. One of these is the autism spectrum disorder (ASD). ASD is a neurodevelopmental disorder manifested by abnormalities in social communication and interaction, as well as by occurrence of repetitive, restricted patterns of behavior or activities. It is believed that adequate knowledge about the oxidative stress biomarkers and the possibility of their reliable measuring could be useful in broadening knowledge on various diseases including ASD. A high number of compounds have been proposed as biomarkers of oxidative stress. Some of these are connected with the severity of ASD. The present review gives a summary of the chromatographic techniques used for the determination of biomarkers for oxidative stress in autism, and of other compounds important in this context. The first part of the review focuses on the correlation between oxidative stress and autism. The second part describes applications of chromatographic and mass spectrometric methods to the analysis of different metabolites connected with oxidative stress in biological fluids of autistic children. Advantages as well as disadvantages of the application of these methods for the analysis of different types of oxidative stress biomarkers are discussed.
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10. Luongo FJ, Horn ME, Sohal VS. {{Putative Microcircuit-Level Substrates for Attention Are Disrupted in Mouse Models of Autism}}. {Biol Psychiatry};2016 (Apr 15);79(8):667-675.
BACKGROUND: Deep layer excitatory circuits in the prefrontal cortex represent the strongest locus for genetic convergence in autism, but specific abnormalities within these circuits that mediate key features of autism, such as cognitive or attentional deficits, remain unknown. Attention normally increases the sensitivity of neural populations to incoming signals by decorrelating ongoing cortical circuit activity. Here, we investigated whether mechanisms underlying this phenomenon might be disrupted within deep layer prefrontal circuits in mouse models of autism. METHODS: We isolated deep layer prefrontal circuits in brain slices then used single-photon GCaMP imaging to record activity from many (50 to 100) neurons simultaneously to study patterns of spontaneous activity generated by these circuits under normal conditions and in two etiologically distinct models of autism: mice exposed to valproic acid in utero and Fmr1 knockout mice. RESULTS: We found that modest doses of the cholinergic agonist carbachol normally decorrelate spontaneous activity generated by deep layer prefrontal networks. This effect was disrupted in both valproic acid-exposed and Fmr1 knockout mice but intact following other manipulations that did not model autism. CONCLUSIONS: Our results suggest that cholinergic modulation may contribute to attention by acting on local cortical microcircuits to decorrelate spontaneous activity. Furthermore, defects in this mechanism represent a microcircuit-level endophenotype that could link diverse genetic and developmental disruptions to attentional deficits in autism. Future studies could elucidate pathways leading from various etiologies to this circuit-level abnormality or use this abnormality itself as a target and identify novel therapeutic strategies that restore normal circuit function.
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11. Mercer AA, Palarz KJ, Tabatadze N, Woolley CS, Raman IM. {{Sex differences in cerebellar synaptic transmission and sex-specific responses to autism-linked mutations in mice}}. {Elife};2016 (Apr 14);5
Neurons of the cerebellar nuclei (CbN) transmit cerebellar signals to premotor areas. The cerebellum expresses several autism-linked genes, including Gabrb3, which encodes GABAA receptor beta3 subunits and is among the maternal alleles deleted in Angelman syndrome. We tested how this Gabrb3 m-/p+ mutation affects CbN physiology in mice, separating responses of males and females. Wild-type mice showed sex differences in synaptic excitation, inhibition, and intrinsic properties. Relative to females, CbN cells of males had smaller synaptically evoked mGluR1/5-dependent currents, slower Purkinje-mediated IPSCs, and lower spontaneous firing rates, but rotarod performances were indistinguishable. In mutant CbN cells, IPSC kinetics were unchanged, but mutant males, unlike females, showed enlarged mGluR1/5 responses and accelerated spontaneous firing. These changes appear compensatory, since mutant males but not females performed indistinguishably from wild-type siblings on the rotarod task. Thus, sex differences in cerebellar physiology produce similar behavioral output, but provide distinct baselines for responses to mutations.
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12. Muotri AR. {{The Human Model: Changing Focus on Autism Research}}. {Biol Psychiatry};2016 (Apr 15);79(8):642-649.
The lack of live human brain cells for research has slowed progress toward understanding the mechanisms underlying autism spectrum disorders. A human model using reprogrammed patient somatic cells offers an attractive alternative, as it captures a patient’s genome in relevant cell types. Despite the current limitations, the disease-in-a-dish approach allows for progressive time course analyses of target cells, offering a unique opportunity to investigate the cellular and molecular alterations before symptomatic onset. Understanding the current drawbacks of this model is essential for the correct data interpretation and extrapolation of conclusions applicable to the human brain. Innovative strategies for collecting biological material and clinical information from large patient cohorts are important for increasing the statistical power that will allow for the extraction of information from the noise resulting from the variability introduced by reprogramming and differentiation methods. Working with large patient cohorts is also important for understanding how brain cells derived from diverse human genetic backgrounds respond to specific drugs, creating the possibility of personalized medicine for autism spectrum disorders.
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13. Nebel MB, Eloyan A, Nettles CA, Sweeney KL, Ament K, Ward RE, Choe AS, Barber AD, Pekar JJ, Mostofsky SH. {{Intrinsic Visual-Motor Synchrony Correlates With Social Deficits in Autism}}. {Biol Psychiatry};2016 (Apr 15);79(8):633-641.
BACKGROUND: Imitation, which is impaired in children with autism spectrum disorder (ASD) and critically depends on the integration of visual input with motor output, likely impacts both motor and social skill acquisition in children with ASD; however, it is unclear what brain mechanisms contribute to this impairment. Children with ASD also exhibit what appears to be an ASD-specific bias against using visual feedback during motor learning. Does the temporal congruity of intrinsic activity, or functional connectivity, between motor and visual brain regions contribute to ASD-associated deficits in imitation, motor, and social skills? METHODS: We acquired resting-state functional magnetic resonance imaging scans from 100 8- to 12-year-old children (50 ASD). Group independent component analysis was used to estimate functional connectivity between visual and motor systems. Brain-behavior relationships were assessed by regressing functional connectivity measures with social deficit severity, imitation, and gesture performance scores. RESULTS: We observed increased intrinsic asynchrony between visual and motor systems in children with ASD and replicated this finding in an independent sample from the Autism Brain Imaging Data Exchange. Moreover, children with more out-of-sync intrinsic visual-motor activity displayed more severe autistic traits, while children with greater intrinsic visual-motor synchrony were better imitators. CONCLUSIONS: Our twice replicated findings confirm that visual-motor functional connectivity is disrupted in ASD. Furthermore, the observed temporal incongruity between visual and motor systems, which may reflect diminished integration of visual consequences with motor output, was predictive of the severity of social deficits and may contribute to impaired social-communicative skill development in children with ASD.
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14. Oien RA, Siper P, Kolevzon A, Grodberg D. {{Detecting Autism Spectrum Disorder in Children With ADHD and Social Disability}}. {J Atten Disord};2016 (Apr 13)
OBJECTIVE: The social disability associated with ADHD often makes diagnostic and treatment decision making challenging. This protocol investigates the test performance of the Autism Mental Status Exam (AMSE) in detecting autism spectrum disorder (ASD) in a sample of 45 children with ADHD and ASD symptomatology. The AMSE is a brief ASD diagnostic assessment administered in the context of a clinical exam. METHOD: All participants received a developmental evaluation, including the AMSE, followed by independent gold standard diagnostic assessments including the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview-Revised (ADI-R). RESULTS: Receiver operating characteristics (ROC) curve analysis indicated strong sensitivity and specificity in this population. Optimal cutoff scores are provided. CONCLUSION: The AMSE holds promise as a brief ASD assessment tool for children with ADHD and ASD symptomatology and as a guide for treatment and referral decisions at the point of care.
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15. Pell PJ, Mareschal I, Calder AJ, von dem Hagen EA, Clifford CW, Baron-Cohen S, Ewbank MP. {{Intact priors for gaze direction in adults with high-functioning autism spectrum conditions}}. {Mol Autism};2016;7:25.
BACKGROUND: Autism Spectrum Conditions (ASC) are associated with a range of perceptual atypicalities, including abnormalities in gaze processing. Pellicano and Burr (Trends Cogn Sci 16(10):504-10, 2012) have argued that these atypicalities might be explained within a Bayesian framework, in which perception represents the combination of sensory information with prior knowledge. They propose that the Bayesian priors of individuals with ASC might be attenuated, such that their perception is less reliant on prior knowledge than neurotypical individuals. An important tenet of Bayesian decision theory is that increased uncertainty about incoming sensory information will lead to a greater influence of the prior on perception. Consistent with this, Mareschal et al. (Curr Biol 23(8):717-21, 2013) showed that when noise is added to the eyes of a face (increasing uncertainty about gaze direction), gaze is more likely to be perceived as direct. METHODS: We adopted the same paradigm as Mareschal et al. to determine whether the influence of a prior on gaze perception is reduced in neurotypical participants with high numbers of autistic traits (experiment 1) and in individuals with a clinical diagnosis of ASC (experiment 2). Participants were presented with synthetic faces and asked to make a judgement about the relative gaze directions of the faces. Uncertainty about gaze direction was manipulated by adding noise to the eyes of a face. RESULTS: Consistent with previous work, in both experiment 1 and experiment 2, participants showed a bias towards perceiving gaze as direct under conditions of uncertainty. However, there was no evidence that the magnitude of this bias was reduced either in the ASC group or in neurotypical controls with a high number of autistic traits. CONCLUSIONS: Our findings challenge the attenuated priors theory of perception in ASC (Trends Cogn Sci 16(10):504-10, 2012) and related proposals (Trends Cogn Sci 17(1):1, 2013, Front Hum Neurosci 8:302, 2014), and suggest priors for gaze direction are intact in high-functioning ASC.
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16. Pierce K, Marinero S, Hazin R, McKenna B, Barnes CC, Malige A. {{Eye Tracking Reveals Abnormal Visual Preference for Geometric Images as an Early Biomarker of an Autism Spectrum Disorder Subtype Associated With Increased Symptom Severity}}. {Biol Psychiatry};2016 (Apr 15);79(8):657-666.
BACKGROUND: Clinically and biologically, autism spectrum disorder (ASD) is heterogeneous. Unusual patterns of visual preference as indexed by eye tracking are hallmarks; however, whether they can be used to define an early biomarker of ASD as a whole or leveraged to define a subtype is unclear. To begin to examine this issue, large cohorts are required. METHODS: A sample of 334 toddlers from six distinct groups (115 toddlers with ASD, 20 toddlers with ASD features, 57 toddlers with developmental delay, 53 toddlers with other conditions [e.g., premature birth, prenatal drug exposure], 64 toddlers with typical development, and 25 unaffected toddlers with siblings with ASD) was studied. Toddlers watched a movie containing geometric and social images. Fixation duration and number of saccades within each area of interest and validation statistics for this independent sample were computed. Next, to maximize power, data from our previous study (n = 110) were added for a total of 444 subjects. A subset of toddlers repeated the eye-tracking procedure. RESULTS: As in the original study, a subset of toddlers with ASD fixated on geometric images >69% of the time. Using this cutoff, sensitivity for ASD was 21%, specificity was 98%, and positive predictive value was 86%. Toddlers with ASD who strongly preferred geometric images had 1) worse cognitive, language, and social skills relative to toddlers with ASD who strongly preferred social images and 2) fewer saccades when viewing geometric images. Unaffected siblings of ASD probands did not show evidence of heightened preference for geometric images. Test-retest reliability was good. Examination of age effects suggested that this test may not be appropriate with children >4 years old. CONCLUSIONS: Enhanced visual preference for geometric repetition may be an early developmental biomarker of an ASD subtype with more severe symptoms.
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17. Rendall AR, Truong DT, Fitch RH. {{Learning delays in a mouse model of Autism Spectrum Disorder}}. {Behav Brain Res};2016 (Apr 15);303:201-207.
Autism Spectrum Disorder (ASD) is a heterogeneous neurodevelopmental disorder with core symptoms of atypical social interactions and repetitive behaviors. It has also been reported that individuals with ASD have difficulty with multisensory integration, and this may disrupt higher-order cognitive abilities such as learning and social communication. Impairments in the integration of sensory information could in turn reflect diminished cross-modal white matter connectivity. Moreover, the genetic contribution in ASD appears to be strong, with heritability estimates as high as 90%. However, no single gene has been identified, and over 1000 risk genes have been reported. One of these genes – contactin-associated-like-protein 2 (CNTNAP2) – was first associated with Specific Language Impairment, and more recently has been linked to ASD. CNTNAP2 encodes a cell adhesion protein regulating synaptic signal transmission. To better understand the behavioral and biological underlying mechanisms of ASD, a transgenic mouse model was created with a genetic knockout (KO) of the rodent homolog Cntnap2. Initial studies on this mouse revealed poor social interactions, behavioral perseveration, and reduced vocalizations-all strongly resembling human ASD symptoms. Cntnap2 KO mice also show abnormalities in myelin formation, consistent with a hypo-connectivity model of ASD. The current study was designed to further assess the behavioral phenotype of this mouse model, with a focus on learning and memory. Cntnap2 KO and wild-type mice were tested on a 4/8 radial arm water maze for 14 consecutive days. Error scores (total, working memory, reference memory, initial and repeated reference memory), latency and average turn angle were independently assessed using a 2×14 repeated measures ANOVA. Results showed that Cntnap2 KO mice exhibited significant deficits in working and reference memory during the acquisition period of the task. During the retention period (i.e., after asymptote in errors), Cntnap2 KO mice performed comparably to wild-type mice. These findings suggest that CNTNAP2 may influence the development of neural systems important to learning and cross-modal integration, and that disruption of this function could be associated with delayed learning in ASD.
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18. Solso S, Xu R, Proudfoot J, Hagler DJ, Jr., Campbell K, Venkatraman V, Carter Barnes C, Ahrens-Barbeau C, Pierce K, Dale A, Eyler L, Courchesne E. {{Diffusion Tensor Imaging Provides Evidence of Possible Axonal Overconnectivity in Frontal Lobes in Autism Spectrum Disorder Toddlers}}. {Biol Psychiatry};2016 (Apr 15);79(8):676-684.
BACKGROUND: Theories of brain abnormality in autism spectrum disorder (ASD) have focused on underconnectivity as an explanation for social, language, and behavioral deficits but are based mainly on studies of older autistic children and adults. METHODS: In 94 ASD and typical toddlers ages 1 to 4 years, we examined the microstructure (indexed by fractional anisotropy) and volume of axon pathways using in vivo diffusion tensor imaging of fronto-frontal, fronto-temporal, fronto-striatal, and fronto-amygdala axon pathways, as well as posterior contrast tracts. Differences between ASD and typical toddlers in the nature of the relationship of age to these measures were tested. RESULTS: Frontal tracts in ASD toddlers displayed abnormal age-related changes with greater fractional anisotropy and volume than normal at younger ages but an overall slower than typical apparent rate of continued development across the span of years. Posterior cortical contrast tracts had few significant abnormalities. CONCLUSIONS: Frontal fiber tracts displayed deviant early development and age-related changes that could underlie impaired brain functioning and impact social and communication behaviors in ASD.
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19. Tebartz van Elst L, Riedel A, Maier S. {{Autism as a Disorder of Altered Global Functional and Structural Connectivity}}. {Biol Psychiatry};2016 (Apr 15);79(8):626-627.
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20. Turcotte P, Mathew M, Shea LL, Brusilovskiy E, Nonnemacher SL. {{Service Needs Across the Lifespan for Individuals with Autism}}. {J Autism Dev Disord};2016 (Apr 15)
The goal of this research was to examine reported service needs among individuals with autism spectrum disorder (ASD) of all ages. Data were generated from a state survey that queried the needs of children, adolescents and adults with ASD. Logistic regression was used to compare service use and need among these age groups. Adults with ASD were less likely to be receiving multiple types of services, and more likely to have a need for services. These findings demonstrate that adults with ASD have more and different needs for services. These results can inform policy and program planning to put in place the services adults with ASD need.
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21. Yahata N, Morimoto J, Hashimoto R, Lisi G, Shibata K, Kawakubo Y, Kuwabara H, Kuroda M, Yamada T, Megumi F, Imamizu H, Nanez JE, Sr., Takahashi H, Okamoto Y, Kasai K, Kato N, Sasaki Y, Watanabe T, Kawato M. {{A small number of abnormal brain connections predicts adult autism spectrum disorder}}. {Nat Commun};2016;7:11254.
Although autism spectrum disorder (ASD) is a serious lifelong condition, its underlying neural mechanism remains unclear. Recently, neuroimaging-based classifiers for ASD and typically developed (TD) individuals were developed to identify the abnormality of functional connections (FCs). Due to over-fitting and interferential effects of varying measurement conditions and demographic distributions, no classifiers have been strictly validated for independent cohorts. Here we overcome these difficulties by developing a novel machine-learning algorithm that identifies a small number of FCs that separates ASD versus TD. The classifier achieves high accuracy for a Japanese discovery cohort and demonstrates a remarkable degree of generalization for two independent validation cohorts in the USA and Japan. The developed ASD classifier does not distinguish individuals with major depressive disorder and attention-deficit hyperactivity disorder from their controls but moderately distinguishes patients with schizophrenia from their controls. The results leave open the viable possibility of exploring neuroimaging-based dimensions quantifying the multiple-disorder spectrum.
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22. Zhang W, Baranek G. {{The Impact of Insurance Coverage Types on Access to and Utilization of Health Services for U.S. Children With Autism}}. {Psychiatr Serv};2016 (Apr 15):appips201500206.
OBJECTIVE: The study examined the association of insurance type with access to and utilization of essential health services among children with autism spectrum disorder (ASD). METHODS: Multivariate logistic regressions were used to illustrate the relationship between the indicators of health services utilization and insurance coverage types among U.S. children with ASD (N=2,041). Analyses used secondary data from the 2011-2012 National Survey of Children’s Health. RESULTS: Privately insured children with ASD were significantly less likely than their publicly insured counterparts to receive therapy (OR=.49). The odds of having any out-of-pocket medical expenses for families with private insurance were 11.0 times greater than for families with public insurance. CONCLUSIONS: The findings reflect current gaps between public and private insurance coverage in the health system for access to and utilization of health services for children with ASD. Special attention should be directed to private insurance plans, where needed health services may be inadequately covered.
