1. Asher A. {{Book Review: Visual supports for people with autism: A guide for parents and professionals Cohen Marlene J. Gerhardt Peter F. ( 2016 ). Visual supports for people with autism: A guide for parents and professionals ( 2nd ed .). Toronto, ON : Woodbine House . 216 pp . US$24.95 . ISBN: 978-1-60613-215-9}}. {Can J Occup Ther};2017 (Jun);84(3):148.
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2. Bellieni CV, Buonocore G. {{Are electromagnetic fields in incubators a risk factor for autism?}}. {Acta Paediatr};2017 (Jul 22)
Hugo Lagercrantz recently argued (1) that a possible cause of infantile autism was the unnatural isolation that babies experienced in neonatal incubators. Atypical brain connectivity has been detected in children with autism and it is possible that this may be also due to environmental factors, including the lack of physiological stimuli that is typically found in the incubator environment. We suggest that also another factor may expose babies in incubators to the risk of developing autistic traits and that is the high electromagnetic fields (EMF) produced by the incubator’s electric engine. This article is protected by copyright. All rights reserved.
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3. Chen H, Uddin LQ, Duan X, Zheng J, Long Z, Zhang Y, Guo X, Zhang Y, Zhao J, Chen H. {{Shared atypical default mode and salience network functional connectivity between autism and schizophrenia}}. {Autism Res};2017 (Jul 21)
Schizophrenia and autism spectrum disorder (ASD) are two prevalent neurodevelopmental disorders sharing some similar genetic basis and clinical features. The extent to which they share common neural substrates remains unclear. Resting-state fMRI data were collected from 35 drug-naive adolescent participants with first-episode schizophrenia (15.6 +/- 1.8 years old) and 31 healthy controls (15.4 +/- 1.6 years old). Data from 22 participants with ASD (13.1 +/- 3.1 years old) and 21 healthy controls (12.9 +/- 2.9 years old) were downloaded from the Autism Brain Imaging Data Exchange. Resting-state functional networks were constructed using predefined regions of interest. Multivariate pattern analysis combined with multi-task regression feature selection methods were conducted in two datasets separately. Classification between individuals with disorders and controls was achieved with high accuracy (schizophrenia dataset: accuracy = 83%; ASD dataset: accuracy = 80%). Shared atypical brain connections contributing to classification were mostly present in the default mode network (DMN) and salience network (SN). These functional connections were further related to severity of social deficits in ASD (p = 0.002). Distinct atypical connections were also more related to the DMN and SN, but showed different atypical connectivity patterns between the two disorders. These results suggest some common neural mechanisms contributing to schizophrenia and ASD, and may aid in understanding the pathology of these two neurodevelopmental disorders. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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4. Cheng GR, Li XY, Xiang YD, Liu D, McClintock SM, Zeng Y. {{The implication of AMPA receptor in synaptic plasticity impairment and intellectual disability in fragile X syndrome}}. {Physiol Res};2017 (Jul 18)
Fragile X syndrome (FXS) is the most frequently inherited form of intellectual disability and prevalent single-gene cause of autism. A priority of FXS research is to determine the molecular mechanisms underlying the cognitive and social functioning impairments in humans and the FXS mouse model. Glutamate ionotropic alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors (AMPARs) mediate a majority of fast excitatory neurotransmission in the central nervous system and are critically important for nearly all aspects of brain function, including neuronal development, synaptic plasticity, and learning and memory. Both preclinical and clinical studies have indicated that expression, trafficking, and functions of AMPARs are altered and result in altered synapse development and plasticity, cognitive impairment, and poor mental health in FXS. In this review, we discuss the contribution of AMPARs to disorders of FXS by highlighting recent research advances with a specific focus on change in AMPARs expression, trafficking, and dependent synaptic plasticity. Since changes in synaptic strength underlie the basis of learning, development, and disease, we suggest that the current knowledge base of AMPARs has reached a unique point to permit a comprehensive re-evaluation of their roles in FXS.
5. Ebihara K, Fujiwara H, Awale S, Dibwe DF, Araki R, Yabe T, Matsumoto K. {{Decrease in endogenous brain allopregnanolone induces autism spectrum disorder (ASD)-like behavior in mice: A novel animal model of ASD}}. {Behav Brain Res};2017 (Jul 22);334:6-15.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with core symptoms of social impairments and restrictive repetitive behaviors. Recent evidence has implicated a dysfunction in the GABAergic system in the pathophysiology of ASD. We investigated the role of endogenous allopregnanolone (ALLO), a neurosteroidal positive allosteric modulator of GABAA receptors, in the regulation of ASD-like behavior in male mice using SKF105111 (SKF), an inhibitor of type I and type II 5alpha-reductase, a rate-limiting enzyme of ALLO biosynthesis. SKF impaired sociability-related performance, as analyzed by three different tests; i.e., the 3-chamber test and social interaction in the open field and resident-intruder tests, without affecting olfactory function elucidated by the buried food test. SKF also induced repetitive grooming behavior without affecting anxiety-like behavior. SKF had no effect on short-term spatial working memory or long-term fear memory, but enhanced latent learning ability in male mice. SKF-induced ASD-like behavior in male mice was abolished by the systemic administration of ALLO (1mg/kg, i.p.) and methylphenidate (MPH: 2.5mg/kg, i.p.), a dopamine transporter inhibitor. The effects of SKF on brain ALLO contents in male mice were reversed by ALLO, but not MPH. On the other hand, SKF failed to induce ASD-like behavior or a decline in brain ALLO contents in female mice. These results suggest that ALLO regulates episodes of ASD-like behavior by positively modulating the function of GABAA receptors linked to the dopaminergic system. Moreover, a sex-dependently induced decrease in brain ALLO contents may provide an animal model to study the main features of ASD.
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6. Fernandez M, Mollinedo-Gajate I, Penagarikano O. {{Neural circuits for social cognition: Implications for autism}}. {Neuroscience};2017 (Jul 17)
Social neuroscience, the study of the neurobiological basis of social behavior, has become a major area of current research in behavioral neuroscience and psychiatry, since many psychiatric disorders are characterized by social deficits. Social behavior refers to the behavioral response with regard to socially relevant information, and requires the perception and integration of social cues through a complex cognition process (i.e. social cognition) that involves attention, memory, motivation and emotion. Neurobiological and molecular mechanisms underlying social behavior are highly conserved across species, and inter- and intra-specific variability observed in social behavior can be explained to large extent by differential activity of this conserved neural network. Human functional magnetic resonance imaging (fMRI) studies have greatly informed about the brain structures and their connectivity networks that are important for social cognition. Animal research has been crucial for identifying specific circuits and molecular mechanisms that modulate this structural network. From a molecular neurobiology perspective, activity in these brain structures is coordinated by neuronal circuits modulated by several neurotransmitters and neuromodulators. Thus, quantitative variation in the levels, release and/or receptor density of these molecules could affect the observed behavioral response. The present review presents an overall framework of the components of the social brain circuitry and its modulation. By integrating multiple research approaches, from human fMRI studies to animal models we can start shedding light into how dysfunction in these circuits could lead to disorders of social-functioning such as Autism.
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7. Khramova TV, Kaysheva AL, Ivanov YD, Pleshakova TO, Iourov IY, Vorsanova SG, Yurov YB, Schetkin AA, Archakov AI. {{Serologic Markers of Autism Spectrum Disorder}}. {J Mol Neurosci};2017 (Aug);62(3-4):420-429.
According to WHO data, about 67 million people worldwide are affected by autism, and this number grows by 14% annually. Among the possible causes of autism are genetic modifications, organic lesions of the central nervous system, metabolic disorders, influence of viral and bacterial infections, chemical influence to the mother’s body during pregnancy, etc. The conducted research shows that research papers published until today do not name any potential protein markers that meet the requirements of the basic parameters for evaluating the efficiency of disease diagnostics, in particular high sensitivity, specificity, and accuracy. Conducting proteomic research on a big scale in order to detect serologic markers of protein nature associated with development of autism spectrum disorders seems to be highly relevant.
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8. McAuliffe T, Cordier R, Vaz S, Thomas Y, Falkmer T. {{Quality of Life, Coping Styles, Stress Levels, and Time Use in Mothers of Children with Autism Spectrum Disorders: Comparing Single Versus Coupled Households}}. {J Autism Dev Disord};2017 (Jul 20)
This study aimed to examine the influence of differences in household status on the parental stress, coping, time use and quality of life (QoL) among mothers of children with autism spectrum disorders. Forty-three single and 164 coupled mothers completed the survey. Data were analysed using multivariate logistic regression. We found that single mothers were 1.05 times more likely to report lower levels of environmental QoL. Whilst they were 1.73 times more likely to use acceptance coping style, this association did not persist after adjusting for total number of children, household income and employment status. There was no difference in time use and stress between these mothers. Possible environmental issues for single mothers and implications for future research are discussed.
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9. Morris G, Puri BK, Frye RE, Maes M. {{The Putative Role of Environmental Mercury in the Pathogenesis and Pathophysiology of Autism Spectrum Disorders and Subtypes}}. {Mol Neurobiol};2017 (Jul 22)
Exposure to organic forms of mercury has the theoretical capacity to generate a range of immune abnormalities coupled with chronic nitro-oxidative stress seen in children with autism spectrum disorder (ASD). The paper discusses possible mechanisms explaining the neurotoxic effects of mercury and possible associations between mercury exposure and ASD subtypes. Environmental mercury is neurotoxic at doses well below the current reference levels considered to be safe, with evidence of neurotoxicity in children exposed to environmental sources including fish consumption and ethylmercury-containing vaccines. Possible neurotoxic mechanisms of mercury include direct effects on sulfhydryl groups, pericytes and cerebral endothelial cells, accumulation within astrocytes, microglial activation, induction of chronic oxidative stress, activation of immune-inflammatory pathways and impairment of mitochondrial functioning. (Epi-)genetic factors which may increase susceptibility to the toxic effects of mercury in ASD include the following: a greater propensity of males to the long-term neurotoxic effects of postnatal exposure and genetic polymorphisms in glutathione transferases and other glutathione-related genes and in selenoproteins. Furthermore, immune and inflammatory responses to immunisations with mercury-containing adjuvants are strongly influenced by polymorphisms in the human leukocyte antigen (HLA) region and by genes encoding effector proteins such as cytokines and pattern recognition receptors. Some epidemiological studies investigating a possible relationship between high environmental exposure to methylmercury and impaired neurodevelopment have reported a positive dose-dependent effect. Retrospective studies, on the other hand, reported no relationship between a range of ethylmercury-containing vaccines and chronic neuropathology or ASD. On the basis of these results, we would argue that more clinically relevant research is required to examine whether environmental mercury is associated with ASD or subtypes. Specific recommendations for future research are discussed.
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10. Papathomas P, Goldschmidt K. {{Utilizing virtual reality and immersion video technology as a focused learning tool for children with autism spectrum disorder}}. {J Pediatr Nurs};2017 (Jul – Aug);35:8-9.
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11. Powell PS, Klinger LG, Klinger MR. {{Patterns of Age-Related Cognitive Differences in Adults with Autism Spectrum Disorder}}. {J Autism Dev Disord};2017 (Jul 20)
Little is known about age-related cognitive differences in autism spectrum disorder (ASD). However, given the overlap in cognitive impairments in ASD to those seen in typical aging, it is possible that adults with ASD will face even greater cognitive difficulties as they age. The current study used a cross-sectional design to examine age-related cognitive differences in adults with ASD and age and IQ-matched adults with typical development (age range 30-67 years). Results indicated that both age and diagnosis were related to poorer cognitive performance. However, adults with ASD exhibited pronounced age effects on measures related to executive functioning compared to adults with typical development, suggesting that aging in ASD may disproportionately affect specific cognitive processes.
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12. Rankin JA, Tomeny TS, Barry TD. {{Multi-informant assessment of siblings of youth with autism spectrum disorder: Parent-child discrepancies in at-risk classification}}. {Res Dev Disabil};2017 (Sep);68:78-87.
BACKGROUND: The behavioral and emotional functioning of typically-developing (TD) siblings of youth with autism spectrum disorder (ASD) has been frequently assessed in the literature; however, these assessments typically include only one informant, rarely considering differences between parent and self-reports of sibling adjustment. AIMS: This study examined parent-youth reported informant discrepancies in behavioral and emotional functioning, including whether parent and youth reports yielded the same conclusions regarding TD sibling risk status. METHODS, PROCEDURES, AND RESULTS: Among 113 parents and TD siblings of youth with ASD, TD siblings self-reported more overall, conduct, hyperactivity, and peer problems (compared to parent reports). Although few siblings were considered at-risk, those who were identified were not usually identified as at-risk on both informants’ reports. Moreover, ASD symptoms, broader autism phenotype symptoms, parent mental health concerns, and social support from parents were all related to differences in at-risk classification between parent- and sibling self-report. CONCLUSIONS AND IMPLICATIONS: This paper highlights the necessity of multi-informant reporting when considering TD sibling psychological functioning. WHAT THIS PAPER ADDS: This study helps to address gaps in the literature on assessment of emotional and behavioral functioning of TD siblings of youth with ASD. The results highlight the importance of utilizing both parent- and self-report when identifying TD siblings at-risk for maladjustment. Although few siblings were considered at-risk, those who were identified were not usually identified as such on both informants’ reports, and a variety of sibling- and parent-factors were associated with differences in at-risk classification. Thus, inclusion and examination of both parent- and self-report of TD sibling psychological functioning is vital for accurately identifying numbers of TD siblings at-risk of maladjustment.
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13. Subramanian K, Brandenburg C, Orsati F, Soghomonian JJ, Hussman JP, Blatt GJ. {{Basal ganglia and autism – a translational perspective}}. {Autism Res};2017 (Jul 21)
The basal ganglia are a collection of nuclei below the cortical surface that are involved in both motor and non-motor functions, including higher order cognition, social interactions, speech, and repetitive behaviors. Motor development milestones that are delayed in autism such as gross motor, fine motor and walking can aid in early diagnosis of autism. Neuropathology and neuroimaging findings in autism cases revealed volumetric changes and altered cell density in select basal ganglia nuclei. Interestingly, in autism, both the basal ganglia and the cerebellum are impacted both in their motor and non-motor domains and recently, found to be connected via the pons through a short disynaptic pathway. In typically developing individuals, the basal ganglia plays an important role in: eye movement, movement coordination, sensory modulation and processing, eye-hand coordination, action chaining, and inhibition control. Genetic models have proved to be useful toward understanding cellular and molecular changes at the synaptic level in the basal ganglia that may in part contribute to these autism-related behaviors. In autism, basal ganglia functions in motor skill acquisition and development are altered, thus disrupting the normal flow of feedback to the cortex. Taken together, there is an abundance of emerging evidence that the basal ganglia likely plays critical roles in maintaining an inhibitory balance between cortical and subcortical structures, critical for normal motor actions and cognitive functions. In autism, this inhibitory balance is disturbed thus impacting key pathways that affect normal cortical network activity. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Habit learning, action selection and performance are modulated by the basal ganglia, a collection of groups of neurons located below the cerebral cortex in the brain. In autism, there is emerging evidence that parts of the basal ganglia are structurally and functionally altered disrupting normal information flow. The basal ganglia through its interconnected circuits with the cerebral cortex and the cerebellum can potentially impact various motor and cognitive functions in the autism brain.
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14. Zauche LH, Darcy Mahoney AE, Higgins MK. {{Predictors of Co-occurring Neurodevelopmental Disabilities in Children With Autism Spectrum Disorders}}. {J Pediatr Nurs};2017 (Jul – Aug);35:113-119.
PURPOSE: Co-occurring neurodevelopmental disabilities (including cognitive and language delays and attention deficit hyperactivity disorder) affect over half of children with ASD and may affect later behavioral, language, and cognitive outcomes beyond the ASD diagnosis. However, no studies have examined predictors of co-occurring neurodevelopmental disabilities in children with ASD. This study investigated whether maternal sociodemographic, perinatal and neonatal factors are associated with co-occurring disabilities. DESIGN AND METHODS: This study involved a retrospective analysis of medical records for children diagnosed with ASD between 2009 and 2010 at an Autism Center in the southeast United States. Logistic regression was used to identify predictors of co-occurring neurodevelopmental disabilities. RESULTS: Of the 385 children in the sample, 61% had a co-occurring neurodevelopmental disability. Children whose mothers had less education (OR: 0.905), had never been married (OR: 1.803), or had bleeding during pregnancy (OR: 2.233) were more likely to have a co-occurring neurodevelopmental disability. Both preterm birth and African American race were associated with bleeding during pregnancy. CONCLUSIONS: Several maternal and perinatal risk factors for ASD were found to put children at risk for further diagnoses of co-occurring neurodevelopmental disabilities. While prematurity, a well-established risk factor for ASD, as well as maternal ethnicity was not found to increase the risk of a co-occurring disability, this study suggests that bleeding during pregnancy may moderate these relationships. PRACTICE IMPLICATIONS: Understanding maternal, perinatal, and neonatal risk factors may inform healthcare provider screening for ASD and co-occurring neurodevelopmental disabilities by helping providers recognize infants who present with multiple risk factors.
