1. Adamo N, Hodsoll J, Asherson P, Buitelaar JK, Kuntsi J. {{Ex-Gaussian, Frequency and Reward Analyses Reveal Specificity of Reaction Time Fluctuations to ADHD and Not Autism Traits}}. {Journal of abnormal child psychology}. 2018.
Both attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) have been linked to increased reaction time variability (RTV), a marker of attentional fluctuation. Here we test whether specificity to either trait emerges when we examine (1) detailed ex-Gaussian and frequency RTV subcomponents, (2) effects while controlling for the other trait and (3) improvement in the RTV measures following rewards or a faster event rate. 1110 children aged 7-10 years from a population-based sample completed a Go/No-Go task under three conditions (slow, fast and incentives). We measured RTV with standard deviation of RT (SDRT), ex-Gaussian distribution measures (Sigma and Tau), RT fluctuations in cycles of ~14-90 s in all conditions (Slow-4 and Slow-5), and RT fluctuations in cycles of 2-14 s in the fast condition (Slow-2 and Slow-3). Parent-rated ADHD and ASD traits were obtained. All refined RTV components were linked to ADHD traits only and not to ASD traits, while Sigma did not relate to either trait. Although both ADHD and ASD social-communication traits were associated with SDRT, the association with social-communication impairments disappeared when controlling for ADHD traits. A reward-induced improvement in RTV measures, indicating malleability, emerged in relation to ADHD traits but not ASD traits. Under closer inspection, specificity emerges of high RTV to ADHD traits. For the clinician, our findings indicate that attentional fluctuation in children with high ASD traits may be due to co-occurring ADHD traits and emphasise how the effectiveness of rewards does not generalise from ADHD to ASD traits.
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2. Akhter S, Hussain A, Shefa J, Kundu GK, Rahman F, Biswas A. {{Prevalence of Autism Spectrum Disorder (ASD) among the children aged 18-36 months in a rural community of Bangladesh: A cross sectional study}}. {F1000Research}. 2018; 7: 424.
Background: Autism spectrum disorder (ASD) refers to a group of complex neurodevelopment disorders characterized by repetitive and characteristic patterns of behavior and difficulties with social communication and interaction. In Bangladesh, autism in children is a significant burden of disease. Early identification of ASD could improve quality of life. The study has explored at the prevalence of ASD among rural community children aged between 18-36 months. Methods: A cross sectional study was conducted among the 5286 children aged between 18-36 months in a rural community. Household level data was collected using screening tool MCHAT. Primarily screening positive 66 children were invited for final diagnosis in a health camp. Diagnosis was made by different staging started from primary screening, followed by validation using MCHAT and flash card. Final diagnosis was made by the paediatric neurologists, child clinical psychologists and development therapist using diagnostic tools (DSM-IV & ADOS). Results: 04 children were diagnosed with autism spectrum disorder (ASD). Prevalence of the ASD in rural community was found 0.75/1000 children. Among the four ASD cases three were boys and one was girl and age range was between 20- 30 months. Whereas, the highest prevalence rate found was for the cerebral palsy which was 5.6/1000 children and Developmental delay (2.6/1000) was the next to that. Conclusions: Age specific autism (18-36 months) in children is found higher in rural community of Bangladesh. In order to get more comprehensive information on autism in other age groups of children in rural community, further study is required. Early detection in rural community could help the policy makers to decentralization of health services among the ASD children in rural community.
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3. Carrick FR, Pagnacco G, Hankir A, Abdulrahman M, Zaman R, Kalambaheti ER, Barton DA, Link PE, Oggero E. {{The Treatment of Autism Spectrum Disorder With Auditory Neurofeedback: A Randomized Placebo Controlled Trial Using the Mente Autism Device}}. {Frontiers in neurology}. 2018; 9: 537.
Introduction: Children affected by autism spectrum disorder (ASD) often have impairment of social interaction and demonstrate difficulty with emotional communication, display of posture and facial expression, with recognized relationships between postural control mechanisms and cognitive functions. Beside standard biomedical interventions and psychopharmacological treatments, there is increasing interest in the use of alternative non-invasive treatments such as neurofeedback (NFB) that could potentially modulate brain activity resulting in behavioral modification. Methods: Eighty-three ASD subjects were randomized to an Active group receiving NFB using the Mente device and a Control group using a Sham device. Both groups used the device each morning for 45 minutes over a 12 week home based trial without any other clinical interventions. Pre and Post standard ASD questionnaires, qEEG and posturography were used to measure the effectiveness of the treatment. Results: Thirty-four subjects (17 Active and 17 Control) completed the study. Statistically and substantively significant changes were found in several outcome measures for subjects that received the treatment. Similar changes were not detected in the Control group. Conclusions: Our results show that a short 12 week course of NFB using the Mente Autism device can lead to significant changes in brain activity (qEEG), sensorimotor behavior (posturography), and behavior (standardized questionnaires) in ASD children.
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4. Kee SE, Mou X, Zoghbi HY, Ji D. {{Impaired spatial memory codes in a mouse model of Rett syndrome}}. {eLife}. 2018; 7.
The Mecp2(+/-) mouse model recapitulates many phenotypes of patients with Rett syndrome (RTT), including learning and memory deficits. It is unknown, however, how the disease state alters memory circuit functions in vivo in RTT mice. Here we recorded from hippocampal place cells, which are thought to encode spatial memories, in freely moving RTT mice and littermate controls. We found that place cells in RTT mice are impaired in their experience-dependent increase of spatial information. This impairment is accompanied by an enhanced baseline firing synchrony of place cells within ripple oscillations during rest, which consequently occludes the increase in synchrony after a novel experience. Behaviorally, contextual memory is normal at short but not long time scale in RTT mice. Our results suggest that hypersynchrony interferes with memory consolidation and leads to impaired spatial memory codes in RTT mice, providing a possible circuit mechanism for memory deficits in Rett Syndrome.
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5. Maier S, Tebartz van Elst L, Perlov E, Duppers AL, Nickel K, Fangmeier T, Endres D, Riedel A. {{Cortical properties of adults with autism spectrum disorder and an IQ>100}}. {Psychiatry research Neuroimaging}. 2018; 279: 8-13.
Previous studies on cortical volume and thickness measures in autism spectrum disorders (ASD) show inconsistent results. We acquired structural magnetic resonance images of 30 individuals with ASD and individually matched controls and extracted surface-based and deformation-based morphometry measures. All participants had an IQ>100. Neither surface-based cortical thickness nor deformation based gyrification measures differed significantly across groups. Significant decreases but no increases of the gyrification index and sulcus depth could only be observed in the ASD group before correcting for multiple comparisons. This finding suggests that possible cortical anomalies in ASD are either weak or, given the heterogeneity of findings in earlier studies, might only apply to small ASD-subgroups.
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6. Nakamura T, Sakaue F, Nasu-Nishimura Y, Takeda Y, Matsuura K, Akiyama T. {{The Autism-Related Protein PX-RICS Mediates GABAergic Synaptic Plasticity in Hippocampal Neurons and Emotional Learning in Mice}}. {EBioMedicine}. 2018.
GABAergic dysfunction underlies many neurodevelopmental and psychiatric disorders. GABAergic synapses exhibit several forms of plasticity at both pre- and postsynaptic levels. NMDA receptor (NMDAR)-dependent inhibitory long-term potentiation (iLTP) at GABAergic postsynapses requires an increase in surface GABAARs through promoted exocytosis; however, the regulatory mechanisms and the neuropathological significance remain unclear. Here we report that the autism-related protein PX-RICS is involved in GABAAR transport driven during NMDAR-dependent GABAergic iLTP. Chemically induced iLTP elicited a rapid increase in surface GABAARs in wild-type mouse hippocampal neurons, but not in PX-RICS/RICS-deficient neurons. This increase in surface GABAARs required the PX-RICS/GABARAP/14-3-3 complex, as revealed by gene knockdown and rescue studies. iLTP induced CaMKII-dependent phosphorylation of PX-RICS to promote PX-RICS-14-3-3 assembly. Notably, PX-RICS/RICS-deficient mice showed impaired amygdala-dependent fear learning, which was ameliorated by potentiating GABAergic activity with clonazepam. Our results suggest that PX-RICS-mediated GABAAR trafficking is a key target for GABAergic plasticity and its dysfunction leads to atypical emotional processing underlying autism.
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7. Ofei SY, Fuchs GJ, 3rd. {{Constipation Burden in Children with Autism Spectrum Disorder: Emergency Department and Healthcare Use}}. {The Journal of pediatrics}. 2018.
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8. Singer AB, Daniele Fallin M, Burstyn I. {{Bayesian Correction for Exposure Misclassification and Evolution of Evidence in Two Studies of the Association Between Maternal Occupational Exposure to Asthmagens and Risk of Autism Spectrum Disorder}}. {Current environmental health reports}. 2018.
PURPOSE OF REVIEW: Inference in epidemiologic studies is plagued by exposure misclassification. Several methods exist to correct for misclassification error. One approach is to use point estimates for the sensitivity (Sn) and specificity (Sp) of the tool used for exposure assessment. Unfortunately, we typically do not know the Sn and Sp with certainty. Bayesian methods for exposure misclassification correction allow us to model this uncertainty via distributions for Sn and Sp. These methods have been applied in epidemiologic literature, but are not considered a mainstream approach, especially in occupational epidemiology. RECENT FINDINGS: Here, we illustrate an occupational epidemiology application of a Bayesian approach to correct for the differential misclassification error generated by estimating occupational exposures from job codes using a job exposure matrix (JEM). We argue that analyses accounting for exposure misclassification should become more commonplace in the literature.
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9. Wong CT, Bestard-Lorigados I, Crawford DA. {{Autism-related behaviours in the cyclooxygenase-2-deficient mouse model}}. {Genes, brain, and behavior}. 2018: e12506.
Prostaglandin E2 (PGE2) is an endogenous lipid molecule involved in normal brain development. Cyclooxygenase-2 (COX2) is the main regulator of PGE2 synthesis. Emerging clinical and molecular research provides compelling evidence that abnormal COX2/PGE2 signalling is associated with autism spectrum disorder (ASD). We previously found that COX2 knockout mice had dysregulated expression of many ASD genes belonging to important biological pathways for neurodevelopment. The current study is the first to demonstrate the connection between irregular COX2/PGE2 signalling and autism-related behaviours in male and female COX2-deficient knockin, (COX)-2(-) , mice at young (4-6 weeks) or adult (8-11 weeks) ages. Autism-related behaviours were prominent in male (COX)-2(-) mice for most behavioural tests. In the open field test, (COX)-2(-) mice travelled more than controls and adult male (COX)-2(-) mice spent less time in the center indicating elevated hyperactive and anxiety-linked behaviours. (COX)-2(-) mice also buried more marbles, with males burying more than females, suggesting increased anxiety and repetitive behaviours. Young male (COX)-2(-) mice fell more frequently in the inverted screen test revealing motor deficits. The three-chamber sociability test found that adult female (COX)-2(-) mice spent less time in the novel mouse chamber indicative of social abnormalities. In addition, male (COX)-2(-) mice showed altered expression of several autism-linked genes: Wnt2, Glo1, Grm5, and Mmp9. Overall, our findings offer new insight into the involvement of disrupted COX2/PGE2 signalling in ASD pathology with age-related differences and greater impact on males. We propose that (COX)-2(-) mice might serve as a novel model system to study specific types of autism.
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10. Zhu L, Wang H. {{Commentary on « Beta-Lactam Antibiotics as A Possible Novel Therapy for Managing Epilepsy and Autism}}. {Iranian journal of child neurology}. 2018; 12(3): 139-40.
