1. Bakheet SA, Alzahrani MZ, Nadeem A, Ansari MA, Zoheir KM, Attia SM, Al-Ayadhi LY, Ahmad SF. {{Resveratrol treatment attenuates chemokine receptor expression in the BTBR T+tf/J mouse model of autism}}. {Mol Cell Neurosci};2016 (Sep 29)
Autism is a neurodevelopmental disorder categorized by qualitative impairments in social interaction, communication, and repetitive stereotypic behavior. Emerging evidence increasingly suggests that chemokine receptors have a pivotal role in the central nervous system and are involved in the pathogenesis of numerous neuroinflammatory diseases. Resveratrol is widely used to treat neurodegenerative diseases, but its effect on autism has not been investigated. We investigated the effect of resveratrol (20 and 40mg/kg) in the spleen and brain tissues of BTBR T+tf/J (BTBR) and C57BL/6J (B6) mice as well as on the C-C chemokine receptor (CCR) and C-X-C motif chemokine receptor (CXCR) (CCR3+, CCR5+, CCR7+ and CCR9+, CXCR3+ and CXCR5+) in cluster of differentiation 4-positive (CD4+) T cells in the spleen. We also assessed the mRNA expression of CCR and CXCR receptors in the spleen and brain tissues. Our study revealed that the BTBR and B6 control mice showed different immune profiles. The BTBR mice showed characteristic higher levels of both CCR and CXCR production and expression in CD4+ T cells than the B6 control mice did. Treatment of B6 and BTBR mice with resveratrol (20 and 40mg/kg) induced a substantial decrease in the CCR and CXCR production and expression in CD4+ T cells compared with the respective untreated control groups. Moreover, resveratrol treatment decreased the mRNA expression levels of CCR and CXCR in the spleen and brain tissues. Resveratrol downregulated the chemokine receptor levels, which might provide unique targets for future therapies for autism.
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2. Bassett E, Heinle R, Johnston D. {{Sleep Apnea in Patients With Rett Syndrome: Roles for Polysomnography and Adenotonsillectomy}}. {J Child Neurol};2016 (Oct 4)
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3. Bertolino B, Crupi R, Impellizzeri D, Bruschetta G, Cordaro M, Siracusa R, Esposito E, Cuzzocrea S. {{Beneficial Effects of Co-Ultramicronized Palmitoylethanolamide/Luteolin in a Mouse Model of Autism and in a Case Report of Autism}}. {CNS Neurosci Ther};2016 (Oct 4)
AIMS: Autism spectrum disorder (ASD) is a condition defined by social communication deficits and repetitive restrictive behaviors. Association of the fatty acid amide palmitoylethanolamide (PEA) with the flavonoid luteolin displays neuroprotective and antiinflammatory actions in different models of central nervous system pathologies. We hypothesized that association of PEA with luteolin might have therapeutic utility in ASD, and we employed a well-recognized autism animal model, namely sodium valproate administration, to evaluate cognitive and motor deficits. METHODS: Two sets of experiments were conducted. In the first, we investigated the effect of association of ultramicronized PEA with luteolin, co-ultramicronized PEA-LUT(R) (co-ultraPEA-LUT(R)) in a murine model of autistic behaviors, while in the second, the effect of co-ultraPEA-LUT(R) in a patient affected by ASD was examined. RESULTS: Co-ultraPEA-LUT(R) treatment ameliorated social and nonsocial behaviors in valproic acid-induced autistic mice and improved clinical picture with reduction in stereotypes in a 10-year-old male child. CONCLUSION: These data suggest that ASD symptomatology may be improved by agents documented to control activation of mast cells and microglia. Co-ultraPEA-LUT(R) might be a valid and safe therapy for the symptoms of ASD alone or in combination with other used drugs.
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4. Bishop-Fitzpatrick L, Minshew NJ, Mazefsky CA, Eack SM. {{Perception of Life as Stressful, Not Biological Response to Stress, is Associated with Greater Social Disability in Adults with Autism Spectrum Disorder}}. {J Autism Dev Disord};2016 (Sep 30)
This study examined differences between adults with autism spectrum disorder (ASD; N = 40) and typical community volunteers (N = 25) on measures of stressful life events, perceived stress, and biological stress response (cardiovascular and cortisol reactivity) during a novel social stress task. Additional analyses examined the relationship between stress and social functioning as measured by the Social Adjustment Scale-II and the Waisman Activities of Daily Living scale. Results indicated that adults with ASD experienced significantly more stressful life events and perceived stress, and greater systolic blood pressure reactivity than typical community volunteers. Results also indicated that perceived stress and stressful life events were significantly associated with social disability. Interventions targeting stress management might improve social function in adults with ASD.
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5. Brimberg L, Mader S, Jeganathan V, Berlin R, Coleman TR, Gregersen PK, Huerta PT, Volpe BT, Diamond B. {{Caspr2-reactive antibody cloned from a mother of an ASD child mediates an ASD-like phenotype in mice}}. {Mol Psychiatry};2016 (Oct 04)
Autism spectrum disorder (ASD) occurs in 1 in 68 births, preferentially affecting males. It encompasses a group of neurodevelopmental abnormalities characterized by impaired social interaction and communication, stereotypic behaviors and motor dysfunction. Although recent advances implicate maternal brain-reactive antibodies in a causative role in ASD, a definitive assessment of their pathogenic potential requires cloning of such antibodies. Here, we describe the isolation and characterization of monoclonal brain-reactive antibodies from blood of women with brain-reactive serology and a child with ASD. We further demonstrate that male but not female mice exposed in utero to the C6 monoclonal antibody, binding to contactin-associated protein-like 2 (Caspr2), display abnormal cortical development, decreased dendritic complexity of excitatory neurons and reduced numbers of inhibitory neurons in the hippocampus, as well as impairments in sociability, flexible learning and repetitive behavior. Anti-Caspr2 antibodies are frequent in women with brain-reactive serology and a child with ASD. Together these studies provide a methodology for obtaining monclonal brain-reactive antibodies from blood B cells, demonstrate that ASD can result from in utero exposure to maternal brain-reactive antibodies of single specificity and point toward the exciting possibility of prognostic and protective strategies.Molecular Psychiatry advance online publication, 4 October 2016; doi:10.1038/mp.2016.165.
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6. Cage E, Bird G, Pellicano E. {{Reputation Management in Children on the Autism Spectrum}}. {J Autism Dev Disord};2016 (Sep 30)
Being able to manage reputation is an important social skill, but it is unclear whether autistic children can manage reputation. This study investigated whether 33 autistic children matched to 33 typical children could implicitly or explicitly manage reputation. Further, we examined whether cognitive processes-theory of mind, social motivation, inhibitory control and reciprocity-contribute to reputation management. Results showed that neither group implicitly managed reputation, and there was no group difference in explicit reputation management. Results suggested different mechanisms contribute to reputation management in these groups-social motivation in typical children and reciprocity in autistic children. Explicit reputation management is achievable for autistic children, and there are individual differences in its relationship to underlying cognitive processes.
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7. Crider A, Pillai A. {{The Neurobiological Basis for Social Affiliation in Autism Spectrum Disorder and Schizophrenia}}. {Curr Behav Neurosci Rep};2016 (Jun);3(2):154-164.
Social interaction and communication are complex behavioral paradigms involving many components. Many different neurotransmitters, hormones, sensory inputs, and brain regions are involved in the act of social engagement and verbal or nonverbal communication. Autism Spectrum Disorder (ASD) and schizophrenia are two neurodevelopmental disorders that have social and language deficits as hallmark symptoms, but show very different etiologies. The output of social dysfunction is common to both ASD and schizophrenia, but this likely arises from very different pathophysiological means. This review will attempt to compile and interpret human and animal studies showing the neurobiological basis for the development of social and language deficits in ASD and schizophrenia as well as a comparison of the two disorders.
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8. Ellis Weismer S, Haebig E, Edwards J, Saffran J, Venker CE. {{Lexical Processing in Toddlers with ASD: Does Weak Central Coherence Play a Role?}}. {J Autism Dev Disord};2016 (Oct 1)
This study investigated whether vocabulary delays in toddlers with autism spectrum disorders (ASD) can be explained by a cognitive style that prioritizes processing of detailed, local features of input over global contextual integration-as claimed by the weak central coherence (WCC) theory. Thirty toddlers with ASD and 30 younger, cognition-matched typical controls participated in a looking-while-listening task that assessed whether perceptual or semantic similarities among named images disrupted word recognition relative to a neutral condition. Overlap of perceptual features invited local processing whereas semantic overlap invited global processing. With the possible exception of a subset of toddlers who had very low vocabulary skills, these results provide no evidence that WCC is characteristic of lexical processing in toddlers with ASD.
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9. Forbes PA, Pan X, de CHAF. {{Reduced Mimicry to Virtual Reality Avatars in Autism Spectrum Disorder}}. {J Autism Dev Disord};2016 (Sep 30)
Mimicry involves unconsciously copying the actions of others. Increasing evidence suggests that autistic people can copy the goal of an observed action but show differences in their mimicry. We investigated mimicry in autism spectrum disorder (ASD) within a two-dimensional virtual reality environment. Participants played an imitation game with a socially engaged avatar and socially disengaged avatar. Despite being told only to copy the goal of the observed action, autistic participants and matched neurotypical participants mimicked the kinematics of the avatars’ movements. However, autistic participants mimicked less. Social engagement did not modulate mimicry in either group. The results demonstrate the feasibility of using virtual reality to induce mimicry and suggest mimicry differences in ASD may also occur when interacting with avatars.
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10. Ganesan S, Khan S, Garel KA, Hamalainen MS, Kenet T. {{Normal Evoked Response to Rapid Sequences of Tactile Pulses in Autism Spectrum Disorders}}. {Front Hum Neurosci};2016;10:433.
Autism spectrum disorder (ASD) is a developmental disorder diagnosed behaviorally, with many documented neurophysiological abnormalities in cortical response properties. While abnormal sensory processing is not considered core to the disorder, most ASD individuals report sensory processing abnormalities. Yet, the neurophysiological correlates of these abnormalities have not been fully mapped. In the auditory domain, studies have shown that cortical responses in the early auditory cortex in ASD are abnormal in multiple ways. In particular, it has been shown that individuals with ASD have abnormal cortical auditory evoked responses to rapid, but not slow, sequences of tones. In parallel, there is substantial evidence of somatosensory processing abnormalities in ASD, including in the temporal domain. Here, we tested the somatosensory domain in ASD for abnormalities in rapid processing of tactile pulses, to determine whether abnormalities there parallel those observed in the auditory domain. Specifically, we tested the somatosensory cortex response to a sequence of two tactile pulses with different (short and long) temporal separation. We analyzed the responses in cortical space, in primary somatosensory cortex. As expected, we found no group difference in the evoked response to pulses with long (700 ms) temporal separation. Contrary to findings in the auditory domain, we also found no group differences in the evoked responses to the sequence with a short (200 ms) temporal separation. These results suggest that rapid temporal processing deficits in ASD are not generalized across multiple sensory domains, and are unlikely to underlie the behavioral somatosensory abnormalities observed in ASD.
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11. Ha S, Park H, Mahmood U, Ra JC, Suh YH, Chang KA. {{Human adipose-derived stem cells ameliorate repetitive behavior, social deficit and anxiety in a VPA-induced autism mouse model}}. {Behav Brain Res};2016 (Oct 4)
Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by impairments in social interaction and communication, and patients often display repetitive behaviors. Although the global prevalence of ASD has increased over time, the etiology and treatments for ASD are poorly understood. Recently, some researchers have suggested that stem cells have therapeutic potential for ASD. Thus, in the present study, we investigated the therapeutic effects of human adipose-derived stem cells (hASCs), a kind of mesenchymal stem cells (MSCs) isolated from adipose tissue, on ASD using valproic acid (VPA)-induced autism model mice. Human ASCs were injected into the neonatal pups (P2 or P3) intraventricularly and then we evaluated major behavior symptoms of ASD. VPA-treated mice showed increased repetitive behaviors, decreased social interactions and increased anxiety but these autistic behaviors were ameliorated through transplantation of hASCs. In addition, hASCs transplantation restored the alteration of phosphatase and tensin homolog (PTEN) expression and p-AKT/AKT ratio in the brains of VPA-induced ASD model mice. The decreased level of vascular endothelial growth factor (VEGF) and interleukin 10 (IL-10) by VPA were rescued in the brains of the hASC-injected VPA mice. With these results, we experimentally showed hASCs’ therapeutic effects on ASD model mice for the first time. This animal model system can be used to elucidate further mechanisms of therapeutic effects of hASCs in ASD.
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12. Hamza M, Halayem S, Mrad R, Bourgou S, Charfi F, Belhadj A. {{[Epigenetics’ implication in autism spectrum disorders: A review]}}. {Encephale};2016 (Sep 27)
BACKGROUND: The etiology of autism spectrum disorders (ASD) is complex and multifactorial, and the roles of genetic and environmental factors in its emergence have been well documented. Current research tends to indicate that these two factors act in a synergistic manner. The processes underlying this interaction are still poorly known, but epigenetic modifications could be the mediator in the gene/environment interface. The epigenetic mechanisms have been implicated in susceptibility to stress and also in the pathogenesis of psychiatric disorders including depression and schizophrenia. Currently, several studies focus on the consideration of the etiological role of epigenetic regulation in ASD. OBJECT: The object of this review is to present a summary of current knowledge of an epigenetic hypothesis in ASD, outlining the recent findings in this field. METHODS: Using Pubmed, we did a systematic review of the literature researching words such as: autism spectrum disorders, epigenetics, DNA methylation and histone modification. RESULTS: Epigenetic refers to the molecular process modulating gene expression without changes in the DNA sequence. The most studied epigenetic mechanisms are those that alter the chromatin structure including DNA methylation of cytosine residues in CpG dinucleotides and post-translational histone modifications. In ASD several arguments support the epigenetic hypothesis. In fact, there is a frequent association between ASD and genetic diseases whose epigenetic etiologies are recognized. A disturbance in the expression of genes involved in the epigenetic regulation has also been described in this disorder. Some studies have demonstrated changes in the DNA methylation of several autism candidate genes including the gene encoding the oxytocin receptor (OXTR), the RELN and the SHANK3 genes. Beyond the analysis of candidate genes, recent epigenome-wide association studies have investigated the methylation level of several other genes and showed hypomethylation of the whole DNA in brain and blood samples of autistic patients. The changes in epigenetic marks following exposure to environmental factors known as autism risk factors are also discussed in many reports. They include nutritional (vitamin D and folate) and toxic (sodium valproate, bisphenol A) factors. Despite a considerable contribution to understanding the complexity of ASD etiology, the epigenetic studies suffer from numerous methodological biases that limit the scope of their results and make their interpretation difficult. The cell samples used in the psychiatric studies are mostly from the post-mortem tissue of the central nervous system, and factors that might change the epigenome (age, gender, treatments received…) are not taken into account. The use of blood and buccal epithelium samples raises in turn the question as to whether the epigenome of these cells reflects that of the nerve cells. DNA methylation can also be influenced by cell subcomposition variability, transcriptional variability and by DNA sequence variants. CONCLUSION: These recent discoveries in epigenetics are the beginnings of an etiopathogenic research revolution in neurodevelopmental disorders. The conceptualization of epigenetic processes is in its early stages and despite its limited means will help integrate disparate data factors previously involved in autism. It could also be the target for the development of new therapeutic modalities.
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13. Hilton CL, Babb-Keeble A, Westover EE, Zhang Y, Adams C, Collins DM, Karmarkar A, Reistetter TA, Constantino JN. {{Sensory Responsiveness in Siblings of Children with Autism Spectrum Disorders}}. {J Autism Dev Disord};2016 (Oct 4)
This study examined sensory responsiveness in unaffected siblings of children with autism spectrum disorder (ASD) and associations between sensory responsiveness and social severity. Sensory Profile Caregiver Questionnaires and Social Responsiveness Scales were completed by parents of 185 children between age 4 and 10.95 years. Significant differences were found between participants with ASD and controls, and between participants with ASD and unaffected siblings for all sensory quadrants and domains, but not between controls and unaffected siblings. Social responsiveness scores were significantly correlated with scores from most sensory profile categories. Sensory responsiveness as an endophenotype of ASD is not indicated from these findings; however, studies with larger numbers of unaffected siblings and controls are needed to confirm the null hypothesis.
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14. Hwang YT, Aliaga SM, Arpone M, Francis D, Li X, Chong B, Slater HR, Rogers C, Bretherton L, Hunter M, Heard R, Godler DE. {{Partially methylated alleles, microdeletion, and tissue mosaicism in a fragile X male with tremor and ataxia at 30 years of age: A case report}}. {Am J Med Genet A};2016 (Oct 1)
CGG repeat expansion >200 within FMR1, termed full mutation (FM), has been associated with promoter methylation, consequent silencing of gene expression and fragile X syndrome (FXS)-a common cause of intellectual disability and co-morbid autism. Unmethylated premutation (55-199 repeats) and FM alleles have been associated with fragile X related tremor/ataxia syndrome (FXTAS), a late onset neurodegenerative disorder. Here we present a 33-year-old male with FXS, with white matter changes and progressive deterioration in gait with cerebellar signs consistent with probable FXTAS; there was no evidence of any other cerebellar pathology. We show that he has tissue mosaicism in blood, saliva, and buccal samples for the size and methylation of his expanded alleles and a de novo, unmethylated microdeletion. This microdeletion involves a approximately 80 bp sequence in the FMR1 promoter as well as complete loss of the CGG repeat in a proportion of cells. Despite FMR1 mRNA levels in blood within the normal range, the methylation and CGG sizing results are consistent with the diagnosis of concurrent FXS and probable FXTAS. The demonstrated presence of unmethylated FM alleles would explain the manifestation of milder than expected cognitive and behavioral impairments and early onset of cerebellar ataxia. Our case suggests that individuals with FXS, who manifest symptoms of FXTAS, may benefit from more detailed laboratory testing. (c) 2016 Wiley Periodicals, Inc.
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15. Ibrahim GM, Morgan BR, Vogan VM, Leung RC, Anagnostou E, Taylor MJ. {{Mapping the Network of Neuropsychological Impairment in Children with Autism Spectrum Disorder: A Graph Theoretical Analysis}}. {J Autism Dev Disord};2016 (Sep 30)
Children with autism spectrum disorder (ASD) exhibit social-communicative impairments. Less is known about the neuropsychological profile of ASD, although cognitive and neuropsychological deficits are evident. We modelled neuropsychological function in 20 children with ASD and 20 sex, age and IQ matched typically-developing controls (ages 7-14) as a network of interacting parameters. Graph theoretical analysis was applied to identify critical topographic regions within this network. Two areas were significantly stronger hubs in typically-developing children, the ability to shift attention (p < 0.001) and overall executive function (p < 0.001). Planning/organization was a stronger hub in the cognitive networks of children with ASD (p = 0.001). We show that ASD is not only characterized by impairments in various neurocognitive domains, but also alterations in their interaction. Lien vers le texte intégral (Open Access ou abonnement)
16. Kleberg JL, Thorup E, Falck-Ytter T. {{Reduced visual disengagement but intact phasic alerting in young children with autism}}. {Autism Res};2016 (Oct 1)
Children with autism may have difficulties with visual disengagement-that is, inhibiting current fixations and orienting to new stimuli in the periphery. These difficulties may limit these children’s ability to flexibly monitor the environment, regulate their internal states, and interact with others. In typical development, visual disengagement is influenced by a phasic alerting network that increases the processing speed of the visual system after salient events. The role of the phasic alerting effect in the putative atypical disengagement performance in autism spectrum disorder (ASD) is not known. Here, we compared visual disengagement in six-year-old children with autism (N = 18) and typically developing children (N = 17) matched for age and nonverbal IQ. We manipulated phasic alerting during a visual disengagement task by adding spatially nonpredictive sounds shortly before the onset of the visual peripheral targets. Children with ASD showed evidence of delayed disengagement compared to the control group. Sounds facilitated visual disengagement similarly in both groups, suggesting typical modulation by phasic alerting in ASD in the context of this task. These results support the view that atypical visual disengagement in ASD is related to other factors than atypicalities in the alerting network. Autism Res 2016. (c) 2016 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research.
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17. Leyser M, Dias BL, Coelho AL, Vasconcelos M, Nascimento OJ. {{12p deletion spectrum syndrome: a new case report reinforces the evidence regarding the potential relationship to autism spectrum disorder and related developmental impairments}}. {Mol Cytogenet};2016;9:75.
BACKGROUND: Autism Spectrum Disorders (ASD) now encompass a broad heterogeneous group of people who present in the early developmental years with a wide range of social and communication deficits, which are typically also associated with complex repetitive behaviors and circumscribed interests. The target goal is to heighten readers’ perception into the trend to personalize the distinct autistic and related developmental conditions encompassing the 12p region. CASE PRESENTATION: This is a case-report of a 4-year-old male who presented the core signs of ASD, which were thought to be related to a rare 12p13.2 deletion. We further reviewed the literature in order to outline the related developmental conditions in the 12p region. Aside from this patient reported here, we found an additional number of 43 cases described in the medical literature since 1974, that have been related to deletions in the 12p region. However, to the best of our knowledge, none of the previous had been specifically linked to the 12p13.2 band. CONCLUSIONS: The 12p deletion spectrum is rarely described as part of the selective genotypes thought to be related to ASD. Even inside of a small piece of the puzzle, there might be ample variation in the behavioral and clinical phenotypes of children and adults presenting with this particular genetic profile. In that regard, the particular 12p13.2 distal deletion presentation is one of the possible genotypes encompassed by the « 12p deletion spectrum syndrome », that might be potentially connected to the diagnosis of ASD and related developmental disorders.
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18. Murphy ER, Norr M, Strang JF, Kenworthy L, Gaillard WD, Vaidya CJ. {{Neural Basis of Visual Attentional Orienting in Childhood Autism Spectrum Disorders}}. {J Autism Dev Disord};2016 (Oct 1)
We examined spontaneous attention orienting to visual salience in stimuli without social significance using a modified Dot-Probe task during functional magnetic resonance imaging in high-functioning preadolescent children with Autism Spectrum Disorder (ASD) and age- and IQ-matched control children. While the magnitude of attentional bias (faster response to probes in the location of solid color patch) to visually salient stimuli was similar in the groups, activation differences in frontal and temporoparietal regions suggested hyper-sensitivity to visual salience or to sameness in ASD children. Further, activation in a subset of those regions was associated with symptoms of restricted and repetitive behavior. Thus, atypicalities in response to visual properties of stimuli may drive attentional orienting problems associated with ASD.
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19. Musova Z, Hancarova M, Havlovicova M, Pourova R, Hrdlicka M, Kraus J, Trkova M, Stejskal D, Sedlacek Z. {{Expanded DMPK repeats in dizygotic twins referred for diagnosis of autism versus absence of expanded DMPK repeats at screening of 330 children with autism}}. {Neuropsychiatr Dis Treat};2016;12:2367-2372.
Myotonic dystrophy type 1 (DM1) belongs to the broad spectrum of genetic disorders associated with autism spectrum disorders (ASD). ASD were reported predominantly in congenital and early childhood forms of DM1. We describe dizygotic twin boys with ASD who were referred for routine laboratory genetic testing and in whom karyotyping, FMR1 gene testing, and single nucleotide polymorphism array analysis yielded negative results. The father of the boys was later diagnosed with suspected DM1, and testing revealed characteristic DMPK gene expansions in his genome as well as in the genomes of both twins and their elder brother, who also suffered from ASD. In accord with previous reports on childhood forms of DM1, our patients showed prominent neuropsychiatric phenotypes characterized especially by hypotonia, developmental and language delay, emotional and affective lability, lowered adaptability, and social withdrawal. The experience with this family and multiple literature reports of ASD in DM1 on the one side but the lack of literature data on the frequency of DMPK gene expansions in ASD patients on the other side prompted us to screen the DMPK gene in a sample of 330 patients with ASD who were first seen by a geneticist before they were 10 years of age, before the muscular weakness, which may signal DM1, usually becomes obvious. The absence of any DMPK gene expansions in this cohort indicates that targeted DMPK gene testing can be recommended only in ASD patients with specific symptoms or family history suggestive of DM1.
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20. Pace M, Dumortier L, Favre-Juvin A, Guinot M, Bricout VA. {{Heart rate variability during sleep in children with autism spectrum disorders}}. {Physiol Behav};2016 (Sep 29);167:309-312.
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21. Poole D, Gowen E, Warren PA, Poliakoff E. {{Brief Report: Which Came First? Exploring Crossmodal Temporal Order Judgements and Their Relationship with Sensory Reactivity in Autism and Neurotypicals}}. {J Autism Dev Disord};2016 (Oct 4)
Previous studies have indicated that visual-auditory temporal acuity is reduced in children with autism spectrum conditions (ASC) in comparison to neurotypicals. In the present study we investigated temporal acuity for all possible bimodal pairings of visual, tactile and auditory information in adults with ASC (n = 18) and a matched control group (n = 18). No group differences in temporal acuity for crossmodal stimuli were observed, suggesting that this may be typical in adults with ASC. However, visual-tactile temporal acuity and bias towards vision when presented with visual-auditory information were both predictors of self-reported sensory reactivity. This suggests that reduced multisensory temporal acuity and/or attention towards vision may contribute to atypical sensory reactivity.
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22. Port RG, Gaetz W, Bloy L, Wang DJ, Blaskey L, Kuschner ES, Levy SE, Brodkin ES, Roberts TP. {{Exploring the relationship between cortical GABA concentrations, auditory gamma-band responses and development in ASD: Evidence for an altered maturational trajectory in ASD}}. {Autism Res};2016 (Oct 1)
Autism spectrum disorder (ASD) is hypothesized to arise from imbalances between excitatory and inhibitory neurotransmission (E/I imbalance). Studies have demonstrated E/I imbalance in individuals with ASD and also corresponding rodent models. One neural process thought to be reliant on E/I balance is gamma-band activity (Gamma), with support arising from observed correlations between motor, as well as visual, Gamma and underlying GABA concentrations in healthy adults. Additionally, decreased Gamma has been observed in ASD individuals and relevant animal models, though the direct relationship between Gamma and GABA concentrations in ASD remains unexplored. This study combined magnetoencephalography (MEG) and edited magnetic resonance spectroscopy (MRS) in 27 typically developing individuals (TD) and 30 individuals with ASD. Auditory cortex localized phase-locked Gamma was compared to resting Superior Temporal Gyrus relative cortical GABA concentrations for both children/adolescents and adults. Children/adolescents with ASD exhibited significantly decreased GABA+/Creatine (Cr) levels, though typical Gamma. Additionally, these children/adolescents lacked the typical maturation of GABA+/Cr concentrations and gamma-band coherence. Furthermore, children/adolescents with ASD additionally failed to exhibit the typical GABA+/Cr to gamma-band coherence association. This altered coupling during childhood/adolescence may result in Gamma decreases observed in the adults with ASD. Therefore, individuals with ASD exhibit improper local neuronal circuitry maturation during a childhood/adolescence critical period, when GABA is involved in configuring of such circuit functioning. Provocatively a novel line of treatment is suggested (with a critical time window); by increasing neural GABA levels in children/adolescents with ASD, proper local circuitry maturation may be restored resulting in typical Gamma in adulthood. Autism Res 2016. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.
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23. Ryan C, Stafford M, King RJ. {{Brief Report: Seeing the Man in the Moon: Do Children with Autism Perceive Pareidolic Faces? A Pilot Study}}. {J Autism Dev Disord};2016 (Sep 30)
Faces are one of the most socially significant visual stimuli encountered in the environment, whereas pareidolias are illusions of faces arising from ambiguous stimuli in the environment. Autism spectrum disorder (ASD) is characterised by deficits in response to social stimuli. We found that children with ASD (n = 60) identify significantly fewer pareidolic faces in a sequence of ambiguous stimuli than typically developing peers. The two groups did not differ in the number of objects identified, indicating that the children with ASD had a specific lack of attention to faces. Pareidolia have considerable potential as naturalistic and easy-to-create materials for the investigation of spontaneous attention to social stimuli in children with ASD.
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24. Sacco C. {{No Map to This Country: One Family’s Journey Through Autismby Jennifer Noonan; Boston, Da Capo Press, 2016, 311 pages}}. {Psychiatr Serv};2016 (Oct 1);67(10):e16-e17.
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25. Schultz ST, Gould GG. {{Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder}}. {Autism Open Access};2016 (Apr);6(2)
Autism Spectrum Disorder (ASD) is characterized by persistent deficits in social communication and restrictive behavior, interests, and activities. Our previous case-control study showed that use of acetaminophen at age 12-18 months is associated with increased likelihood for ASD (OR 8.37, 95% CI 2.08-33.7). In this study, we again show that acetaminophen use is associated with ASD (p = 0.013). Because these children are older than in our first study, the association is reversed; fewer children with ASD vs. non-ASD children use acetaminophen as a « first choice » compared to « never use » (OR 0.165, 95% CI 0.045, 0.599). We found significantly more children with ASD vs. non- ASD children change to the use of ibuprofen when acetaminophen is not effective at reducing fever (p = 0.033) and theorize this change in use is due to endocannabinoid system dysfunction. We also found that children with ASD vs. non-ASD children are significantly more likely to show an increase in sociability when they have a fever (p = 0.037) and theorize that this increase is due to anandamide activation of the endocannabinoid system in ASD children with low endocannabinoid tone from early acetaminophen use. In light of this we recommend that acetaminophen use be reviewed for safety in children.
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26. Tan P, Alant E. {{Using peer-mediated instruction to support communication involving a student with autism during mathematics activities: A case study}}. {Assist Technol};2016 (Oct 3):1-7.
This study employed an A-B singled subject design to explore the extent to which a peer-mediated intervention supported a first-grade student with autism’s usage both in purpose and frequency of a speech-generating device (SGD) during mathematics activities. The intervention involved teaching a peer without a disability to encourage the student with autism to use the SGD during partnered mathematics activities. Our analysis involved visual and descriptive examination of trends and patterns over time, and comparison of means between and within phases. We found during the course of this study that (1) the student with autism’s level of overall communication, which included the relevancy of these communicative behaviors, increased; (2) the student with autism’s level of spontaneous communication acts increased; and (3) the peer became more independent with supporting the student with autism’s communication. Implications for future research and practice are provided.
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27. Wang X, Mu Y, Sun M, Han J. {{Bidirectional regulation of fragile X mental retardation protein phosphorylation controls rhodopsin homeostasis}}. {J Mol Cell Biol};2016 (Oct 4)
Homeostatic regulation of the light sensor, rhodopsin, is critical for the maintenance of light sensitivity and survival of photoreceptors. The major fly rhodopsin, Rh1, undergoes light-induced endocytosis and degradation, but its protein and mRNA levels remain constant during light/dark cycles. It is not clear how translation of Rh1 is regulated. Here, we show that adult photoreceptors maintain a constant, abundant quantity of ninaE mRNA, which encodes Rh1. We demonstrate that the Fmr1 protein associates with ninaE mRNA and represses its translation. Further, light exposure triggers a calcium-dependent dephosphorylation of Fmr1, which relieves suppression of Rh1 translation. We demonstrate that the catalytic subunit of PP2A (Mts) mediates light-induced Fmr1 dephosphorylation in a regulatory B subunit of PP2A (CKa)-dependent manner. Finally, we show that blocking light-induced Rh1 translation results in reduced light sensitivity. Our results reveal the molecular mechanism of Rh1 homeostasis and physiological consequence of Rh1 dysregulation.
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28. Watson LR. {{Autism Spectrum Disorder: From Pensieve to Crystal Ball}}. {Semin Speech Lang};2016 (Nov);37(4):231-238.
In the next decade, professionals in communication sciences and disorders will encounter a wealth of needs, opportunities, and challenges in research and practice related to autism spectrum disorder. What lies ahead will reflect both transformations of and continuities with past perspectives (psychodynamic, biological, and learning theory). Among our largest challenges as individuals and as a discipline will be to determine the most important needs to address and the most productive opportunities to seize. Interprofessional collaboration, community engagement, and partnerships among researchers, practitioners, and community stakeholder are all strategies that can better guide our selection of priorities.
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29. Yao Z, Hu B, Xie Y, Zheng F, Liu G, Chen X, Zheng W. {{Resting-State Time-Varying Analysis Reveals Aberrant Variations of Functional Connectivity in Autism}}. {Front Hum Neurosci};2016;10:463.
Recently, studies based on time-varying functional connectivity have unveiled brain states diversity in some neuropsychiatric disorders, such as schizophrenia and major depressive disorder. However, time-varying functional connectivity analysis of resting-state functional Magnetic Resonance Imaging (fMRI) have been rarely performed on the Autism Spectrum Disorder (ASD). Hence, we performed time-varying connectivity analysis on resting-state fMRI data to investigate brain states mutation in ASD children. ASD showed an imbalance of connectivity state and aberrant ratio of connectivity with different strengths in the whole brain network, and decreased connectivity associated precuneus/posterior cingulate gyrus with medial prefrontal gyrus in default mode network. As compared to typical development children, weak relevance condition (the strength of a large number of connectivities in the state was less than means minus standard deviation of all connection strength) was maintained for a longer time between brain areas of ASD children, and ratios of weak connectivity in brain states varied dramatically in the ASD. In the ASD, the abnormal brain state might be related to repetitive behaviors and stereotypical interests, and macroscopically reflect disruption of gamma-aminobutyric acid at the cellular level. The detection of brain states based on time-varying functional connectivity analysis of resting-state fMRI might be conducive for diagnosis and early intervention of ASD before obvious clinical symptoms.
