Deficits In Autism Research Articles

Hippocampal contributions to biologic, behavioral and cognitive deficits in autism: An update review

The most characteristic symptoms for the diagnosis of autism spectrum disorder (ASD) and the future life of the individual are deterioration in social communication and stereotyped or repetitive behaviors. ASD is associated with diverse atypical difficulties, including memory, learning, language, emotion, and cognitive impairment. Consequently, the hippocampus is important for memory, learning, language ability, emotional regulation, and cognitive mapping. Thus, the hippocampus plays an influential role in the pathophysiological mechanisms of ASD. Here, we provide an updated review of hippocampal structural and functional abnormalities and highlight the hippocampus as an important area for future research.

Is it up to language? Pragmatic competence in Croatian preschool children with autism and typical development

Objectives The relationship between structural language ability and pragmatics is not fully understood, in either individuals with autism or those with typical development (TD). Despite the well-established understanding that core deficits in autism lie in pragmatics, specific pragmatic behaviours that distinguish autistic children (AC) from their TD peers are not sufficiently described. The aims of this study were as follows: to investigate the differences in language abilities and pragmatic competence between AC and those with TD; to examine the relationship between language comprehension/production and pragmatic competence in both groups; and to identify the items of pragmatic composite that are most discriminative in detecting AC. Methods The participants in this study were preschool-aged children with TD (N = 45; mean age 65.5 months) and AC with average nonverbal IQ scores (N = 32; mean age 72.9 months). Language production and comprehension abilities were assessed using the New Reynell Developmental Language Scales (4th edition), and pragmatic competence was measured using the Children’s Communication Checklist (CCC). Results For all language and pragmatic variables, AC performed worse than those with TD. Pragmatic competencies did not correlate with structural language skills in either group, except for a correlation between language production and coherence in the TD. Finally, certain pragmatic behaviours common to many AC and rarely found in children with TD were identified as potential distinguishing features between the two groups. Conclusions This study underscores the importance of incorporating pragmatic assessments alongside traditional language evaluations and suggests that interventions should target pragmatic competence specifically, especially in preschool AC.

Cross-neurotype communication from an autistic point of view: Insights on autistic Theory of Mind from a focus group study.

The conceptualisation of autism as a disorder where Theory of Mind (ToM) and pragmatics are fundamentally impaired has prompted a wealth of research on autistic deficits, most of which is characterised by two main assumptions: first, that autistic people would display said deficits, if present, with any conversation partner and in any situation; second, that neurotypical people do not present these deficits, regardless of the conversation partner. However, this is not necessarily reflected in autistic accounts of the way they experience social cognition and pragmatics. The present paper aims to investigate the autistic experience of communication with both autistic and neurotypical people, with a particular focus on their perception of the ability of autistic and neurotypical people to understand their communicative intentions. Participants, 23 adult Italian autistic people without intellectual disability or language disorders, were recruited online. Two virtual focus groups of 2 hours each were conducted, transcribed and analysed through thematic analysis with a descriptive phenomenological approach by two independent researchers. Six themes were developed from the analysis, the most relevant being Autistic-Autistic communication and Autistic ToM. The results, in line with the Double Empathy theory, suggest there seem to be important differences between neurotypical and autistic people's ToM. These appear to make it easier for autistic people to communicate with one another, as well as to create difficulties for neurotypical people to understand autistic people, not just the other way around. These results seem to confirm that challenges in cross-neurotype communication are better interpreted as mutual miscomprehension and reciprocal differences in ToM rather than deficits on the autistic part. This calls for a reframing of ToM and/or the need for autistic ToM as a construct, of which neurotypical people seem to be lacking. Moreover, these insights should be taken into account for speech and language therapy and clinical practice in general, advocating for a neurodiversity-informed view of co-constructed communication as well as for a broader societal change in which therapists can play a crucial role, through participatory approaches or raising awareness in their daily practice. What is already known on the subject Autism is conceived as characterised by social cognition and communication difficulties, often linked to Theory of Mind (ToM) deficits. However, recent research suggested variations in ToM abilities within the autistic population and proposed alternative theories like the Double Empathy theory. Nevertheless, only a few studies examined how autistic individuals perceive communication across neurotypes. What this study adds Autistic individuals seem to find it easier to communicate with other autistic people, and they identify specific characteristics of neurotypical communication that hinder successful communication. Moreover, neurotypical people are perceived as having difficulties in autistic ToM, which seems to emerge as a relevant and needed construct in light of the Double Empathy problem. What are the clinical implications of this work? These findings can inform speech and language therapy and clinical practice about the potential gains of raising awareness on the Double Empathy problem and the higher communication ease inside the autistic community, alongside individualised support. Participatory approaches and closer collaboration with the autistic community also seem to be crucial for therapists to help improve communication experiences for autistic individuals.

Altered white matter connectivity of ventral language networks in autism spectrum disorder: An automated fiber quantification analysis with multi-site datasets

Comprehension and pragmatic deficits are prevalent in autism spectrum disorder (ASD) and are potentially linked to altered connectivity in the ventral language networks. However, previous magnetic resonance imaging studies have not sufficiently explored the microstructural abnormalities in the ventral fiber tracts underlying comprehension dysfunction in ASD. Additionally, the precise locations of white matter (WM) changes in the long tracts of patients with ASD remain poorly understood. In the current study, we applied the automated fiber-tract quantification (AFQ) method to investigate the fine-grained WM properties of the ventral language pathway and their relationships with comprehension and symptom manifestation in ASD. The analysis included diffusion/T1 weighted imaging data of 83 individuals with ASD and 83 age-matched typically developing (TD) controls. Case-control comparisons were performed on the diffusion metrics of the ventral tracts at both the global and point-wise levels. We also explored correlations between diffusion metrics, comprehension performance, and ASD traits, and conducted subgroup analyses based on age range to examine developmental moderating effects. Individuals with ASD exhibited remarkable hypoconnectivity in the ventral tracts, particularly in the temporal portions of the left inferior longitudinal fasciculus (ILF) and the inferior fronto-occipital fasciculus (IFOF). These WM abnormalities were associated with poor comprehension and more severe ASD symptoms. Furthermore, WM alterations in the ventral tract and their correlation with comprehension dysfunction were more prominent in younger children with ASD than in adolescents. These findings indicate that WM disruptions in the temporal portions of the left ILF/IFOF are most notable in ASD, potentially constituting the core neurological underpinnings of comprehension and communication deficits in autism. Moreover, impaired WM connectivity and comprehension ability in patients with ASD appear to improve with age.

Autism impairs face perception? Opposite associations between different subclusters of autistic traits and illusory face detection

ABSTRACT Despite common beliefs about facial processing deficits in autism, many studies have failed to confirm qualitative impairments. Individual differences within the autistic population are likely key confounding factors. The dichotomy of the Autism Spectrum Quotient (AQ) has been recognized in psychometric literature among subclinical and clinical population, enabling large-sample research on how heterogeneous autistic traits affect face perception. Here we innovatively used face pareidolia, the illusion of seeing faces in non-face objects, to investigate how different autistic traits affect face perception. Our results showed that higher AQ-social scores (social and communication aspects) were linked to a lower likelihood of seeing illusory faces, while higher AQ-attention-to-detail scores (rigidity and pattern aspects) increased susceptibility to face pareidolia. A mediation model revealed that imagination mediates the relationship between autistic traits and face perception, suggesting diverse mechanisms in autism's impact on face-related processes.

T1w/T2w ratio maps identify children with autism spectrum disorder and the relationships between myelin-related changes and symptoms

BackgroundModern neuroimaging methods have revealed that autistic symptoms are associated with abnormalities in brain morphology, connectivity, and activity patterns. However, the changes in brain microstructure underlying the neurobiological and behavioral deficits of autism remain largely unknown. Methodswe characterized the associated abnormalities in intracortical myelination pattern by constructing cortical T1-weighted/T2-weighted ratio maps. Voxel-wise comparisons of cortical myelination were conducted between 150 children with autism spectrum disorder (ASD) and 139 typically developing (TD) children. Group differences in cortical T1-weighted/T2-weighted ratio and gray matter volume were then examined for associations with autistic symptoms. A convolutional neural network (CNN) model was also constructed to examine the utility of these regional abnormalities in cortical myelination for ASD diagnosis. ResultsCompared to TD children, the ASD group exhibited widespread reductions in cortical myelination within regions related to default mode, salience, and executive control networks such as the inferior frontal gyrus, bilateral insula, left fusiform gyrus, bilateral hippocampus, right calcarine sulcus, bilateral precentral, and left posterior cingulate gyrus. Moreover, greater myelination deficits in most of these regions were associated with more severe autistic symptoms. In addition, children with ASD exhibited reduced myelination in regions with greater gray matter volume, including left insula, left cerebellum_4_5, left posterior cingulate gyrus, and right calcarine sulcus. Notably, the CNN model based on brain regions with abnormal myelination demonstrated high diagnostic efficacy for ASD. ConclusionsOur findings suggest that microstructural abnormalities in myelination contribute to autistic symptoms and so are potentially promising therapeutic targets as well as biomarkers for ASD diagnosis.

Investigation of the Fasciola Cinereum, Absent in BTBR mice, and Comparison with the Hippocampal Area CA2.

The arginine vasopressin 1b receptor (Avpr1b) plays an important role in social behaviors including social learning, memory, and aggression, and is known to be a specific marker for the cornu ammonis area 2 (CA2) regions of the hippocampus. The fasciola cinereum (FC) is an anatomical region in which Avpr1b expressing neurons are prominent, but the functional roles of the FC have yet to be investigated. Surprisingly, the FC is absent in the inbred BTBR T+tf/J (BTBR) mouse strain used to study core behavioral deficits of autism. Here, we characterized and compared transcriptomic expression profiles using single nucleus RNA sequencing and identified 7 different subpopulations and heterogeneity within the dorsal CA2 (dCA2) and FC. Mef2c, involved in autism spectrum disorder, is more highly expressed in the FC. Using Hiplex in situ hybridization, we examined the neuroanatomical locations of these subpopulations in the proximal and distal regions of the hippocampus. Anterograde tracing of Avpr1b neurons specific for the FC showed projections to the IG, dCA2, lacunosum molecular layer of CA1, dorsal fornix, septofibrial nuclei, and intermediate lateral septum (iLS). In contrast to the dCA2, inhibition of Avpr1b neurons in the FC by the inhibitory DREADD system during behavioral testing did not impair social memory. We performed single nucleus RNA sequencing in the dCA2 region and compared between wildtype (WT) and BTBR mice. We found that transcriptomic profiles of dCA2 neurons between BTBR and WT mice are very similar as they did not form any unique clusters; yet, we found there were differentially expressed genes between the dCA2s of BTBR and WT mice. Overall, this is a comprehensive study of the comparison of Avpr1b neuronal subpopulations between the FC and dCA2. The fact that FC is absent in BTBR mice, a mouse model for autism spectrum disorder, suggests that the FC may play a role in understanding neuropsychiatric disease.

Crocin Exerts Neuroprotective Effect in Valproate Exposed Rat Model of Autistic Spectrum Disorder by Ameliorating Behavioural and Biochemical Reversions

Autistic spectrum disorder (ASD) is associated with oxidative stress and neuron damage triggered by valproic acid (VPA) in a post-natal rat model of ASD. It was hypothesized that crocin (CRO), may have beneficial effects in ASD due to its antioxidant activities. The study investigated the neuro-behavioural and biochemical modifications of crocin in VPA-induced ASD. Wistar albino rat pups aged 13 days were divided into five groups (06 each). 400 mg/kg VPA subcutaneously on PND 14 successfully induced autism. From PND 14 to 40, crocin was dispensed daily. Different neuro-behavioral markers were examined while the groups were receiving therapy. Animals were sacrificed at the completion of the research for biochemical calculations. Crocin treatment significantly improved behavioral activity and oxidative changes compared to animals treated with the VPA-exposed group. The effects were more pronounced at higher dose of crocin, providing evidence of reversing the valproic acid-induced autistic deficits. Crocin could be a viable option for ASD treatment due to its potential neuronal cytoprotective effects, likely attributed to its antioxidant properties

Segregated Dynamical Networks for Biological Motion Perception in the Mu and Beta Range Underlie Social Deficits in Autism.

Biological motion perception (BMP) correlating with a mirror neuron system (MNS) is attenuated in underage individuals with autism spectrum disorder (ASD). While BMP in typically-developing controls (TDCs) encompasses interconnected MNS structures, ASD data hint at segregated form and motion processing. This coincides with less fewer long-range connections in ASD than TDC. Using BMP and electroencephalography (EEG) in ASD, we characterized directionality and coherence (mu and beta frequencies). Deficient BMP may stem from desynchronization thereof in MNS and may predict social-communicative deficits in ASD. Clinical considerations thus profit from brain-behavior associations. Point-like walkers elicited BMP using 15 white dots (walker vs. scramble in 21 ASD (mean: 11.3 ± 2.3 years) vs. 23 TDC (mean: 11.9 ± 2.5 years). Dynamic Imaging of Coherent Sources (DICS) characterized the underlying EEG time-frequency causality through time-resolved Partial Directed Coherence (tPDC). Support Vector Machine (SVM) classification validated the group effects (ASD vs. TDC). TDC showed MNS sources and long-distance paths (both feedback and bidirectional); ASD demonstrated distinct from and motion sources, predominantly local feedforward connectivity, and weaker coherence. Brain-behavior correlations point towards dysfunctional networks. SVM successfully classified ASD regarding EEG and performance. ASD participants showed segregated local networks for BMP potentially underlying thwarted complex social interactions. Alternative explanations include selective attention and global-local processing deficits. This is the first study applying source-based connectivity to reveal segregated BMP networks in ASD regarding structure, cognition, frequencies, and temporal dynamics that may explain socio-communicative aberrancies.

MDGA2 Constrains Glutamatergic Inputs Selectively onto CA1 Pyramidal Neurons to Optimize Neural Circuits for Plasticity, Memory, and Social Behavior.

Synapse organizers are essential for the development, transmission, and plasticity of synapses. Acting as rare synapse suppressors, the MAM domain containing glycosylphosphatidylinositol anchor (MDGA) proteins contributes to synapse organization by inhibiting the formation of the synaptogenic neuroligin-neurexin complex. A previous analysis of MDGA2 mice lacking a single copy of Mdga2 revealed upregulated glutamatergic synapses and behaviors consistent with autism. However, MDGA2 is expressed in diverse cell types and is localized to both excitatory and inhibitory synapses. Differentiating the network versus cell-specific effects of MDGA2 loss-of-function requires a cell-type and brain region-selective strategy. To address this, we generated mice harboring a conditional knockout of Mdga2 restricted to CA1 pyramidal neurons. Here we report that MDGA2 suppresses the density and function of excitatory synapses selectively on pyramidal neurons in the mature hippocampus. Conditional deletion of Mdga2 in CA1 pyramidal neurons of adult mice upregulated miniature and spontaneous excitatory postsynaptic potentials, vesicular glutamate transporter 1 intensity, and neuronal excitability. These effects were limited to glutamatergic synapses as no changes were detected in miniature and spontaneous inhibitory postsynaptic potential properties or vesicular GABA transporter intensity. Functionally, evoked basal synaptic transmission and AMPAR receptor currents were enhanced at glutamatergic inputs. At a behavioral level, memory appeared to be compromised in Mdga2 cKO mice as both novel object recognition and contextual fear conditioning performance were impaired, consistent with deficits in long-term potentiation in the CA3-CA1 pathway. Social affiliation, a behavioral analog of social deficits in autism, was similarly compromised. These results demonstrate that MDGA2 confines the properties of excitatory synapses to CA1 neurons in mature hippocampal circuits, thereby optimizing this network for plasticity, cognition, and social behaviors.

Melanocortin agonism in a social context selectively activates nucleus accumbens in an oxytocin-dependent manner

Social deficits are debilitating features of many psychiatric disorders, including autism. While time-intensive behavioral therapy is moderately effective, there are no pharmacological interventions for social deficits in autism. Many studies have attempted to treat social deficits using the neuropeptide oxytocin for its powerful neuromodulatory abilities and influence on social behaviors and cognition. However, clinical trials utilizing supplementation paradigms in which exogenous oxytocin is chronically administered independent of context have failed. An alternative treatment paradigm suggests pharmacologically activating the endogenous oxytocin system during behavioral therapy to enhance the efficacy of therapy by facilitating social learning. To this end, melanocortin receptor agonists like Melanotan II (MTII), which induces central oxytocin release and accelerates formation of partner preference, a form of social learning, in prairie voles, are promising pharmacological tools. To model pharmacological activation of the endogenous oxytocin system during behavioral therapy, we administered MTII prior to social interactions between male and female voles. We assessed its effect on oxytocin-dependent activity in brain regions subserving social learning using Fos expression as a proxy for neuronal activation. In non-social contexts, MTII only activated hypothalamic paraventricular nucleus, a primary site of oxytocin synthesis. However, during social interactions, MTII selectively increased oxytocin-dependent activation of nucleus accumbens, a site critical for social learning. These results suggest a mechanism for the MTII-induced acceleration of partner preference formation observed in previous studies. Moreover, they are consistent with the hypothesis that pharmacologically activating the endogenous oxytocin system with a melanocortin agonist during behavioral therapy has potential to facilitate social learning.

Predictive coding deficits in autism: Abnormalities in feedback or feedforward connectivities?

Predictive coding deficits in autism: Abnormalities in feedback or feedforward connectivities?

Evidence of mutual non-verbal synchrony in learners with severe learning disability and autism, and their support workers: a motion energy analysis study.

Some research indicates that neurodivergent people are less likely than "neurotypical" people to adapt their movements to a partner's movements to facilitate interpersonal motor synchrony. Researchers therefore suggest synchrony deficits underlie the social differences associated with autism and other neurodivergences. Intensive Interaction (II) is a client-led approach, where Learning Support Workers (LSW) follow the lead of learners to create balanced and reciprocal interactions. We aimed to examine the balance of synchrony in learners with autism and Severe Learning Disabilities and their LSWs in a special education college where learners had prior experience with II. Using Motion Energy Analysis, we assessed the degree to which each partner acted as a leader, and hence which partner acted as a follower, during moments of close synchrony. Overall, learners and LSWs showed higher than chance synchrony. There were no differences in the degree to which each partner led the moments of synchrony, or the amount pairs synchronized with zero-lag, where there was no delay between each partners' movements. The equal balance of leading and following in the learner and LSW pairs demonstrates that both partners consistently adapted their movements to their partner's movements to facilitate synchrony. The findings tentatively challenge the notion of a synchrony deficit in autism and suggest synchrony can be present in cross-neurotype pairs in comfortable and engaging conditions. We discuss the potential for client-led, movement-based approaches to support smooth interactions across neurotypes.

Factors associated with receptive and expressive language in autistic children and siblings: A systematic review.

Language abilities of autistic children and children at elevated likelihood for autism (EL-siblings) are highly heterogeneous, and many of them develop language deficits. It is as of yet unclear why language abilities of autistic children and EL-siblings vary, although an interaction of multiple influential factors is likely at play. In this review, we describe research articles that identify one or multiple of such factors associated with the receptive or expressive language abilities of autistic children and EL-siblings since the introduction of the DSM-5. Our aim was to identify and summarize factors that are linked to language development in autistic children and siblings in the recent literature to ultimately gain insight into the heterogeneity of language abilities in these children. The search strategy of this review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The following databases were consulted: Embase, MEDLINE, Web of Science Core Collection, and Scopus. Inclusion criteria for studies were the presence of a sample of autistic children no older than 7 years old who were diagnosed with autism spectrum disorder per the criteria of the DSM-5. Intervention studies and studies without an explicitly reported language measure were excluded. Risk of bias assessment was completed using the Newcastle-Ottawa Scales. Ultimately, 55 articles were included in this review. Fifty-six factors were identified to be related to receptive or expressive language abilities of autistic children and EL-siblings. They were grouped into three main categories: biological factors; psychosocial and environmental factors; and age-related and developmental factors, each with different subcategories. Although many of the identified variables were only examined in one article, some well-researched associated factors were reported across multiple studies and were present in both autistic children and EL-siblings, in particular joint attention, nonverbal cognitive abilities and frontal EEG power. Better insight in these factors associated with language abilities in autistic children and siblings at elevated likelihood can inform future intervention strategies to reduce language deficits and its corresponding negative consequences in these children. Our results confirm that multiple different factors likely underlie language deficits in autism. Important aspects that should be considered are, among others, social factors such as joint attention, child characteristics such as nonverbal cognition, and neurocognitive factors.

The Impact of Virtual Reality on the Skill Acquisition and Cognitive Development of Children and Adolescents with Autism Spectrum Disorder

Recent years have witnessed a growing occurrence of autism spectrum disorder (ASD) in children and adolescents. ASD is acknowledged as a neurodevelopmental disease, which can trigger serious developmental impairments and delays in language development, social and communication abilities, interest construction and behavioral patterns. Virtual reality (VR) technology is gaining increasing attention as a potential effective tool to prevent and rehabilitate ASD. Numerous studies have summarized the application of VR technology in autism developmental deficits. This review focuses on whether VR-based cognitive and performance training can hone the daily living skills, social communication capacities and academic abilities of children and teenagers diagnosed with ASD. The summary of several evidence-based studies demonstrates that VR platforms offer an innovative and efficacious option for the treatment of some deficits in autism. Despite its low cost and ease of accessibility, VR still has noteworthy limitations that need to be resolved. Future research might look into its application in other skill acquisition, correlation with brain function, adjunctive function in therapeutic treatment, and cross-cultural inquiry.

The enteric nervous system deficits in autism spectrum disorder.

Gastrointestinal (GI) disorders are common comorbidities in individuals with autism spectrum disorder (ASD), and abnormalities in these issues have been found to be closely related to the severity of core behavioral deficits in autism. The enteric nervous system (ENS) plays a crucial role in regulating various aspects of gut functions, including gastrointestinal motility. Dysfunctional wiring in the ENS not only results in various gastrointestinal issues, but also correlates with an increasing number of central nervous system (CNS) disorders, such as ASD. However, it remains unclear whether the gastrointestinal dysfunctions are a consequence of ASD or if they directly contribute to its pathogenesis. This review focuses on the deficits in the ENS associated with ASD, and highlights several high-risk genes for ASD, which are expressed widely in the gut and implicated in gastrointestinal dysfunction among both animal models and human patients with ASD. Furthermore, we provide a brief overview of environmental factors associated with gastrointestinal tract in individuals with autism. This could offer fresh perspectives on our understanding of ASD.

The Novel Somatosensory Nose-Poke Adapted Paradigm (SNAP) Is an Effective Tool to Assess Differences in Tactile Sensory Preferences in Autistic-Like Mice.

One of the most prevalent deficits in autism spectrum disorder (ASD) are sensitivities to sensory stimuli. Despite the prevalence of sensory deficits in autism, there are few paradigms capable of easily assessing sensory behaviors in ASD-like mouse models. We addressed this need by creating the Somatosensory Nose-poke Adapted Paradigm (SNAP), which consists of an elevated platform with 6 holes in the center, half of which are lined with sandpaper and half are smooth, requiring mice to use their whiskers to sense the texture. The SNAP paradigm assesses tactile sensory preferences as well as stereotypy, anxiety, and locomotion. We used two wild-type (neurotypical) mouse strains, C57BL/6J (C57) inbred and CD-1 outbred mice, and two ASD mouse models, BTBR (a model of idiopathic ASD) and Cntnap2 -/- mice (a model of syndromic ASD). We found that both ASD models produced more nose pokes into the rough condition than the smooth condition, suggesting an increased preference for complex tactile stimulation when compared with the neurotypical groups, wherein no differences were observed. Furthermore, we found increased stereotypy and time spent in the center, suggestive of decreased anxiety, only for BTBR mice compared with the other mouse strains. Overall, SNAP is an easy to implement task to assess the degree of preference for complex tactile stimulation in ASD mouse models that can be further modified to exclude possible confounding effects of novelty or anxiety on the sensory preferences.

Effect of sex differences and time of oxytocin administration on treatment of rat model of autism spectrum disorder: Focused on necroptosis markers.

Autism is a neurodevelopmental disorder. A variety of molecular and cellular abnormalities leads to behavioral deficits in autism. Nevertheless, its etiology and treatment strategy are not completely understood. Oxytocin has recently shown improvements in social functioning. This study aimed to evaluate the necroptosis pathway for the neuroprotective effects of oxytocin in the valproic acid-induced autism spectrum disorder model. The autism spectrum disorder was induced by valproic acid on gestational day 12.5 (600 mg/kg, intraperitoneally). Offspring received intranasal oxytocin (1μg/μL) on the 21st and 40th days after birth. The offspring behaviors were scrutinized by self-grooming, marble-burying, three-chamber, and Morris water maze tests. Western blot was performed on the hippocampus and amygdala tissues to investigate the expression of RIP3 and MLKL markers. The valproic acid group demonstrated more anxiety, repetitive behaviors, and expression of RIP3 and MLKL markers, and less social interaction and spatial memory compared with the control group. Oxytocin considerably improved social interactions, preference for social novelty, and memory. The elevated expression of RIP3 and MLKL markers in valproic acid-induced autistic rats were alleviated after treatment with oxytocin. We also highlighted the importance of age and gender in autism spectrum disorder interventions. Our findings suggested that oxytocin administration was as an effective treatment in two areas of repetitive/stereotyped behaviors, social interactions/cognitive function. Notably, early administration of oxytocin resulted in better therapeutic responses in autism-like behaviors. The molecular tests introduce oxytocin as a potential candidate for reducing the expression of necroptosis mediators in the brain. This reinforced our hypothesis that the necroptosis pathway takes part in autism spectrum disorder.

Motor deficits in autism differ from that of developmental coordination disorder.

A vast majority of individuals with autism spectrum disorder experience impairments in motor skills. Those are often labelled as additional developmental coordination disorder despite the lack of studies comparing both disorders. Consequently, motor skills rehabilitation programmes in autism are often not specific but rather consist in standard programmes for developmental coordination disorder. Here, we compared motor performance in three groups of children: a control group, an autism spectrum disorder group and a developmental coordination disorder group. Despite similar level of motor skills evaluated by the standard movement assessment battery for children, in a Reach-to-Displace Task, children with autism spectrum disorder and developmental coordination disorder showed specific motor control deficits. Children with autism spectrum disorder failed to anticipate the object properties, but could correct their movement as well as typically developing children. In contrast, children with developmental coordination disorder were atypically slow, but showed a spared anticipation. Our study has important clinical implications as motor skills rehabilitations are crucial to both populations. Specifically, our findings suggest that individuals with autism spectrum disorder would benefit from therapies aiming at improving their anticipation, maybe through the support of their preserved representations and use of sensory information. Conversely, individuals with developmental coordination disorder would benefit from a focus on the use of sensory information in a timely fashion.

The Use of One-Part Directives in Developing Play Skills in Children With Autism During Trial-Based Instructions

Play is one of the core deficits in autism. Children with autism have very different play behavior. The current study examines the of using a one-part directive during trial-based instructions on developing play skills in young children with autism. With the use of Single-subject research as an in-depth type of quantitative study of the response of an individual or a group of individuals to intervention. Participants were five children diagnosed with autism ages three to five years old. The task was introduced in a single case design across all sessions in both generalization settings. The participants seemed to have no apparent intervention effects, and one showed a decrease in play following the intervention. The possible reasons for the variability across participants and suggestions for improving methods in developing play skills are discussed. Acquisition and generalization of play skills may be affected not only by which play skills are taught but also by how play skills are taught. The careful selection of play activities may develop spontaneous play among children with autism and their peers.