Impaired Social Interaction Research Articles

Construction of an animal model of autism based on interaction between cerebellar histological, immunohistochemical, and biochemical changes in adult male albino rat

ABSTRACT Autism spectrum disorder (ASD) represents a heterogeneous group of neurodevelopmental conditions characterized by impaired social interaction, language deficit, and stereotype behavior. This study was designed to construct an autistic animal model on the basis of histological and immunohistochemical changes in the rat cerebellum. Methods Twelve pregnant female rats were divided into a control group and a valproic acid (VPA) treated group (injected intraperitoneally on embryonic day 12 with 600 mg/kg body weight of VPA). Neurobehavioral tests were conducted on the offspring of both groups. The cerebellum was studied by light and electron microscopy as well as GFAP and caspase-3 immunohistochemical staining. Results The VPA-treated group showed signs of neuronal degeneration, such as congested blood vessels, vacuolations, irregularly shrunken with dark small heterochromatic nuclei and numerous apoptotic blebs in the Purkinje and granule cells with vacuolated cerebellar glomeruli. The myelinated nerve fibers showed rarefaction and loss of their neurofilaments. GFAP and caspase-3 immune expression were significantly altered in the VPA-treated group. Conclusion The VPA rat model can serve as an excellent model of autism at the structural level, which may be used as a validated model in preclinical studies to evaluate novel drugs.

Pain-Associated Diagnoses in Childhood Before the Diagnosis of Attention-Deficit/Hyperactivity Disorder: A Population-Based Study.

Background: Pediatric pain significantly affects children's lives, leading to school absenteeism, impaired social interactions, and psychological distress. The perception of sensory signals as pain is influenced by the brain's noradrenergic system, and recent evidence suggests that chronic pain may impact cognitive functioning and emotional regulation. Attention-Deficit/Hyperactivity Disorder (ADHD) is associated with alterations in the dopaminergic/noradrenergic systems, which could affect pain perception. Pain-associated conditions and frequent analgesic use in childhood may be linked to ADHD development and could serve as early indicators, yet data on this potential association remain limited. Study Aim: This population-based case-control study in Israel aimed to assess the prevalence of pain-related diagnoses prior to ADHD diagnosis in children aged 5 to 18. The study included children registered with Leumit Health Services (LHS) between 1 January 2006, and 30 June 2021. Children diagnosed with ADHD were compared to matched controls, selected based on age, gender, socioeconomic status, and other sociodemographic factors, who were never diagnosed with ADHD during the study period. Results: Children with ADHD (N = 18,756) and controls (N = 37,512) were precisely matched for sociodemographic characteristics. Individuals with ADHD exhibited significantly higher frequencies of diverse pain conditions, including those associated with illness [headache, earaches, and throat pain (odds ratios [OR] = 1.156 [95%CI 1.085, 1.232], 1.295 [95%CI 1.217, 1.377], and 1.080 [95%CI 1.019, 1.145], respectively; p < 0.01)] and injury [sprains and strains (OR = 1.233 [95% CI 1.104,1.376)]. Analgesics were more frequently purchased by individuals with ADHD, particularly paracetamol (OR = 1.194 [95%CI 1.152, 1.237], p < 0.001) and ibuprofen (OR = 1.366 [95%CI 1.318, 1.416], p = 0.001). Conclusions: This study highlights a potential connection between ADHD and pediatric pain. The elevated rates of pain diagnoses and analgesic usage among children with ADHD underscore the need for further research.

The Use of Joyce J. Fitzpatrick's "Life Perspective Rhythm Theory" in a Case with Substance Use Disorder Diagnosed with Craving Severity: Case Report

Objective: In this study, it was aimed to plan the patient care of a male patient with craving severity diagnosed with substance use disorder according to Joyce J. Fitzpatrick's "Life Perspective Rhythm Theory". Theoretical Framework: In this study, nursing care was applied based on the Life Perspectives Rhythm theory. Method: A male patient with severe cravings diagnosed with substance use disorder treated in a psychiatric ward was evaluated according to the rhythmic patterns in Joyce J. Fitzpatrick's "Life Perspective Rhythm Theory". Patient care was planned and implemented based on the five main assumptions of the theory. Results and Discussion: Based on Fitzpatrick's Life Perspective Rhythm Theory, it was determined that the 32-year-old male patient with craving severity who was followed up with a diagnosis of substance use disorder had problems in the process of adaptation to life perspectives in the temporal behavior pattern, increased the number of cigarettes smoked daily in the motor behavior pattern, had impulse uncontrol in the cognitive behavior pattern, and had discourses that his parents mistreated him in the perceptual behavior pattern. According to Fitzpatrick, we determined the priority of care of this case as ineffective coping, decreased self-esteem, denial, risk of violence against self or others, anxiety, ineffectiveness in maintaining health, impaired social interaction and impaired family processes. Research Implications: In this study, the planning, implementation and evaluation stages of the patient care of a male patient with craving severity diagnosed with substance use disorder were carried out according to the Life Perspective Rhythm Theory with the priorities determined by using observation and communication skills. At the end of the process, the patient stated that his level of knowledge increased in order to maintain his physical and mental well-being, and that he knew the symptoms of craving severity and the measures to be taken when these symptoms occur. Since there are very few studies based on the theory developed by Fitzpatrick, it is recommended to study with different patient groups in order to obtain precise results by concretizing the usability of the theory in patterns.

Amelioration of propionic acid-induced autism-like behaviors in rats by fenofibrate: A focus on reduction of brain galectin-3 levels.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions and repetitive behaviors. This study examines the effects of fenofibrate on a propionic acid (PPA)-induced rat model of ASD, focusing on behavioral changes, inflammatory markers, and histological findings. Thirty male Wistar rats were divided into three groups: a control group, a group receiving PPA and saline, and a group treated with PPA and fenofibrate for 15 days. Behavioral assessments, including the three-chamber sociability test, open-field test, and passive avoidance learning, were conducted. Biochemical analyses measured TNF-α, NGF, IL-17, IL-2, and galectin-3 levels in brain tissues. Histological evaluations focused on Purkinje neuron counts in the cerebellum and neuronal changes in the CA1 and CA3 regions of the hippocampus, along with glial fibrillary acidic protein (GFAP) levels. Fenofibrate treatment significantly improved behavioral outcomes, reducing autism-like behaviors compared to the PPA/saline group. Biochemically, the PPA/saline group showed elevated levels of malondialdehyde, TNF-α, IL-2, IL-17, and galectin-3, which were reduced following fenofibrate treatment. Histologically, the PPA/saline group exhibited fewer, dysmorphic Purkinje neurons and increased glial activity in the CA1 region, both of which were ameliorated by fenofibrate treatment. Fenofibrate shows promise in mitigating autism-like behaviors in a rat model of ASD, likely due to its antioxidative and neuroprotective properties, which contribute to preserving neuronal integrity and reducing inflammation.

Effect of the social environment on olfaction and social skills in wild-type and a mouse model of autism

Autism spectrum disorders (ASD) are complex, polygenic and heterogenous neurodevelopmental conditions. The severity of autism-associated variants is influenced by environmental factors, particularly social experiences during the critical neurodevelopmental period. While early behavioral interventions have shown efficacy in some children with autism, pharmacological support for core features — impairments in social interaction and communication, and stereotyped or restricted behaviors — is currently lacking. In this study, we examined how the social environment influences both wild-type (WT) and Shank3 knockout (KO) mice, a model reflecting core autism-like traits. Our findings revealed that chronic social isolation enhanced social interaction and olfactory neuron responses in WT animals. Furthermore, it restored impairments in social novelty preference and olfactory function, as well as self-grooming in Shank3 KO mice. Conversely, an enriched social environment heightened social interest toward novel conspecifics in WT mice, but elicited the opposite effect in Shank3 KO mice. Notably, Shank3 KO mice displayed distinct social responses when exposed to WT or Shank3 KO mice. These results offer novel insights that could favor the implementation of behavioral interventions and inclusive classroom programs for children with ASD.

Language, Theory of Mind and Cognitive skills in Arabic-speaking children with and without autism: Evidence from network and cluster analyses

IntroductionAutism spectrum disorder (ASD) is characterized by impairments in social interactions, social communication, and repetitive and stereotyped patterns of behavior. Previous studies have reported mixed findings regarding the links between language (i.e., phonology, morphosyntax, lexicon and pragmatics), theory of mind (ToM), executive functions (EFs), and central coherence measures in children with ASD. MethodsA total of 163 Palestinian-Arabic-speaking children aged 4-11 participated: 76 with ASD and 87 with typical language development (TLD). The children`s phonological, morphosyntactic, lexical, and pragmatic skills and verbal and non-verbal ToM abilities were evaluated. Additionally, cognitive assessments included non-verbal IQ, EF, and central coherence processing. ResultsGroup-level results showed that children with ASD scored lower than their TLD peers in all measures. Network analysis revealed robust interconnections between language, ToM, and cognitive skills in both groups. In autistic children, language was a central node, with pragmatics prevailing over morphosyntax and lexicon, while age was central in the TLD group. Cluster analysis identified four language clusters within the ASD group, demonstrating dissociations between language domains: (1) high performance across all domains, (2) moderate performance in phonology and morphosyntax with low pragmatic abilities, (3) moderate performance in phonology and lexicon with low morphosyntax and pragmatics, and (4) moderate phonology and lexicon with extremely poor morphosyntax and pragmatics. Autistic children with enhanced language abilities performed better in verbal and non-verbal ToM and EF tasks. ConclusionsOur findings underscore the variability in language, ToM, and cognitive profiles of autistic children, showing dissociation within and between different domains in some autistic children. These results offer insights for applied interventions.

Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior.

The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. In this work, we found that group 2 innate lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory interneurons to increase inhibitory synapse density in the developing mouse brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social interaction. These data define a type 2 neuroimmune circuit in early life that shapes inhibitory synapse development and behavior.

Oseltamivir phosphate (Tamiflu) alters neurobehavior of zebrafish larvae by inducing mitochondrial dysfunction

Antiviral drugs are widely used, yet their potential risks during early development, particularly within the central nervous system, remain contentious. Oseltamivir phosphate (OSE), a commonly prescribed antiviral, is increasingly detected in various environments. However, its toxicity to organisms and the underlying mechanisms are not well understood. In this study, we employed the zebrafish model to evaluate the developmental neurotoxic effects of OSE at environmentally and therapeutically relevant doses, through high-throughput behavioral analysis, in vivo two-photon imaging, transcriptomic sequencing, pharmacological intervention, and biochemical and molecular assays. Our results indicated that OSE exposure increased heart rate and induced pericardial edema in zebrafish larvae. Additionally, OSE-exposed larvae exhibited hyperactive behavior, impaired social interactions, and reduced habitual learning capacity. Although OSE at our selected levels did not significantly affect neuron count in the brain, it activated neuroinflammatory responses, altered blood vessel morphology, modulated neurotransmitter levels and the expression of neurodevelopment-related genes. Transcriptomic analysis revealed upregulation of mitochondria-related genes associated with oxidative phosphorylation. Further assessments of mitochondrial function demonstrated altered activities of respiratory chain complexes, reduced mitochondrial membrane potential (MMP), and decreased ATP content. Notably, co-treatment with mitochondrial protectants acetyl-l-carnitine-hydrochloride (ALC) or nicotinamide riboside (NR) effectively mitigated OSE-induced neurobehavioral disorders. These findings suggest that overuse of OSE can pose neurodevelopmental risks for both humans and animals, potentially attributable to mitochondrial dysfunction.

Proposed Hypothesis of TWEAK/Fn14 Receptor Modulation in Autism Spectrum Disorder.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with a complex, multiple etiology that is marked by impaired social interaction, communication, and repetitive behaviour. There is presently no pharmaceutical treatment for the core symptoms of ASD, even though the prevalence of ASD is increasing worldwide. Treatment of autism spectrum disorder involves the interaction of numerous signalling pathways, such as the Wnt/beta-catenin pathway, probiotics and kynurenine pathway, PPAR pathway, PI3K-AKT-mTOR pathway, Hedgehog signaling pathway, etc. The scientific literature has revealed TWEAK/Fn14 to not be explored in the autism spectrum disorder. In vitro and in vivo, TWEAK can control a wide range of cellular responses. Recent research has revealed that TWEAK and Fn14 are expressed in the Central Nervous System (CNS) and upregulated in perivascular endothelial cells, astrocytes, neurons, and microglia in response to various stimuli, including cerebral ischemia. This upregulation is followed by cell death and an increase in Blood-brain Barrier (BBB) permeability. The study has revealed that Aurintricarboxylic Acid (ATA) acts as an agent that suppresses TWEAK/Fn14 signaling. Similarly, from the discussion, it has been emphasized that the proposed molecular TWEAK/Fn14 signalling pathway can be considered as a therapeutic approach in the management of autism spectrum disorder.

Unraveling the socio-cognitive consequences of KCC2 disruption in zebrafish: implications for neurodevelopmental disorders and therapeutic interventions.

During postnatal brain development, maintaining a delicate balance between excitation and inhibition (E/I) is essential for the precise formation of neuronal circuits. The K+/cl- cotransporter 2 (KCC2) is instrumental in this process, and its dysregulation is implicated in various neurological disorders. This study utilized zebrafish (Danio rerio) to investigate the socio-cognitive consequences of KCC2 disruption. Through CRISPR-Cas9 technology, biallelic kcc2a knockout zebrafish larvae were generated, revealing behavioral abnormalities, including impaired social interactions and memory deficits. Molecular analyses unveiled alterations in key genes associated with the GABAergic and glutamatergic systems, potentially contributing to E/I imbalance. Additionally, KCC2 disruption influenced the expression of oxytocin and BDNF, crucial regulators of social behaviors, synaptic plasticity, and memory formation. The study also explored the therapeutic potential of KCC2 modulation using pharmaceuticals, showing the rescuing effects of CLP-290 and LIT-001 on social abnormalities. However, the selective impact of LIT-001 on social behaviors, not memory, highlights the complexity of neurobehavioral modulation. In summary, this study sheds light on the pivotal role of KCC2 in shaping socio-cognitive functions and suggests potential therapeutic avenues for KCC2-related neurological disorders.

Salubrious effects of proanthocyanidins on behavioral phenotypes and DNA repair deficiency in the BTBR mouse model of autism

Autism is a neurodevelopmental disorder distinguished by impaired social interaction and repetitive behaviors. Global estimates indicate that autism affects approximately 1.6% of children, with the condition progressively becoming more prevalent over time. Despite noteworthy progress in autism research, the condition remains untreatable. This serves as a driving force for scientists to explore new approaches to disease management. Autism is linked to elevated levels of oxidative stress and disturbances in the DNA repair mechanism, which may potentially play a role in its comorbidities development. The current investigation aimed to evaluate the beneficial effect of the naturally occurring flavonoid proanthocyanidins on the behavioral characteristics and repair efficacy of autistic BTBR mice. Moreover, the mechanisms responsible for these effects were clarified. The present findings indicate that repeated administration of proanthocyanidins effectively reduces altered behavior in BTBR animals without altering motor function. Proanthocyanidins decreased oxidative DNA strand breaks and accelerated the rate of DNA repair in autistic animals, as evaluated by the modified comet test. In addition, proanthocyanidins reduced the elevated oxidative stress and recovered the disrupted DNA repair mechanism in the autistic animals by decreasing the expressions of Gadd45a and Parp1 levels and enhancing the expressions of Ogg1, P53, and Xrcc1 genes. This indicates that proanthocyanidins have significant potential as a new therapeutic strategy for alleviating autistic features.

Deciphering autism heterogeneity: a molecular stratification approach in four mouse models

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by impairments in social interaction and communication, as well as restrained or stereotyped behaviors. The inherent heterogeneity within the autism spectrum poses challenges for developing effective pharmacological treatments targeting core features. Successful clinical trials require the identification of robust markers to enable patient stratification. In this study, we identified molecular markers within the oxytocin and immediate early gene families across five interconnected brain structures of the social circuit. We used wild-type and four heterogeneous mouse models, each exhibiting unique autism-like behaviors modeling the autism spectrum. While dysregulations in the oxytocin family were model-specific, immediate early genes displayed widespread alterations, reflecting global changes across the four models. Through integrative analysis, we identified Egr1, Foxp1, Homer1a, Oxt, and Oxtr as five robust and discriminant molecular markers that allowed the successful stratification of the four models. Importantly, our stratification demonstrated predictive values when challenged with a fifth mouse model or identifying subgroups of mice potentially responsive to oxytocin treatment. Beyond providing insights into oxytocin and immediate early gene mRNA dynamics, this proof-of-concept study represents a significant step toward the potential stratification of individuals with ASD. This work has implications for the success of clinical trials and the development of personalized medicine in autism.

THE BENEFITS OF NON-BIOLOGICAL THERAPY IN CHILDREN WITH AUTISM SPECTRUM DISORDER (ASD)

Introduction – Autism Spectrum Disorders (ASD) are a group of neurodevelopmental disorders characterized by three main problems, namely the presence of communication disorders, impaired reciprocal social interaction with the surrounding environment, and restricted, repetitive, and stereotyped behavior patterns in the first 3 years of age. In Indonesia, there were around 112,000 ASD sufferers in 2012, while in 2015 it was estimated that 1 in 250 children had ASD, or around 134,000 people. Methods – The author used the literature review method by collecting the results of several kinds of literature on ASD, and non-biological therapy and their benefits in ASD children. The literature on non-biological therapy and its benefits in ASD children is limited to 2011-2021. Results – Autism is a lifelong disorder, so it is important to recognize it as early as possible, and parents need to understand the problem. It's important to remember that the cause of autism is unknown, and no single drug has been found that can cure ASD, but some therapies can suppress ASD symptoms that can help ASD lead a more productive life by reducing symptoms and improving skills. Discuss – There is no definitive therapy that can cure ASD, but therapy is aimed at improving ASD symptoms. Non-biological therapy which includes behavioral therapy (such as TEACCH or ABA) is currently used as first-line therapy for ASD. Conclusion – Symptoms that appear in ASD children vary widely, therefore the therapy given is individual and depends on the circumstances and symptoms that appear. There are many types of non-biological therapies for ASD, such as ABA, TEACCH, PECS, Caregiver-mediated Intervention, Parent-mediated Communication, SIT, and AIT. These therapies have been shown to have benefits in improving ASD symptoms such as communication skills, social interaction, and behavior, where each therapy has different benefits in each type. These therapies are given to everyone as needed. Keywords: non-biological, children, autism.

Key Synaptic Pathology in Autism Spectrum Disorder: Genetic Mechanisms and Recent Advances.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions and verbal communication, accompanied by symptoms of restricted and repetitive patterns of behavior or interest. Over the past 30 years, the morbidity of ASD has increased in most areas of the world. Although the pathogenesis of ASD is not fully understood, it has been associated with over 1000 genes or genomic loci, indicating the importance and complexity of the genetic mechanisms involved. This review focuses on the synaptic pathology of ASD and particularly on genetic variants involved in synaptic structure and functions. These include SHANK, NLGN, NRXN, FMR1, and MECP2 as well as other potentially novel genes such as CHD8, CHD2, and SYNGAP1 that could be core elements in ASD pathogenesis. Here, we summarize several pathological pathways supporting the hypothesis that synaptic pathology caused by genetic mutations may be the pathogenic basis for ASD.

Dysregulated plasma autoantibodies are associated with B cell dysfunction in young Arab children with autism spectrum disorder in Qatar.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and communication, as well as the occurrence of stereotyped and repetitive behaviors. Previous studies have provided solid evidence of dysregulated immune system in ASD; however, limited studies have investigated autoantibody profiles in individuals with ASD. This study aims to screen plasma autoantibodies in a well-defined cohort of young children with ASD (n = 100) and their matched controls (n = 60) utilizing a high-throughput KoRectly Expressed (KREX) i-Ome protein-array technology. We identified differential protein expression of 16 autoantibodies in ASD, which were correlated with differential gene expression of these markers in independent ASD cohorts. Meanwhile, we identified a distinct list of 33 autoantibodies associated with ASD severity; several of which were correlated with maternal age and birth weight in ASD. In addition, we found dysregulated numbers of circulating B cells and activated HLADR+ B cells in ASD, which were correlated with altered levels of several autoantibodies. Further in-depth analysis of B cell subpopulations revealed an increased frequency of activated naïve B cells in ASD, as well as an association of resting naïve B cells and transitional B cells with ASD severity. Pathway enrichment analysis revealed disrupted MAPK signaling in ASD, suggesting a potential relevance of this pathway to altered autoantibodies and B cell dysfunction in ASD. Finally, we found that a combination of eight autoantibodies associated with ASD severity showed an area under the curve (ROC-AUC) of 0.937 (95% CI = 0.890, 0.983; p < 0.001), which demonstrated the diagnostic accuracy of the eight-marker signature in the severity classification of ASD cases. Overall, this study determined dysregulated autoantibody profiles and B cell dysfunction in children with ASD and identified an eight-autoantibody panel for ASD severity classification.

Unveiling the role of IGF1R in autism spectrum disorder: a multi-omics approach to decipher common pathogenic mechanisms in the IGF signaling pathway.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition marked by impairments in social interaction, communication, and repetitive behaviors. Emerging evidence suggests that the insulin-like growth factor (IGF) signaling pathway plays a critical role in ASD pathogenesis; however, the precise pathogenic mechanisms remain elusive. This study utilizes multi-omics approaches to investigate the pathogenic mechanisms of ASD susceptibility genes within the IGF pathway. Whole-exome sequencing (WES) revealed a significant enrichment of rare variants in key IGF signaling components, particularly the IGF receptor 1 (IGF1R), in a cohort of Chinese Han individuals diagnosed with ASD, as well as in ASD patients from the SFARI SPARK WES database. Subsequent single-cell RNA sequencing (scRNA-seq) of cortical tissues from children with ASD demonstrated elevated expression of IGF receptors in parvalbumin (PV) interneurons, suggesting a substantial impact on their development. Notably, IGF1R appears to mediate the effects of IGF2R on these neurons. Additionally, transcriptomic analysis of brain organoids derived from ASD patients indicated a significant association between IGF1R and ASD. Protein-protein interaction (PPI) and gene regulatory network (GRN) analyses further identified ASD susceptibility genes that interact with and regulate IGF1R expression. In conclusion, IGF1R emerges as a central node within the IGF signaling pathway, representing a potential common pathogenic mechanism and therapeutic target for ASD. These findings highlight the need for further investigation into the modulation of this pathway as a strategy for ASD intervention.

Exploring the role of orexins in the modulation of social reward

Abstract Rationale positive social interactions are essential for mental health, by offering emotional support, reducing stress levels, and promoting resilience against drugs of abuse effects. However, not all individuals perceive social interaction as rewarding. Objectives the goal of this study was to investigate whether the modulation of the orexin system can shift passive coping and non-social behavior (vulnerable) to active coping and social behavior (resilient). This knowledge is primordial for stress- and addiction-related disorders, and for other psychiatric disorders involving impairment in social interaction. Methods male C57/BL6N mice categorized into social and non-social groups, received injections of SB334867, a selective orexin 1 receptor (OX1R) antagonist, before the conditioning sessions with a male conspecific of the same weight and age. Results our results from the conditioned place preference test (CPP) show that SB334867 has no effect on social preference in non-social mice, but it reduces their stress levels and depression-like behavior. These effects appear to be due to a higher OX1R expression in the basolateral amygdala (BLA), a stress-related brain area, of non-social mice compared to their social counterparts. Conclusions these data suggest that the orexin system may be a target to alleviate stress and depression-like behavior in non-social individuals rather than to promote social reward.

Psychosocial impact of adverse home environment on primary school performance in Cambodia

There is lack of an in-depth understanding of the impact of psychosocial problems at home on learning performance among primary school children in Cambodia. Hereafter, the aim of this study is to gain a better understanding of the psychosocial challenges that primary school children in Cambodia face at home and how those affect their school performance. The semi-structure interviews were conducted with 86 participants in Battambang and Kampong Cham provinces, including students, parents/caregivers, and school officers. The thematic analysis was utilized. The findings show that primary school children who are exposed to family adversity, including domestic violence, family division, and household socio-economic crisis, demonstrate symptoms of psychological distress, impaired social interaction, and poor school performance. Low school performance was often anticipated by the lack of parental involvement and the overall deficient quality of teaching.

Amelioration of social impairments in autism: Possible role of vagal afferent stimulation in modification of the prefrontal-amygdala connectivity

Impairment in social interactions is a prominent feature of autism spectrum disorder (ASD). The present hypothesis explains the possible role of vagal afferent stimulation in the modification of prefrontal-amygdala connectivity in the amelioration of social impairments in ASD. Currently, there is no definitive treatment for ASD. However, there is documented evidence showing that interventions that increase vagal tone lead to the improvement of autism-related social symptoms. However, the exact mechanism that explains the correlation between the elevation of vagal tone and the amelioration of autism-related symptoms has not been elucidated. In the present hypothesis, it is proposed that the increase in vagal tone affects the nucleus tractus solitarius (NTS) in the brainstem. The NTS has strong connections with other brainstem nuclei, such as the locus coeruleus and dorsal raphe nucleus. The aforementioned nuclei are the main sources of norepinephrine and serotonin, with extensive projections to various brain areas, especially the prefrontal cortex (PFC) and amygdala. PFC-amygdala functional connectivity plays an important role in social behavior and emotion regulation. Therefore, visceral stimulation, which subsequently increases the vagal tone, possibly leads to the improvement of autistic social deficits through the enhancement of PFC-amygdala functional connectivity. Further investigations are needed to evaluate the function of the mentioned neural pathways during visceral stimulation in individuals with ASD.

Assessment of auditory hypersensitivity in children and adolescents with Autism Spectrum Disorder: integrative review

Introduction: Individuals with Autism Spectrum Disorder may present impairments in communication, behavior, social interaction and changes in sensory processing with atypical responses to information from the senses, such as auditory hypersensitivity. Objective: to describe the methods of evaluating auditory hypersensitivity used in babies, children and/or adolescents with Autism Spectrum Disorder, through an integrative review. Data Synthesis: The study was carried out with the PVO strategy, in the months of October and November 2023, with the search key: “Infant” OR “Child” OR “Adolescent” AND “Autism Spectrum Disorder” AND “Hyperacusis” OR “ Hyperacuses” OR "Hearing” in 11 databases. Results: 7,071 studies were identified, after reading titles and abstracts, 59 were selected, 30 of which were duplicates and 29 were read in full. In the end, 10 articles were included. The majority of studies carried out audiological exams followed by a questionnaire, with the Sensory Profile questionnaire being the most common and the Otoacoustic Emissions, Brainstem Auditory Evoked Potential and Immittance Tests being the most common. The sounds that cause the most discomfort are: sounds of strong intensity in general, such as, vacuum cleaner and hairdryer. The most common emotional reaction was crying and physical reactions, covering the ears and running away. Conclusion: It was noticed that the majority of studies reported in this review demonstrate that for the investigation of auditory hypersensitivity, it can be both questionnaires and hearing exams were used in children and adolescents with auditory hypersensitivity, making it necessary to carry out more studies on the subject to standardize an assessment for auditory hypersensitivity.