Autism Spectrum Disorder Symptomatology Research Articles

Demands and stress before and during the COVID-19 pandemic of parents to children with autism spectrum disorder.

Parents to children with Autism Spectrum Disorder (ASD) face diverse daily demands that can lead to stress. The aim of this study was to examine to which extent stress in parents to children with ASD can be explained by daily demands before and during the COVID-19 pandemic (after lockdowns; first half of 2022), and whether there are differences between the two time periods in this regard. Data from parents to children with ASD living in Germany from two independent questionnaire studies (before the pandemic: N = 168, during the pandemic: N = 105) were matched for comparability. Simple and multiple linear regression analyses were used to answer the research question. Parental stress as well as all demands examined showed higher levels during the COVID-19 pandemic than before. Significant predictors of parental stress before and during the COVID-19 pandemic were (1) the daily demands to deal with the child's problem behavior, (2) the restriction of one's personal way of life, and (3) the challenge to cooperate with the partner. During the COVID-19 pandemic, the child's problem behavior was particularly relevant. It was also found that the demand to deal with stigmatizing reactions did not explain parental stress during the COVID-19 pandemic whereas before the pandemic it had been a significant predictor. Although parental stress and the demands of daily life increased during the pandemic, most of the stress can be explained by the same demands. It is suggested that the increased levels may be due to an increase in the child's ASD symptomatology, which is why it is advisable to install therapeutic and care structures that prepare children with ASD for future crises.

Cortical responses to social stimuli in infants at elevated likelihood of ASD and/or ADHD: A prospective cross-condition fNIRS study

Autism spectrum disorders (ASD) and attention-deficit hyperactivity disorder (ADHD) are highly prevalent neurodevelopmental conditions that often co-occur and present both common and distinct neurodevelopmental profiles. Studying the developmental pathways leading to the emergence of ASD and/or ADHD symptomatology is crucial in understanding neurodiversity and discovering the mechanisms that underpin it. This study used functional near-infrared spectroscopy (fNIRS) to investigate differences in cortical specialization to social stimuli between 4- to 6-month-old infants at typical and elevated likelihood of ASD and/or ADHD. Results showed that infants at both elevated likelihood of ASD and ADHD had reduced selectivity to vocal sounds in left middle and superior temporal gyrus. Furthermore, infants at elevated likelihood of ASD showed attenuated responses to visual social stimuli in several cortical regions compared to infants at typical likelihood. Individual brain responses to visual social stimuli were associated with later autism traits, but not ADHD traits. These outcomes support our previous observations showing atypical social brain responses in infants at elevated likelihood of ASD and align with later atypical brain responses to social stimuli observed in children and adults with ASD. These findings highlight the importance of characterizing antecedent biomarkers of atypicalities in processing socially relevant information that might contribute to both phenotypic overlap and divergence across ASD and ADHD conditions and their association with the later emergence of behavioural symptoms.

Seeking contexts that promote neurodiverse social success: Patterns of behavior during minimally-structured interaction settings in autistic and non-autistic youth.

While peer interaction differences are considered a central feature of autism, little is known regarding the nature of these interactions via directly-observed measurement of naturalistic (i.e., minimally-structured) groups of autistic and non-autistic adolescent peers. 148 autistic and non-autistic adolescents (111 male, Mage = 14.22, SDage = 1.90; MIQ = 103.22, SDIQ = 15.80) participated in a 50-minute, minimally-structured, naturalistic peer interaction paradigm with activities of varying social demands: an incidental social demand (eating in a room with peers), a physical social demand (playing a physically-interactive game), and a verbal social demand (playing a verbal game). While autistic youth exhibited fewer overall interaction behaviors than non-autistic youth, the two groups did not differ in amount of positive, negative, and low-level interaction behaviors. Within activities, autistic and non-autistic youth only differed in positive interaction behaviors during the context of a verbal social demand. Youth who displayed more positive interaction behaviors during this same activity had less autism spectrum disorder symptomatology, controlling for nested group effects and relevant covariates. These results point toward subtle differences in social demands across naturalistic settings that can either support or impede prosocial interaction for autistic youth, providing a guidepost for identifying settings that best promote social success for neurodiverse populations.

Barriers and facilitators of physical activity participation in adolescents with autism

ABSTRACT Adolescents with autism are less physically active compared to neurotypical peers. Little is known concerning the meanings and processes that influence their physical activity (PA) participation. Therefore, we aimed to explore the barriers/facilitators of PA participation adolescents with autism experience. Guided by the principles of the socio-ecological model, semi-structured interviews with 17 adolescents with autism (n = 11 males, 14.4 ± 1.6 years) were conducted. In every PA context (i.e. unorganized PA, sports club, and physical education classes), a variety of intrapersonal, interpersonal, environmental and policy barriers/facilitators of PA participation were found. These barriers/facilitators can be context-specific and related to autism spectrum disorder symptomatology.

Autism Spectrum Disorder in Children with an Early History of Paediatric Acquired Brain Injury.

Autism spectrum disorder (ASD) is a neurodevelopmental condition that arises from a combination of both genetic and environmental risk factors. There is a lack of research investigating whether early acquired brain injury (ABI) may be a risk factor for ASD. The current study comprehensively reviewed all hospital records at The Brain Injury Service, Kids Rehab at the Children's Hospital at Westmead (Australia) from January 2000 to January 2020. Of the approximately 528 cases, 14 children with paediatric ABI were subsequently given an ASD diagnosis (2.7%). For this ASD sample, the mean age at the time of the ABI was 1.55 years, indicating a high prevalence of early ABI in this diagnostic group. The mean age of ASD diagnosis was, on average, 5 years later than the average ASD diagnosis in the general population. Furthermore, 100% of children had at least one medical comorbidity and 73% had three or more co-occurring DSM-5 diagnoses. Although based on a small data set, results highlight early paediatric ABI as a potential risk factor for ASD and the potential for a delayed ASD diagnosis following early ABI, with comorbidities possibly masking symptoms. This study was limited by its exploratory case series design and small sample size. Nonetheless, this study highlights the need for longitudinal investigation into the efficacy of early screening for ASD symptomatology in children who have sustained an early ABI to maximise potential intervention.

Therapeutic Profile of Cannabidiol in the Broad Symptomatology of Autism Spectrum Disorder: Evidence From Basic Science to Clinical Approaches

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders whose symptoms include impaired communication and social interaction, stereotypies, and varying levels of intellectual disability. Together with these symptoms are co-occurring psychiatric or neurological conditions, often with hyperactivity and attention disorders, anxiety, depression, and epilepsy. So far, no effective treatment for ASD is available, possibly because its neurobiological basis and heterogeneous nature are not clearly understood. Clinical and preclinical trials support the involvement of the endocannabinoid system in the patho-physiology of ASD. Cannabidiol (CBD), the main nonpsychotomimetic compound of the cannabis plant, interacts with the endocannabinoid system and has significant therapeutic potential in treating several psychiatric disorders and manifestations of ASD. After this article, readers are expected to have a broad understanding of current scientific evidence and perspectives on the use of CBD in cases of ASD. [ Psychiatr Ann . 2023;53(6):247–251.]

Criminal Sexual Behavior of Individuals With Autism Spectrum Disorder and Recommendations for Correctional Professionals.

Continued uncertainty on overrepresentation of autism spectrum disorder (ASD) in the criminal justice system (CJS), although important, has shifted focus away from other questions of CJS treatment of neurodiverse individuals and left little guidance on best practice for people with ASD. For ASD individuals involved in sex offenses, there remains even less guidance. Because aspects of ASD symptomatology can highly influence sexual behaviors in ways that differ from neurotypical sex offending, it is imperative that clinicians and correctional professionals know more about this potential influence of ASD on sex offending behaviors. This knowledge should then inform efforts to enact more effective and equitable policies when interacting with the ASD population. This article reviews the connection between ASD symptoms and sexual behaviors as well as the lack of ASD-oriented sex education that could result in sex offending charges. A review of literature examining sex offending risk and its relation to ASD follows. Recommendations for more equitable treatment are discussed for different aspects of the correctional system, including forensic assessment, treatment efforts, and correctional staff interactions.

Associations between thalamocortical functional connectivity and sensory over-responsivity in infants at high likelihood for ASD.

Despite growing evidence implicating thalamic functional connectivity atypicalities in autism spectrum disorder (ASD), it remains unclear how such alterations emerge early in human development. Because the thalamus plays a critical role in sensory processing and neocortical organization early in life, its connectivity with other cortical regions could be key for studying the early onset of core ASD symptoms. Here, we investigated emerging thalamocortical functional connectivity in infants at high (HL) and typical (TL) familial likelihood for ASD in early and late infancy. We report significant thalamo-limbic hyperconnectivity in 1.5-month-old HL infants, and thalamo-cortical hypoconnectivity in prefrontal and motor regions in 9-month-old HL infants. Importantly, early sensory over-responsivity (SOR) symptoms in HL infants predicted a direct trade-off in thalamic connectivity whereby stronger thalamic connectivity with primary sensory regions and basal ganglia was inversely related to connectivity with higher order cortices. This trade-off suggests that ASD may be characterized by early differences in thalamic gating. The patterns reported here could directly underlie atypical sensory processing and attention to social vs. nonsocial stimuli observed in ASD. These findings lend support to a theoretical framework of ASD whereby early disruptions in sensorimotor processing and attentional biases early in life may cascade into core ASD symptomatology.

Role of cortical excitatory/inhibitory imbalance in autism spectrum disorders from a symptom severity trajectories framework: a study protocol

BackgroundThere is considerable evidence reporting an excitatory/inhibitory (E/I) cortical imbalance in autism spectrum disorders (ASD). However, previous findings on the direction of this imbalance and its relationship to ASD symptomatology are heterogeneous. Some factors contributing to these mixed results might be the methodological differences between studies assessing the E/I ratio and the intrinsic variability within the autistic spectrum. Studying the evolution of ASD symptoms and the factors that modulate it might help to explain and reduce this variability. Here we present a study protocol to explore the longitudinal role of E/I imbalance in ASD symptoms, combining different approaches to measure the E/I ratio and using the trajectories of symptom severity as a framework.MethodsThis observational two time-point prospective study assesses the E/I ratio and the evolution of the behavioural symptoms in a sample of at least 98 participants with ASD. Participants are enrolled at 12 to 72 months of age and followed from 18 to 48 months after. A comprehensive battery of tests is applied to evaluate ASD clinical symptoms. The E/I ratio is approached from electrophysiology, magnetic resonance, and genetics. We will calculate the individual change for the main ASD symptoms and, based on that, we will define the trajectories of symptom severity. Then, we will investigate the correlation between measures of excitation/inhibition balance and autistic symptomatology cross-sectionally, as well as the ability of these measurements to predict changes in symptoms over time.DiscussionThis study presents a robust multisystemic approach to the E/I imbalance theory in autism and its relation to divergent symptom trajectories. That setting will allow us to relate and compare the neurobiological information coming from different sources and its impact on behavioural symptoms while accounting for the high variability in ASD. The findings derived from this study could contribute to the ASD biomarkers research and might provide valuable evidence for the development of more personalized treatments in ASD.

Infant sleep predicts trajectories of social attention and later autism traits.

Children with neurodevelopmental disorders including autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) often experience sleep disturbances, but little is known about when these sleep differences emerge and how they relate to later development. We used a prospective longitudinal design in infants with a family history of ASD and/or ADHD to examine infant sleep and its relation to trajectories of attention and later neurodevelopmental disorders. We formed factors of Day and Night Sleep from parent-reported measures (including day/night sleep duration, number of naps in the day, frequency of night awakenings and sleep onset problems). We examined sleep in 164 infants at 5-, 10- and 14-months with/without a first-degree relative with ASD and/or ADHD who underwent a consensus clinical assessment for ASD at age 3. By 14-months, infants with a first-degree relative with ASD (but not ADHD) showed lower Night Sleep scores than infants with no family history of ASD; lower Night Sleep scores in infancy were also associated with a later ASD diagnosis, decreased cognitive ability, increased ASD symptomatology at 3-years, and developing social attention (e.g., looking to faces). We found no such effects with Day Sleep. Sleep disturbances may be apparent at night from 14-months in infants with a family history of ASD and also those with later ASD, but were not associated with a family history of ADHD. Infant sleep disturbances were also linked to later dimensional variation in cognitive and social skills across the cohort. Night Sleep and Social Attention were interrelated over the first 2 years of life, suggesting that this may be one mechanism through which sleep quality influences neurodevelopment. Interventions targeted towards supporting families with their infant's sleep problems may be useful in this population.

Callous unemotional traits mediate the presence of challenging behaviors in adults with autism spectrum disorder and intellectual disability

Background: Callous-unemotional traits (CUT) are an antisocial personality trait, which can be present in people with autism spectrum disorder (ASD), especially in relation to difficulties in empathy. These traits are related to challenging behaviors, such as aggressive behavior, which may occur in people with ASD. Method: This study aimed to expand the understanding of the role of CUT in adults with ASD and intellectual disability (ID). Eighty-three adults with a diagnosis of ASD and ID participated in the study. Results: Mediation analyses found that CUT indirectly mediated the relationship between ASD symptomatology and the frequency of self-injuries and stereotypies, but not aggression. Conclusions: It is considered that CUT may have a protective effect on the presence of individual challenging behaviors in adults with ASD and ID. The apparent relationship between CUT and executive functioning was discussed. CUT traits may be considered as a variable to contemplate in relation to interventions in challenging behaviors in the ASD population, especially in those individuals who show aggression-related behaviors and who have a higher executive level.

Comparing autism phenotypes in children born extremely preterm and born at term.

Children born preterm are at increased risk for autism spectrum disorder (ASD). There is limited knowledge about whether ASD phenotypes in children born preterm differ from children born at term. The objective of this study was to compare ASD core symptoms and associated characteristics among extremely preterm (EP) and term-born children with ASD. EP participants (n=59) from the Extremely Low Gestational Age Newborn Study who met diagnostic criteria for ASD at approximately 10 years of age were matched with term-born participants from the Simons Simplex Collection on age, sex, spoken language level, and nonverbal IQ. Core ASD symptomatology was evaluated with the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS). Developmental milestones, anthropometrics, seizure disorder, and psychiatric symptoms were also investigated. The EP group had lower parent-reported symptom scores on ADI-R verbal communication, specifically stereotyped language, and restricted, repetitive behaviors. There were no between-group differences on ADI-R nonverbal communication and ADI-R reciprocal social interaction or with direct observation on the ADOS-2. The EP group was more likely to have delayed speech milestones and lower physical growth parameters. Results from female-only analyses were similar to those from whole-group analyses. In sum, behavioral presentation was similar between EP and IQ- and sex-matched term-born children assessed at age 10 years, with the exception of less severe retrospectively reported stereotyped behaviors, lower physical growth parameters, and increased delays in language milestones among EP-born children with ASD.

Linking ADHD and ASD Symptomatology with Social Impairment: The Role of Emotion Dysregulation.

Children with attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) often experience social impairments. These children also frequently struggle with emotion regulation, and extant literature suggests that emotion dysregulation predicts social impairment in both clinical and neurotypical populations. However, the evidence base linking ADHD/ASD with social impairment comes primarily from samples meeting full diagnostic criteria for ADHD and/or ASD despite evidence that both syndromes reflect extreme ends of natural continuums that are normally distributed across the general population. To our knowledge, the present study is the first to concurrently examine unique and overlapping relations among ADHD/ASD symptoms, emotion regulation, and social difficulties using multi-informant measures (parent, teacher) with a clinically-evaluated sample of 108 children ages 8-13 (40 girls; 66% White/Non-Hispanic) with and without clinically-elevated ASD and ADHD symptoms and other common clinical disorders. Bias-corrected, bootstrapped conditional effects modeling revealed that ADHD-inattentive (β=-0.23) and ASD-social communication (β=-0.20) symptoms predicted social impairment directly, whereas ADHD-hyperactive/impulsive (β=-0.06) and ASD-restricted/repetitive behavior/interests (β=-0.06) symptoms predicted social impairment only via their shared associations with emotion dysregulation. Sensitivity analyses revealed that most relations were robust to control for item overlap across measures. In contrast, only the ADHD-inattention/social impairment link was robust to control for mono-informant bias, highlighting the importance of multi-informant methods and the potential for different determinants of social functioning across settings. Overall, this study implicates emotion regulation skills and all four ADHD/ASD symptom clusters as potential influences on children's social functioning, albeit with a more nuanced and potentially setting-specific pattern than suggested by prior work.

Comparison of serum thrombospondin-1 and thrombospondin-2 levels among children with autism spectrum disorder and healthy controls

Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder, the etiology of which has not been clearly determined yet. There is increasing evidence that synaptic and dendritic changes are involved in the etiology of ASD. The aim of this study is to determine whether serum Thrombospondin-1 and Thrombospondin-2 differ between ASD patients and healthy controls. This study also investigates possible correlations between clinical symptomatology of ASD and serum Thrombospondin-1 and Thrombospondin-2 levels. Method: A total of 44 children with ASD and 21 healthy controls under 6 years of age were included in the study. Symptom severity and behavioral problems among children with ASD were evaluated by using Childhood Autism Rating Scale and Abnormal Behavior Checklist. Serum levels of Thrombospondin-1 and Thrombospondin-2 were measured by using commercial enzyme-linked immunosorbent assay kits. Result: No statistically significant differences were found between the two groups in terms of serum Thrombospondin-1 and Thrombospondin-2 levels. In addition, no correlation was determined between Thrombospondin-2 levels and clinical symptomatology and severity of ASD. However, the Thrombospondin-1 level was found to negatively correlated with the total score of Childhood Autism Rating Scale, inappropriate speech and stereotype subscale scores of Aberrant Behavior Checklist scale. Conclusion: Thrombospondin-1 might have a potential role in the etiopathogenesis of ASD. Further studies are required to clearly elucidate the association between Trombospondin-1 and ASD.

Slower Peak Pupillary Response to Emotional Faces in Parents of Autistic Individuals.

BackgroundAtypical autonomic arousal has been consistently documented in autism spectrum disorder (ASD) and is thought to contribute to the social-communication phenotype of ASD. Some evidence suggests that clinically unaffected first-degree relatives of autistic individuals may also show subtle differences in indices of autonomic arousal, potentially implicating heritable pathophysiological mechanisms in ASD. This study examined pupillary responses in parents of autistic individuals to investigate evidence that atypical autonomic arousal might constitute a subclinical physiological marker of ASD heritability within families of autistic individuals.MethodsPupillary responses to emotional faces were measured in 47 ASD parents and 20 age-matched parent controls. Macro-level pupillary responses (e.g., mean, peak, latency to peak) and dynamic pupillary responses over the course of the stimulus presentation were compared between groups, and in relationship to subclinical ASD-related features in ASD parents. A small ASD group (n = 20) and controls (n = 17) were also included for exploratory analyses of parent–child correlations in pupillary response.ResultsParents of autistic individuals differed in the time course of pupillary response, exhibiting a later primary peak response than controls. In ASD parents, slower peak response was associated with poorer pragmatic language and larger peak response was associated with poorer social cognition. Exploratory analyses revealed correlations between peak pupillary responses in ASD parents and mean and peak pupillary responses in their autistic children.ConclusionDifferences in pupillary responses in clinically unaffected parents, together with significant correlations with ASD-related features and significant parent–child associations, suggest that pupillary responses to emotional faces may constitute an objective physiological marker of ASD genetic liability, with potential to inform the mechanistic underpinnings of ASD symptomatology.

Investigating the contributions of circadian pathway and insomnia risk genes to autism and sleep disturbances

Sleep disturbance is prevalent in youth with Autism Spectrum Disorder (ASD). Researchers have posited that circadian dysfunction may contribute to sleep problems or exacerbate ASD symptomatology. However, there is limited genetic evidence of this. It is also unclear how insomnia risk genes identified through GWAS in general populations are related to ASD and common sleep problems like insomnia traits in ASD. We investigated the contribution of copy number variants (CNVs) encompassing circadian pathway genes and insomnia risk genes to ASD risk as well as sleep disturbances in children with ASD. We studied 5860 ASD probands and 2092 unaffected siblings from the Simons Simplex Collection (SSC) and MSSNG database, as well as 7509 individuals from two unselected populations (IMAGEN and Generation Scotland). Sleep duration and insomnia symptoms were parent reported for SSC probands. We identified 335 and 616 rare CNVs encompassing circadian and insomnia risk genes respectively. Deletions and duplications with circadian genes were overrepresented in ASD probands compared to siblings and unselected controls. For insomnia-risk genes, deletions (not duplications) were associated with ASD in both cohorts. Results remained significant after adjusting for cognitive ability. CNVs containing circadian pathway and insomnia risk genes showed a stronger association with ASD, compared to CNVs containing other genes. Circadian genes did not influence sleep duration or insomnia traits in ASD. Insomnia risk genes intolerant to haploinsufficiency increased risk for insomnia when duplicated. CNVs encompassing circadian and insomnia risk genes increase ASD liability with little to no observable impacts on sleep disturbances.

Social and sensory influences on linguistic alignment

Abstract Previous research has demonstrated that speakers adapt individual characteristics of speech production to the social context, for example via phonetic convergence. Studies have measured the impact of social dynamics on convergence in typical speakers, but the impact of individual differences is less well-explored. The present study measures phonetic convergence before and after a cooperative interaction with an undergraduate student by comparing teens with a history of autism spectrum disorder (ASD) and with typical development. Results revealed a small temporal convergence effect for typically developing dyads; in contrast, dyads including autistic teens showed no convergence. Furthermore, the degree of convergence was negatively related to severity of ASD symptomatology and atypical sensory profiles. While social and sensory processing abilities may play a role in phonetic convergence, high covariance between these measures makes it difficult to differentiate their contributions in isolation.

Eczema and related atopic diseases are associated with increased symptom severity in children with autism spectrum disorder

Growing evidence indicates that autism spectrum disorder (ASD) has diverse genetic, neurological, and environmental factors that contribute to its neurodevelopmental course. Interestingly, childhood ASD is often accompanied by skin disorders, such as eczema, and other related atopic manifestations. This link may be due to the shared embryonic origin of epidermal and neural tissue. Accordingly, we consider the potential influence of a skin-brain co-vulnerability and ensuing atopic cascade on ASD symptomatology by investigating whether atopic disorders (asthma, allergies, eczema and hay fever) are associated with increased symptom severity in children with ASD. Overall, 45 atopic and 93 non-atopic children with ASD were assessed using the ADOS-2 on scores of total, social and non-social symptoms. Differences in ASD symptom severity were further evaluated as a function of atopic disease type. Atopic children displayed greater symptom severity overall and in the social domain, relative to non-atopic participants. Atopic children were 2.4 times more likely to experience overall impairments classified within the ADOS-2 highest-level severity bracket and 2.7 times more likely to show social difficulties in this range. Moreover, those reporting comorbid eczema displayed increased symptom severity relative to both their non-atopic peers and those reporting asthma and allergies. Taken together, findings indicate that atopic disorders, and particularly comorbid eczema, are associated with increases in ASD symptom severity. Findings provide grounds for future investigations into this link between childhood skin diseases and ASD symptom severity to advance our understanding of neurodevelopment and to develop targeted assessment and intervention opportunities.

Homotaurine ameliorates the core ASD symptomatology in VPA rats through GABAergic signaling: Role of GAD67

Dysregulated GABAergic signaling is reported in Autism Spectrum disorder (ASD). In the present study, we evaluated a GABA structural mimicker homotaurine (HT) via in-silico docking and investigated the therapeutic efficacy of this drug to ameliorate ASD symptoms in the valproic acid (VPA) rat model of ASD. For the in-vivo study, animals were divided into two groups [Normal control (NC, 0.9 % saline; i.p) and disease control (VPA 600 mg/kg; i.p)] on gestational day (GD) 12.5. Male pups from VPA-exposed mothers were further divided into five groups (n = 6 in each group): disease control (DC, no-further treatment), standard treatment (risperidone (RES) 2.5 mg/kg; i.p, consecutively from PND 23-43), HT (10, 25 and 50 mg/kg; i.p, consecutively from PND 23-43). In in-silico studies, the binding pattern of homotaurine to GABA-A receptor was found similar to GABA with Tyr205, Glu155, Tyr157, Arg6, and Thr 130 as shared residues. In the in-vivo phase, the early developmental parameters (from PND 7-23) and behavioral parameters (from PND 43-54) were assessed. The offsprings of the VPA exposed group exhibited significant (p < 0.05) developmental delays, behavioral deficits [decreased sociability and social novelty (three-chamber sociability test), spatial memory (Morris water maze), increased stereotypy (self-grooming)], increased oxidative stress (decreased GSH, SOD, Catalase, and increased MDA), increased pro-inflammatory (IL-1β, 6, TNF-α) and decreased anti-inflammatory (IL-10) cytokines, Purkinje cell loss in the cerebellum and pyknosis in PFC (H/E, Nissil staining) and decreased GAD67 expression in the cerebellum (RT-PCR & immunohistochemistry). Compared to the DC, HT treatment (50 mg/kg) was able to ameliorate the aberrant core behavioral deficits, decreased oxidative stress, decreased pro-inflammatory and increased anti-inflammatory cytokine profile with preservation of the Purkinje cell density in the cerebellum, decreased pyknosis in the prefrontal cortex and normalized the expression of GAD67. Thus, HT can be a useful therapeutic agent in ASD and requires further clinical evaluation.

Online administration of the ADOS for research with adolescents and adults in response to the pandemic.

This study evaluates an online ADOS-2 Module 4 administration. Adolescents and adults with (n=24; 7 females) and without (n=13; 5 females) a history of autism spectrum disorder (ASD) completed the ADOS-2 Module 4 via videoconference. Parents or caregivers completed the Parent/Caregiver Form of the Vineland Adaptive Behavior Scales and the Achenbach Adult Behavior Checklist. The ADOS-2 was reviewed and scored by five trained clinicians and supervised by a senior clinician with established research reliability. The autistic group's scores differed on ADOS total (Calibrated Severity Score, WPS instrument) and domain scores, KSADS domain scores, and Achenbach T-scores. Inter-rater reliability was "moderate" (κ=0.732), and percentage item-wise agreement was r=0.69. The online ADOS-2 showed significant convergence with parent-reported assessments of ASD-relevant symptoms and characteristics, suggesting it was a valid assessment. While any online assessments must be used with caution, results suggest that the approach described here could have sufficient validity and reliability to fill the urgent need to assess and evaluate ASD symptomatology, as one component of a thorough clinical evaluation of ASD-related behaviors. LAY SUMMARY: In this exploratory study, we asked whether it was possible to givethe ADOS-2 to adolescents and adults in a completely online way. Results showed that expert clinicians agreed on 69% of ADOS-2 items; also, participants with autism had higher scores on all parts of the ADOS-2. The online ADOS-2 scores had strong and significant relationships with parents' reports of friendship and social skills. While we need more research that tests this method, this way of doing the ADOS-2 online may be useful for clinicians and researchers who have an urgent need to evaluate autism during the pandemic.