Reciprocal Social Interaction Research Articles

Relationships between the social communication questionnaire and pragmatic language, socialization skills, and behavioral problems in children with autism spectrum disorders

The Social Communication Questionnaire (SCQ) is one of the most widely used screening instruments for autism spectrum disorder (ASD). This study examined the relationships between the reciprocal social interaction, communication, and repetitive/stereotyped factors on the Strength and Difficulties Questionnaire (SDQ) and pragmatic, socialization, and behavioral problems in children with ASD and children with typical development (TD). Participants were seven- to 11-year-old children with ASD without intellectual disability (n = 52) and with TD (n = 37). The two groups were matched on age and intelligence quotient. Significant differences were found between the two groups on the SCQ domains and the outcome measures (pragmatic language, socialization skills, and behavioral problems). Furthermore, multiple regression analysis exploring the relationships between the SCQ and the criterion variables showed that reciprocal social interaction and repetitive/stereotyped behaviors had an important weight in the prediction of daily life social skills in typically developing children (34%). However, the model with the highest percentage of explained variance in children with ASD involved pragmatic language, with reciprocal social interaction as the best predictor, even reaching 41%. The findings highlight the suitability of routinely including the SCQ in the first stage of assessment protocols for ASD, and, in particular, they show its capacity to predict a valuable repertoire of behaviors.

A Review on Autism

Autism is a developmental disorder characterized by difficulties with social interaction and communication and by restricted and repetitive behavior. It is a group of neurodevelopment disorders known as pervasive developmental disorders(PDD). These disorders are characterized by three core deficits: impaired communication, impaired reciprocal social interaction and restricted, repetitive and stereotyped patterns of behaviors or interests. The presentation of these impairments is variable in range and severity and often changes with the acquisition of other developmental skills. Autism Spectrum Disorder (ASD) is typically diagnosed in childhood and has a wide range symptoms, some being more severe than others. These symptoms consist of communication, socialization, behavioral and interest impairments, as well as minimal social skills. Due to these symptoms, a child with ASD may have trouble relating to peers and forming meaningful relationships. Children diagnosed with autism communicate verbally, nonverbally or a combination of both. Autism is associated with a combination of genetic and environmental. Risk factors during pregnancy include certain infections, such as rubella, toxins including valproic acid, alcohol, cocaine, pesticides and air pollution, fetal growth restriction, and autoimmune diseases. Controversies surround other proposed environmental causes; for example, the vaccine hypothesis, which has been disproven. Autism affects information processing in the brain by altering connections and organization of nerve cells and their synapses. The types of autism is Autistic Disorder, Asperger Syndrome, Pervasive development disorder. Diagnosis is based on behavior, not cause or mechanism. Treatment included Education, high dose vitamin, melatonin to address sleep issues, Medication and drugs included Atypical drugs risperidone and aripiprazole.

Parent-Adolescent Reciprocity in a Conflictual Situation Predicts Peer Interaction in Adolescents With ASD.

Parent-child reciprocity plays a signicant role in shaping children's social interaction skills. The development of conflict management skills throughout childhood and adolescence impacts the individual's social adjustment. The increase in conflictual interaction with one's parents during adolescence affects the transformation of parent-adolescent interaction into a more mutual, equal relationship. Adolescents with ASD and their parents may struggle in this type of interaction due to the adolescents' social and regulatory impairments, in addition to their dependence on their parents' involvement and guidance. The current study aimed to evaluate differences in the way adolescents with and without ASD interact with their parents in a conflictual situation. In addition, the association between parent-adolescent reciprocity and the adolescent's social interaction with an unfamiliar peer was examined in the ASD group. Thirty adolescents with ASD and their parents and 30 typically developing (TD) controls were assessed during a standardized conflict interaction. In addition, adolescents with ASD took part in a conversation with an unfamiliar peer. Interactions were videotaped and coded. Results revealed that during the conflictual interaction, compared to their TD peers, adolescents with ASD were more involved in the conversation and less withdrawn from the parent, while their parents were more sensitive and less intrusive toward them. Parent-adolescent reciprocity was poorer in the ASD (compared to the TD) dyad and was positively associated with the adolescents' social-conversational skills with a peer. These findings emphasize the different developmental trajectory parent-adolescent relationship takes in adolescents with ASD, and its impact on the adolescent's social skills. Autism Res 2019, 12: 263-273 © 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: The development of conflict management skills throughout childhood and adolescence impacts the individual's social adjustment. The ability of parents to engage in reciprocal social interaction with the children plays a significant role in shaping children's social interaction skills with peers and with other adults. The transition to adolescence is characterized by an increase in conflictual interaction with one's parents, which transforms the interaction between adolescents and their parents into a more mutual, equal relationship. Adolescents with ASD and their parents may struggle in this type of interaction due to the adolescents' social and emotional difficulties, and their dependence on their parents' involvement and guidance. However, the nature of parent-adolescent interaction, and particularly conflict management has rarely been studied. This study evaluated the way parents and their adolescents with ASD interact in a conflictual conversation, compared to parents and their typically developing adolescents. In addition, we examined how this type of interaction associated with adolescents' social conversation skills with a peer, in the ASD group. A videotaped interaction between adolescents and their parents indicated that parents and their adolescents with ASD engaged more positively in the conflict, but were less reciprocal with each other. In addition, higher reciprocity among parents and their adolescents with ASD was associated with better conversation skills with an unfamiliar peer. These findings demonstrate the different ways parent-adolescent relationships evolve in families affected by ASD, and the important role parents have in shaping the adolescent's social communication skills.

Interviewing individuals with an autism spectrum disorder in forensic settings

Autism spectrum disorders (ASD) encompass the neurodevelopmental conditions including autism, atypical autism, high functioning autism, and Asperger’s syndrome. In addition to difficulties with social communication, reciprocal social interaction and within different dimensions of imagination, individuals with an ASD typically present with sensory hypersensitivities, a specific cognitive style and characteristics, emotional regulation issues, as well as other co-morbid neurodevelopmental or psychiatric conditions. All these features can raise significant issues when formally interviewing an individual with an ASD, especially within forensic contexts where individuals may be interviewed as a witness, victim or perpetrator of an offense for a range of reasons. To date, there has been limited discussion in the literature regarding how the difficulties associated with having an ASD and co-morbidities can impact on forensic interviews. Using the available literature and clinical experience this article summarizes some key issues and possible solutions related to conducting forensic interviews with adults who have ASD.

Protection by tyrosine kinase inhibitor, tyrphostin AG126, through the suppression of IL-17A, RORγt, and T-bet signaling, in the BTBR mouse model of autism

Autism spectrum disorder (ASD) is an extremely predominant neurodevelopmental disorder expressed as impairment in reciprocal social interaction along with repetitive, restricted, and stereotyped behaviors. The protein tyrosine kinase inhibitor, tyrphostin AG126 (AG126), regulates the expression of several genes that play an important role in the development of neuroinflammatory disorders. Here, we investigate the possible effects of AG126 (5 mg/kg daily through intraperitoneal injection) on self-grooming, marble burying, and hot plate test results in BTBR T + Itpr3tf/J mice (BTBR is a model of autism). We also explore the effects of AG126 administration on IL-17 A, RORγt, T-bet, and IFN-γ production in CD4+ T cells and on CCR6+ chemokine receptors in splenic cells. We further investigated the effect of AG126 administration on the mRNA and protein expression of IL-17 A, RORγt, T-bet, IFN-γ, and NF-κB in the brain tissue. Our results demonstrate that treatment of BTBR mice with AG126 reduced repetitive self-grooming scores and lowered hot plate sensitivity potentials. Furthermore, AG126 administration also caused a substantial reduction of IL-17 A, RORγt, T-bet, and IFN-γ production in CD4+ T cells and on CCR6+ chemokine receptors in splenic cells. BTBR mice treated with AG126 also show decreased mRNA and protein expression levels of IL-17 A, RORγt, T-bet, IFN-γ, and NF-κB activation in brain tissue. Our results indicate that treating BTBR mice with AG126 leads to protection against neuroimmune dysfunction/dysregulation through the inhibition of cytokines and transcription factor signaling. This mechanism may be useful in the development of future therapies for neuroimmune disorders.

Juvenile Shank3b deficient mice present with behavioral phenotype relevant to autism spectrum disorder

Autism spectrum disorder (ASD) is a pervasive, multifactorial neurodevelopmental disorder diagnosed according to deficits in three behavioral domains: communication, social interaction, and stereotyped/repetitive behaviors. Mutations in Shank genes account for ∼1% of clinical ASD cases with Shank3 being the most common gene variant. In addition to maintaining synapses and facilitating dendritic maturation, Shank genes encode master scaffolding proteins that build core complexes in the postsynaptic densities of glutamatergic synapses. Male mice with a deletion of the PDZ domain of Shank3 (Shank3B KO) were previously shown to display ASD-like behavioral phenotypes with reported self-injurious repetitive grooming and aberrant social interactions. Our goal was to extend these previous findings and use a comprehensive battery of highly detailed ASD-relevant behavioral assays including an assessment of mouse ultrasonic communication carried out on key developmental days and male and female Shank3B KO mice. We demonstrate that ASD-related behaviors, atypical reciprocal social interaction and indiscriminate repetitive grooming, are apparent in juvenile stages of development of Shank3B KO mice. Our findings underscore the importance of utilizing Shank mutant models to understand the impact of this gene in ASD etiology, whichmay enable future studies focusing on etiological gene-environment interactions in ASD.

Social interaction recruits mentalizing and reward systems in middle childhood.

Social cognition develops in the context of reciprocal social interaction. However, most neuroimaging studies of mentalizing have used noninteractive tasks that may fail to capture important aspects of real-world mentalizing. In adults, social-interactive context modulates activity in regions linked to social cognition and reward, but few interactive studies have been done with children. The current fMRI study examines children aged 8-12 using a novel paradigm in which children believed they were interacting online with a peer. We compared mental and non-mental state reasoning about a live partner (Peer) versus a story character (Character), testing the effects of mentalizing and social interaction in a 2 × 2 design. Mental versus Non-Mental reasoning engaged regions identified in prior mentalizing studies, including the temporoparietal junction, superior temporal sulcus, and dorsomedial prefrontal cortex. Moreover, peer interaction, even in conditions without explicit mentalizing demands, activated many of the same mentalizing regions. Peer interaction also activated areas outside the traditional mentalizing network, including the reward system. Our results demonstrate that social interaction engages multiple neural systems during middle childhood and contribute further evidence that social-interactive paradigms are needed to fully capture how the brain supports social processing in the real world.

Oxytocin and vasopressin flatten dominance hierarchy and enhance behavioral synchrony in part via anterior cingulate cortex

The neuropeptides oxytocin (OT) and arginine vasopressin (AVP) influence social functions in many mammals. In humans and rhesus macaques, OT delivered intranasally can promote prosocial behavior in certain contexts. Yet the precise neural mechanisms mediating these behavioral effects remain unclear. Here we show that treating a group of male macaque monkeys intranasally with aerosolized OT relaxes their spontaneous social interactions with other monkeys. OT reduces differences in social behavior between dominant and subordinate monkeys, thereby flattening the status hierarchy. OT also increases behavioral synchrony within a pair. Intranasal delivery of aerosolized AVP reproduces the effects of OT with greater efficacy. Remarkably, all behavioral effects are replicated when OT or AVP is injected focally into the anterior cingulate gyrus (ACCg), a brain area linked to empathy and other-regarding behavior. ACCg lacks OT receptors but is rich in AVP receptors, suggesting exogenous OT may shape social behavior, in part, via nonspecific binding. Notably, OT and AVP alter behaviors of both the treated monkey and his untreated partner, consistent with enhanced feedback through reciprocal social interactions. These findings bear important implications for use of OT in both basic research and as a therapy for social impairments in neurodevelopmental disorders.

Autistic traits in a sample of adult patients with schizophrenia: prevalence and correlates.

Schizophrenia and autism spectrum disorder (ASD) are currently conceptualized as distinct disorders. However, the relationship between these two disorders has been revisited in recent years due to evidence that they share phenotypic and genotypic expressions. This study aimed to identify ASD traits in patients with schizophrenia, and to define their demographic, psychopathological, cognitive and functional correlates. Seventy-five schizophrenia patients (20 females, mean age 42 ± 12) were evaluated with the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview-Revised (ADI-R). Participants were also assessed with clinical, neuropsychological, and psychosocial functioning measures. Of the 75 patients, 47 were negative to all the autism scales administered (ADOS-TOT-NEG), 21 patients were positive to the ADOS Language sub-domain (ADOS-L-POS), 21 patients were positive to the ADOS Reciprocal Social Interaction (RSI) sub-domain (ADOS-RSI-POS), 14 patients were positive to the ADOS Total scale (ADOS-TOT-POS), and nine patients were positive to the ADI-R scale (ADI-R-POS). Demographic (duration of illness), psychopathological (negative symptoms and general psychopathology), and cognitive (working memory and processing speed) differences emerged between schizophrenic patients with and without ASD traits, while no differences in psychosocial functioning were detected. Results of this study indicate the existence, in a sample of patients with a diagnosis of schizophrenia, of a distinct group of subjects with ASD features, characterized by specific symptomatological and cognitive profile. These findings may contribute to better characterize patients with schizophrenia in order to develop new procedures and therapeutic tools in a more personalized perspective.

Impaired social behaviors and minimized oxytocin signaling of the adult mice deficient in the N-methyl-d-aspartate receptor GluN3A subunit

The N-methyl-d-aspartate receptor (NMDAR) has been implicated in the pathophysiology of neurological diseases, such as schizophrenia, autism spectrum disorders (ASD), and Alzheimer's disease (AD), whose unique clinical hallmark is a constellation of impaired social and/or cognitive behaviors. GluN3A (NR3A) is a unique inhibitory subunit in the NMDAR complex. The role of GluN3A in social behavioral activities is obscure. In this study, we sought to evaluate altered social activities in adult GluN3A knockout (KO) mice. GluN3A KO mice spent less time in reciprocal social interaction in the social interaction test compared to wild-type (WT) mice. A social approach test using a three-chamber system confirmed that mice lacking GluN3A had lower sociability and did not exhibit a preference for social novelty. GluN3A KO mice displayed abnormal food preference in the social transmission of food preference task and low social interaction activity in the five-trial social memory test, but without social memory deficits. Using a home cage monitoring system, we observed reduced social grooming behavior in GluN3A KO mice. Signaling genes that might mediate the altered social behaviors were examined in the prefrontal cortex, hippocampus, and thalamus. Among nine genes examined, the expression of the oxytocin receptor was significantly lower in the prefrontal cortex of GluN3A KO mice than that in WT mice. Oxytocin treatment rescued social activity deficits in GluN3A KO mice. These findings support a novel idea that a chronic state of moderate increases in NMDAR activities may lead to downregulation of the oxytocin signaling and impaired behavioral activities that are seen in psychiatric/neurodegenerative disorders.

Conditional deletion of Cadherin 13 perturbs Golgi cells and disrupts social and cognitive behaviors.

Inhibitory interneurons mediate the gating of synaptic transmission and modulate the activities of neural circuits. Disruption of the function of inhibitory networks in the forebrain is linked to impairment of social and cognitive behaviors, but the involvement of inhibitory interneurons in the cerebellum has not been assessed. We found that Cadherin 13 (Cdh13), a gene implicated in autism spectrum disorder and attention‐deficit hyperactivity disorder, is specifically expressed in Golgi cells within the cerebellar cortex. To assess the function of Cdh13 and utilize the manipulation of Cdh13 expression in Golgi cells as an entry point to examine cerebellar‐mediated function, we generated mice carrying Cdh13‐floxed alleles and conditionally deleted Cdh13 with GlyT2::Cre mice. Loss of Cdh13 results in a decrease in the expression/localization of GAD67 and reduces spontaneous inhibitory postsynaptic current (IPSC) in cerebellar Golgi cells without disrupting spontaneous excitatory postsynaptic current (EPSC). At the behavioral level, loss of Cdh13 in the cerebellum, piriform cortex and endopiriform claustrum have no impact on gross motor coordination or general locomotor behaviors, but leads to deficits in cognitive and social abilities. Mice lacking Cdh13 exhibit reduced cognitive flexibility and loss of preference for contact region concomitant with increased reciprocal social interactions. Together, our findings show that Cdh13 is critical for inhibitory function of Golgi cells, and that GlyT2::Cre‐mediated deletion of Cdh13 in non‐executive centers of the brain, such as the cerebellum, may contribute to cognitive and social behavioral deficits linked to neurological disorders.

Behavioral alterations in autism model induced by valproic acid and translational analysis of circulating microRNA

Autism spectrum disorder (ASD) is characterized by difficulties in social interaction, communication and language, and restricted repertoire of activities and interests. The etiology of ASD remains unknown and no clinical markers for diagnosis were identified. Environmental factors, including prenatal exposure to valproic acid (VPA), may contribute to increased risk of developing ASD. MicroRNA (miRNA) are small noncoding RNA that regulate gene expression and are frequently linked to biological processes affected in neurodevelopmental disorders. In this work, we analyzed the effects of resveratrol (an antioxidant and anti-inflammatory molecule) on behavioral alterations of the VPA model of autism, as well as the levels of circulating miRNA. We also evaluated the same set of miRNA in autistic patients. Rats of the VPA model of autism showed reduced total reciprocal social interaction, prevented by prenatal treatment with resveratrol (RSV). The levels of miR134–5p and miR138–5p increased in autistic patients. Interestingly, miR134–5p is also upregulated in animals of the VPA model, which is prevented by RSV. In conclusion, our findings revealed important preventive actions of RSV in the VPA model, ranging from behavior to molecular alterations. Further evaluation of preventive mechanisms of RSV can shed light in important biomarkers and etiological triggers of ASD.

17-\u03b2 estradiol increases parvalbumin levels in Pvalb heterozygous mice and attenuates behavioral phenotypes with relevance to autism core symptoms

BackgroundAutism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by two core symptoms: impaired social interaction and communication, and restricted, repetitive behaviors and interests. The pathophysiology of ASD is not yet fully understood, due to a plethora of genetic and environmental risk factors that might be associated with or causal for ASD. Recent findings suggest that one putative convergent pathway for some forms of ASD might be the downregulation of the calcium-binding protein parvalbumin (PV). PV-deficient mice (PV−/−, PV+/−), as well as Shank1−/−, Shank3−/−, and VPA mice, which show behavioral deficits relevant to all human ASD core symptoms, are all characterized by lower PV expression levels.MethodsBased on the hypothesis that PV expression might be increased by 17-β estradiol (E2), PV+/− mice were treated with E2 from postnatal days 5–15 and ASD-related behavior was tested between postnatal days 25 and 31.ResultsPV expression levels were significantly increased after E2 treatment and, concomitantly, sociability deficits in PV+/− mice in the direct reciprocal social interaction and the 3-chamber social approach assay, as well as repetitive behaviors, were attenuated. E2 treatment of PV+/+ mice did not increase PV levels and had detrimental effects on sociability and repetitive behavior. In PV−/− mice, E2 obviously did not affect PV levels; tested behaviors were not different from the ones in vehicle-treated PV−/− mice.ConclusionOur results suggest that the E2-linked amelioration of ASD-like behaviors is specifically occurring in PV+/− mice, indicating that PV upregulation is required for the E2-mediated rescue of ASD-relevant behavioral impairments.

Processing Speed is Impaired in Adults with Autism Spectrum Disorder, and Relates to Social Communication Abilities.

Autism spectrum disorder (ASD) is characterized by a variety of social and non-social behavioral deficits. One potential mechanism that could unify this diverse profile of behaviors is slower processing speed. Seventy-six high-functioning adults with ASD were compared to 64 matched controls on standardized measures of processing speed. Participants with ASD were significantly slower on all measures, and on the composite score from the three tests (d's > .65). ASD participants with slower processing speeds scored higher on the ADOS Communication and Reciprocal Social Interaction scale (r = .34). These findings provide evidence of slower processing speeds in adults with ASD, and that this may be contributing to impairments in social communication skills. Interventions that improve processing speed might improve social communication abilities in ASD.

Impaired Object Recognition but Normal Social Behavior and Ultrasonic Communication in Cofilin1 Mutant Mice

Autism spectrum disorder (ASD), schizophrenia (SCZ) and intellectual disability (ID) show a remarkable overlap in symptoms, including impairments in cognition, social behavior and communication. Human genetic studies revealed an enrichment of mutations in actin-related genes for these disorders, and some of the strongest candidate genes control actin dynamics. These findings led to the hypotheses: (i) that ASD, SCZ and ID share common disease mechanisms; and (ii) that, at least in a subgroup of affected individuals, defects in the actin cytoskeleton cause or contribute to their pathologies. Cofilin1 emerged as a key regulator of actin dynamics and we previously demonstrated its critical role for synaptic plasticity and associative learning. Notably, recent studies revealed an over-activation of cofilin1 in mutant mice displaying ASD- or SCZ-like behavioral phenotypes, suggesting that dysregulated cofilin1-dependent actin dynamics contribute to their behavioral abnormalities, such as deficits in social behavior. These findings let us hypothesize: (i) that, apart from cognitive impairments, cofilin1 mutants display additional behavioral deficits with relevance to ASD or SCZ; and (ii) that our cofilin1 mutants represent a valuable tool to study the underlying disease mechanisms. To test our hypotheses, we compared social behavior and ultrasonic communication of juvenile mutants to control littermates, and we did not obtain evidence for impaired direct reciprocal social interaction, social approach or social memory. Moreover, concomitant emission of ultrasonic vocalizations was not affected and time-locked to social activity, supporting the notion that ultrasonic vocalizations serve a pro-social communicative function as social contact calls maintaining social proximity. Finally, cofilin1 mutants did not display abnormal repetitive behaviors. Instead, they performed weaker in novel object recognition, thereby demonstrating that cofilin1 is relevant not only for associative learning, but also for “non-matching-to-sample” learning. Here we report the absence of an ASD- or a SCZ-like phenotype in cofilin1 mutants, and we conclude that cofilin1 is relevant specifically for non-social cognition.

False Belief Reasoning in Adults with and without Autistic Spectrum Disorder: Similarities and Differences.

A central diagnostic criteria for autism spectrum disorder (ASD) is the qualitative impairment in reciprocal social interaction and a prominent hypotheses that tried to explain this impairment is the Theory of Mind (ToM) deficit hypotheses. On a behavioral level the critical test for having a ToM, the understanding of false beliefs (FB), is often used for testing ToM abilities in individuals with ASD. Investigating the neural underpinnings several neuroimaging studies revealed a network of areas involved in FB reasoning in neurotypical individuals. For ASD individuals the neural correlates of false belief processing are largely unknown. Using functional magnetic resonance imaging and an adapted unexpected transfer task, that makes it possible to distinguish between the computation of diverging beliefs and the selection of a belief-associated response, we investigated a group of adult high-functioning individuals with ASD (N = 15) and an age and IQ matched group of neurotypical adults (NT; N = 15). On the behavioral level we found no group differences. On the neural level, results were two-fold: In the story phase, in which participants had to compute whether the character's belief is congruent or incongruent to their own belief, there were no differences between neurotypical participants and those diagnosed with ASD. But, in the subsequent question phase, participants with ASD showed increased activity in the bilateral anterior prefrontal cortex, the left posterior frontal cortex, the left superior temporal gyrus, and the left temporoparietal area. These results suggest that during the story phase in which the participants processed observable actions the neural correlates do not differ between adult individuals with ASD and NT individuals. But in the question phase in which participants had to infer an unobservable mental state results revealed neural differences between the two groups. Possibly, these subtle neural processing differences may contribute to the fact that adult ASD individuals are able to master explicit false belief tasks but fail to apply their strategies during everyday social interaction.

Laser-based spectrometer for optical trace gas detection in young adults with autism

Autism is known as a complex neurodevelopmental disability that involve a combination of impairments in communication, reciprocal social interaction, and stereotypic behaviors. Many studies linked oxidative stress (OS) with the etiopathogenesis of Autism Spectrum Disorders (ASD), but the literature reports somewhat contradictory results. The aim of our study was to evaluate ethylene as a by-products of OS in human body, in people with autism. We used a laser-based spectrometer for optical trace ethylene detection. The results indicated that OS was not significantly increased in this disorder. As a by-product of OS exhaled ethylene from adults with autism presented very small concentration differences compared to healthy controls. The possible responsible factor for the normality between the concentrations of breath ethylene at young adults with autism and control adults could be explained by the antioxidants intake together with the lifestyle and dietary patterns. Additional studies are needed to determine carefully which antioxidant will have the greatest therapeutic benefit considering the importance of oxidative stress in many biological reactions.

Precocious development of self-awareness in dolphins.

Mirror-self recognition (MSR) is a behavioral indicator of self-awareness in young children and only a few other species, including the great apes, dolphins, elephants and magpies. The emergence of self-awareness in children typically occurs during the second year and has been correlated with sensorimotor development and growing social and self-awareness. Comparative studies of MSR in chimpanzees report that the onset of this ability occurs between 2 years 4 months and 3 years 9 months of age. Studies of wild and captive bottlenose dolphins (Tursiops truncatus) have reported precocious sensorimotor and social awareness during the first weeks of life, but no comparative MSR research has been conducted with this species. We exposed two young bottlenose dolphins to an underwater mirror and analyzed video recordings of their behavioral responses over a 3-year period. Here we report that both dolphins exhibited MSR, indicated by self-directed behavior at the mirror, at ages earlier than generally reported for children and at ages much earlier than reported for chimpanzees. The early onset of MSR in young dolphins occurs in parallel with their advanced sensorimotor development, complex and reciprocal social interactions, and growing social awareness. Both dolphins passed subsequent mark tests at ages comparable with children. Thus, our findings indicate that dolphins exhibit self-awareness at a mirror at a younger age than previously reported for children or other species tested.

The behavioural phenotype of Potocki-Lupski syndrome: a cross-syndrome comparison

BackgroundPotocki-Lupski syndrome (PTLS) and Smith-Magenis syndrome (SMS) are related genomic disorders, as duplication 17p11.2 (associated with PTLS) is the reciprocal recombination product of the SMS microdeletion. While SMS has a relatively well-delineated behavioural phenotype, the behavioural profile in PTLS is less well defined, despite purported associations with autism spectrum disorder (ASD) and the suggestion that some behaviours may be diametric to those seen in SMS.MethodsCaregivers of individuals with PTLS (N = 34; M age = 12.43, SD = 6.78) completed online behavioural questionnaires, including the Challenging Behaviour Questionnaire (CBQ), the Activity Questionnaire (TAQ), the Repetitive Behaviour Questionnaire (RBQ), the Mood, Interest and Pleasure Questionnaire-Short Form (MIPQ-S) and the Social Communication Questionnaire (SCQ), which assesses behaviours associated with ASD. Individuals with PTLS were matched on age and adaptive functioning to individuals with SMS (N = 31; M age = 13.61, SD = 6.85) and individuals with idiopathic ASD (N = 33; M age = 12.04, SD = 5.85) from an existing dataset.ResultsIndividuals with PTLS and SMS were less impaired than those with idiopathic ASD on the communication and reciprocal social interaction subscales of the SCQ, but neither syndrome group differed from idiopathic ASD on the restricted, repetitive and stereotyped behaviours subscale. On the repetitive behaviour measure, individuals with PTLS and idiopathic ASD scored higher than individuals with SMS on the compulsive behaviour subscale. Rates of self-injury and property destruction were significantly lower in PTLS and idiopathic ASD than in SMS. No between-syndrome differences were found in relation to overactivity or mood; however, impulsivity was greater in SMS than in PTLS.ConclusionsFindings suggest some overlap in the behavioural phenotype of PTLS and features of ASD symptomatology; however, the overall profile of behaviours in PTLS appears to be divergent from both idiopathic ASD and SMS. Relative to idiopathic ASD, PTLS is not characterised by communication or social interaction deficits. However, restricted and repetitive behaviours were evident in PTLS, and these may be characterised specifically by compulsive behaviours. While several behavioural differences were identified between PTLS and SMS, there was little evidence of diametric behavioural phenotypes, particularly in relation to social behaviour.

Computer-analyzed facial expression as a surrogate marker for autism spectrum social core symptoms.

To develop novel interventions for autism spectrum disorder (ASD) core symptoms, valid, reliable, and sensitive longitudinal outcome measures are required for detecting symptom change over time. Here, we tested whether a computerized analysis of quantitative facial expression measures could act as a marker for core ASD social symptoms. Facial expression intensity values during a semi-structured socially interactive situation extracted from the Autism Diagnostic Observation Schedule (ADOS) were quantified by dedicated software in 18 high-functioning adult males with ASD. Controls were 17 age-, gender-, parental socioeconomic background-, and intellectual level-matched typically developing (TD) individuals. Statistical analyses determined whether values representing the strength and variability of each facial expression element differed significantly between the ASD and TD groups and whether they correlated with ADOS reciprocal social interaction scores. Compared with the TD controls, facial expressions in the ASD group appeared more “Neutral” (d = 1.02, P = 0.005, PFDR < 0.05) with less variation in Neutral expression (d = 1.08, P = 0.003, PFDR < 0.05). Their expressions were also less “Happy” (d = −0.78, P = 0.038, PFDR > 0.05) with lower variability in Happy expression (d = 1.10, P = 0.003, PFDR < 0.05). Moreover, the stronger Neutral facial expressions in the ASD participants were positively correlated with poorer ADOS reciprocal social interaction scores (ρ = 0.48, P = 0.042). These findings indicate that our method for quantitatively measuring reduced facial expressivity during social interactions can be a promising marker for core ASD social symptoms.