Developmental Paths to Anxiety in an Autism-Enriched Infant Cohort: The Role of Temperamental Reactivity and Regulation.
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ABSTRACT:
SUBMITTER: Ersoy M
PROVIDER: S-EPMC8254725 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:This study examined the effects of individual differences in temperamental reactivity (fear) and self-regulation (attentional control) on attentional biases toward threat in a sample of school-aged children (age range was between 9 years 1 month and 13 years 10 months). Attentional biases were assessed with pictorial Dot-probe task, comparing attention allocation toward angry (threat-related) vs. neutral and happy faces. Children also completed self-report temperamental measures of fear and attentional control. We compared attentional bias scores in 4 groups of children: high/low fear and high/low attentional control. Results indicated that, in the case of children with high fear and low attentional control, attention was significantly biased toward angry faces compared with children who had low fear and low attentional control. Findings are discussed in terms of the moderating role of individual differences in attentional control in the context of threat, anxiety-related attentional biases in children.
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Project description:Internalising problems are common within Autism Spectrum Disorder (ASD); early intervention to support those with emerging signs may be warranted. One promising signal lies in how individual differences in temperament are shaped by parenting. Our longitudinal study of infants with and without an older sibling with ASD investigated how parenting associates with infant behavioural inhibition (8-14 months) and later effortful control (24 months) in relation to 3-year internalising symptoms. Mediation analyses suggest nondirective parenting (8 months) was related to fewer internalising problems through an increase in effortful control. Parenting did not moderate the stable predictive relation of behavioural inhibition on later internalising. We discuss the potential for parenting to strengthen protective factors against internalising in infants from an ASD-enriched cohort.
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Project description:Developmental theories suggest affect-biased attention, preferential attention to emotionally salient stimuli, emerges during infancy through coordinating individual differences. Here we examined bidirectional relations between infant affect-biased attention, temperamental negative affect, and maternal anxiety symptoms using a Random Intercepts Cross-Lagged Panel model (RI-CLPM). Infant-mother pairs from Central Pennsylvania and Northern New Jersey (N = 342; 52% White; 50% reported as assigned female at birth) participated when infants were 4, 8, 12, 18 and 24 months of age. Infants completed the overlap task while eye-tracking data were collected. Mothers reported their infant's negative affect and their own anxiety symptoms. In an RI-CLPM, after accounting for between-person variance (random intercepts representing the latent average of a construct), it is possible to assess within-person variance (individual deviations from the latent average of a construct). Positive relations represent stability in constructs (smaller within-person deviations). Negative relations represent fluctuation in constructs (larger within-person deviations). At the between-person level (random intercepts), mothers with greater anxiety symptoms had infants with greater affect-biased attention. However, at the within-person level (deviations), greater fluctuation in maternal anxiety symptoms at 12- and 18 months prospectively related to greater stability in attention to angry facial configurations. Additionally, greater fluctuation in maternal anxiety symptoms at 18 months prospectively related to greater stability in attention to happy facial configurations. Finally, greater fluctuation in maternal anxiety symptoms at 4- and 12 months prospectively related to greater stability in infant negative affect. These results suggest that environmental uncertainty, linked to fluctuating maternal anxiety, may shape early socioemotional development. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
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Project description:BACKGROUND:Although temperament has been recognized as an important contributor to childhood psychopathology, its role in emergent autism spectrum phenotypes is not well understood. This study examined whether toddlers with autism spectrum disorder (ASD) display temperamental vulnerabilities compared to toddlers with other developmental challenges, whether these characteristics are distinct from core autism symptoms, if they are stable over time, and if they contribute to social outcomes in preschool. METHODS:Parents of 165 toddlers with ASD, 58 nonverbal ability- and chronological age- (CA) matched developmentally delayed (DD) toddlers, and 92 CA-matched typically developing (TD) toddlers completed the Toddler Behavior Assessment Questionnaire-Supplemental (TBAQ-S) at 26 months (SD = 6; Time 1). TBAQ-S data were also available for a subset of toddlers with ASD (n = 126) at 43 months (SD = 9; Time 2). RESULTS:Compared to the DD and TD groups, toddlers with ASD exhibited vulnerabilities within the Effortful Control domain as well as the Surgency domain. They also displayed greater Negative Emotionality compared to TD peers. In the ASD group, temperamental characteristics were not concurrently related to autism severity or developmental level and individual differences were highly stable over time. Changes in Perceptual Sensitivity, Inhibitory Control, and Low-Intensity Pleasure from age 2 to 3.5 uniquely predicted autism symptom severity and adaptive social skill level at Time 2. CONCLUSIONS:Temperamental vulnerabilities in toddlers with ASD are stable over time and involve attentional and behavioral control as well as affective reactivity. They contribute uniquely to social outcomes in preschool and are likely to signal risk for developing later maladaptive attentional, affective, and behavioral symptoms. Considering biologically based dimensions may shed light on noncore facets of the early ASD phenotype that are potentially relevant to the emergence of comorbid conditions later in childhood.
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Project description:Canine aggression is one of the most frequent problems in veterinary behavioral medicine, which in severe cases may result in relinquishment or euthanasia. As it is important to reveal underlying factors of aggression for both treatment and prevention, we recently developed a questionnaire on aggression and temperamental traits and found that "reactivity to stimuli" was associated with aggression toward owners, children, strangers, and other dogs of the Shiba Inu breed. In order to examine whether these associations were consistent in other breeds, we asked the owners of insured dogs of Anicom Insurance Inc. to complete our questionnaire. The top 17 contracted breeds were included. The questionnaire consisted of dogs' general information, four items related to aggression toward owners, children, strangers, and other dogs, and 20 other behavioral items. Aggression-related and behavioral items were rated on a five-point frequency scale. Valid responses (n = 5610) from owners of dogs aged 1 through 10 years were collected. Factor analyses on 18 behavioral items (response rate over 95%) extracted five largely consistent factors in 14 breeds: "sociability with humans," "fear of sounds," "chase proneness," "reactivity to stimuli," and "avoidance of aversive events." By stepwise multiple regression analyses, using the Schwartz's Bayesian information criterion (BIC) method with aggression points as objective variables and general information and temperamental factor points as explanatory variables, "reactivity to stimuli," i.e., physical reactivity to sudden movement or sound at home, was shown to be significantly associated with owner-directed aggression in 13 breeds, child-directed aggression in eight breeds, stranger-directed aggression in nine breeds, and dog-directed aggression in five breeds. These results suggest that "reactivity to stimuli" is simultaneously involved in several types of aggression. Therefore, it would be worth taking "reactivity to stimuli" into account in the treatment and prevention of canine aggression.
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Project description:Anxiety disorders are among the most prevalent psychiatric disorders, causing significant suffering and disability. Behavioral inhibition is a temperament that is linked to an increased risk for the later development of anxiety disorders and other stress-related psychopathology, and understanding the neural systems underlying this dispositional risk could provide insight into novel treatment targets for anxiety disorders. Nonhuman primates (NHPs) have anxiety-related temperaments that are similar to those of humans with behavioral inhibition, facilitating the design of translational models related to human psychopathology. Characterization of our NHP model of behavioral inhibition, which we term anxious temperament (AT), reveals that it is trait-like. Exploration of the neural substrates of AT in NHPs has revealed a distributed neural circuit that is linked to individual differences in AT, which includes the dorsal amygdala. AT-related metabolism in the dorsal amygdala, including the central nucleus, is stable across time and can be detected even in safe contexts, suggesting that AT has trait-like neural signatures within the brain. The use of lesioning and novel chemogenetic methods allows for mechanistic perturbation of the amygdala to determine its causal contribution to AT. Studies characterizing the molecular bases for individual differences in AT in the dorsal amygdala, which take advantage of novel methods for probing cellular and molecular systems, suggest involvement of neurotrophic systems, which point to the importance of neuroplasticity in AT. These novel methods, when used in combination with translational NHP models such as AT, promise to provide insights into the brain systems underlying the early risk for anxiety disorder development.
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Project description:BackgroundEpigenetic mechanisms such as altered DNA methylation have been suggested to play a role in autism, beginning with the classical association of Prader-Willi syndrome, an imprinting disorder, with autistic features.ObjectivesHere we tested for the relationship of paternal sperm DNA methylation with autism risk in offspring, examining an enriched-risk cohort of fathers of autistic children.MethodsWe examined genome-wide DNA methylation (DNAm) in paternal semen biosamples obtained from an autism spectrum disorder (ASD) enriched-risk pregnancy cohort, the Early Autism Risk Longitudinal Investigation (EARLI) cohort, to estimate associations between sperm DNAm and prospective ASD development, using a 12-month ASD symptoms assessment, the Autism Observation Scale for Infants (AOSI). We analysed methylation data from 44 sperm samples run on the CHARM 3.0 array, which contains over 4 million probes (over 7 million CpG sites), including 30 samples also run on the Illumina Infinium HumanMethylation450 (450K) BeadChip platform (∼485 000 CpG sites). We also examined associated regions in an independent sample of post-mortem human brain ASD and control samples for which Illumina 450K DNA methylation data were available.ResultsUsing region-based statistical approaches, we identified 193 differentially methylated regions (DMRs) in paternal sperm with a family-wise empirical P-value [family-wise error rate (FWER)] <0.05 associated with performance on the Autism Observational Scale for Infants (AOSI) at 12 months of age in offspring. The DMRs clustered near genes involved in developmental processes, including many genes in the SNORD family, within the Prader-Willi syndrome gene cluster. These results were consistent among the 75 probes on the Illumina 450K array that cover AOSI-associated DMRs from CHARM. Further, 18 of 75 (24%) 450K array probes showed consistent differences in the cerebellums of autistic individuals compared with controls.ConclusionsThese data suggest that epigenetic differences in paternal sperm may contribute to autism risk in offspring, and provide evidence that directionally consistent, potentially related epigenetic mechanisms may be operating in the cerebellum of individuals with autism.
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