Differences in sensory responses among children with autism spectrum disorder and typical development: Links to joint attention and social competence

Dakopolos, Andrew Jacob; Jahromi, Laudan B.

doi:10.1002/icd.2117

Cited by 15 publications

(11 citation statements)

References 59 publications

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“…Moreover, domain general processes such as ocular motor control (271), sex differences (272), or predictive processing (213) may moderate the development of social attention symptoms development in ASD. Atypical sensory processing may also influence social attention development (273)(274)(275). However, joint attention may also predict the second-year sensory regulation in infants at risk for ASD (276).…”

Section: Social and Non-social Attention Developmentmentioning

confidence: 99%

The Bidirectional Social-Cognitive Mechanisms of the Social-Attention Symptoms of Autism

Mundy

Bullen

2022

Front. Psychiatry

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Differences in social attention development begin to be apparent in the 6th to 12th month of development in children with Autism Spectrum Disorder (ASD) and theoretically reflect important elements of its neurodevelopmental endophenotype. This paper examines alternative conceptual views of these early social attention symptoms and hypotheses about the mechanisms involved in their development. One model emphasizes mechanism involved in the spontaneous allocation of attention to faces, or social orienting. Alternatively, another model emphasizes mechanisms involved in the coordination of attention with other people, or joint attention, and the socially bi-directional nature of its development. This model raises the possibility that atypical responses of children to the attention or the gaze of a social partner directed toward themselves may be as important in the development of social attention symptoms as differences in the development of social orienting. Another model holds that symptoms of social attention may be important to early development, but may not impact older individuals with ASD. The alterative model is that the social attention symptoms in infancy (social orienting and joint attention), and social cognitive symptoms in childhood and adulthood share common neurodevelopmental substrates. Therefore, differences in early social attention and later social cognition constitute a developmentally continuous axis of symptom presentation in ASD. However, symptoms in older individuals may be best measured with in vivo measures of efficiency of social attention and social cognition in social interactions rather than the accuracy of response on analog tests used in measures with younger children. Finally, a third model suggests that the social attention symptoms may not truly be a symptom of ASD. Rather, they may be best conceptualized as stemming from differences domain general attention and motivation mechanisms. The alternative argued for here that infant social attention symptoms meet all the criteria of a unique dimension of the phenotype of ASD and the bi-directional phenomena involved in social attention cannot be fully explained in terms of domain general aspects of attention development.

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Section: Social and Non-social Attention Developmentmentioning

confidence: 99%

The Bidirectional Social-Cognitive Mechanisms of the Social-Attention Symptoms of Autism

Mundy

Bullen

2022

Front. Psychiatry

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“…Groups did not significantly differ in household income, t (31) = 0.645, p = 0.52, d = 0.47; mother’s ethnicity, χ 2 (4, N = 38) = 6.05, p = 0.20; or father’s ethnicity, χ 2 (4, N = 36) = 5.63, p = 0.23. Finally, as group differences in children’s effortful control (ASD < TD), executive function (ASD < TD), emotion regulation (ASD < TD), and joint attention (ASD < TD) have been reported in our prior work (Dakopolos & Jahromi, 2018; Jahromi et al, 2013), these were not reported as part of the present study.…”

Section: Resultsmentioning

confidence: 76%

Delay of gratification in preschoolers with and without autism spectrum disorder: Individual differences and links to executive function, emotion regulation, and joint attention

Jahromi

Chen

Dakopolos

et al. 2019

Autism

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This study examined delay of gratification behaviors in preschool-aged children with and without autism spectrum disorder. Recent research has found that elementary-aged children with autism spectrum disorder showed challenges with delay of gratification and that there were individual differences in terms of children’s behaviors during the wait. We extend this work to a younger sample of children with autism spectrum disorder to understand whether these difficulties emerge by the preschool years. Moreover, we assessed whether individual differences in other key self-regulatory capacities (i.e. effortful control, emotion regulation, executive function, and joint attention) were related to delay of gratification wait durations or behavioral strategies. Findings revealed that preschoolers with autism spectrum disorder waited for a shorter duration, demonstrated more temptation-focused behaviors, and expressed less positive affect than their typical peers during the delay of gratification task. At the full-sample level, individual differences in children’s temptation-focused behaviors (i.e. visual attention and verbalizations focused on the temptation) were related to children’s executive function, joint attention, and parents’ ratings of emotion regulation. When we examined associations within groups, the associations were not significant for the autism spectrum disorder group, but for typically developing children, there was a positive association between temptation-focused behaviors and emotion regulation.

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“…Based on these findings, Molenhuis et al (2016) concluded that Cntn4-deficiency does not affect ASD-specific phenotypes, but rather results in subtle non-ASD-specific changes in responsiveness to stimuli and cognitive performance. Notably, hyper-responsiveness to acoustic stimuli is a phenotype that has been associated with ASD and other neuropsychiatric disorders ( Baranek et al, 2013 ; Green et al, 2013 ; Acevedo et al, 2018 ; Dakopolos and Jahromi, 2019 ; Hornix et al, 2019 ).…”

Section: Neurophysiological Roles Of Chl1 Cntn6 mentioning

confidence: 99%

Cell Adhesion Molecules Involved in Neurodevelopmental Pathways Implicated in 3p-Deletion Syndrome and Autism Spectrum Disorder

Gandawijaya

Bamford

Burbach

et al. 2021

Front. Cell. Neurosci.

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Autism spectrum disorder (ASD) is characterized by impaired social interaction, language delay and repetitive or restrictive behaviors. With increasing prevalence, ASD is currently estimated to affect 0.5–2.0% of the global population. However, its etiology remains unclear due to high genetic and phenotypic heterogeneity. Copy number variations (CNVs) are implicated in several forms of syndromic ASD and have been demonstrated to contribute toward ASD development by altering gene dosage and expression. Increasing evidence points toward the p-arm of chromosome 3 (chromosome 3p) as an ASD risk locus. Deletions occurring at chromosome 3p result in 3p-deletion syndrome (Del3p), a rare genetic disorder characterized by developmental delay, intellectual disability, facial dysmorphisms and often, ASD or ASD-associated behaviors. Therefore, we hypothesize that overlapping molecular mechanisms underlie the pathogenesis of Del3p and ASD. To investigate which genes encoded in chromosome 3p could contribute toward Del3p and ASD, we performed a comprehensive literature review and collated reports investigating the phenotypes of individuals with chromosome 3p CNVs. We observe that high frequencies of CNVs occur in the 3p26.3 region, the terminal cytoband of chromosome 3p. This suggests that CNVs disrupting genes encoded within the 3p26.3 region are likely to contribute toward the neurodevelopmental phenotypes observed in individuals affected by Del3p. The 3p26.3 region contains three consecutive genes encoding closely related neuronal immunoglobulin cell adhesion molecules (IgCAMs): Close Homolog of L1 (CHL1), Contactin-6 (CNTN6), and Contactin-4 (CNTN4). CNVs disrupting these neuronal IgCAMs may contribute toward ASD phenotypes as they have been associated with key roles in neurodevelopment. CHL1, CNTN6, and CNTN4 have been observed to promote neurogenesis and neuronal survival, and regulate neuritogenesis and synaptic function. Furthermore, there is evidence that these neuronal IgCAMs possess overlapping interactomes and participate in common signaling pathways regulating axon guidance. Notably, mouse models deficient for these neuronal IgCAMs do not display strong deficits in axonal migration or behavioral phenotypes, which is in contrast to the pronounced defects in neuritogenesis and axon guidance observed in vitro. This suggests that when CHL1, CNTN6, or CNTN4 function is disrupted by CNVs, other neuronal IgCAMs may suppress behavioral phenotypes by compensating for the loss of function.

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Differences in sensory responses among children with autism spectrum disorder and typical development: Links to joint attention and social competence

Cited by 15 publications

References 59 publications

The Bidirectional Social-Cognitive Mechanisms of the Social-Attention Symptoms of Autism

The Bidirectional Social-Cognitive Mechanisms of the Social-Attention Symptoms of Autism

Delay of gratification in preschoolers with and without autism spectrum disorder: Individual differences and links to executive function, emotion regulation, and joint attention

Cell Adhesion Molecules Involved in Neurodevelopmental Pathways Implicated in 3p-Deletion Syndrome and Autism Spectrum Disorder

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