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Shared and distinct developmental pathways to ASD and ADHD phenotypes among infants at familial risk.

ABSTRACT: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are believed to share partially overlapping causal mechanisms suggesting that early risk markers may also overlap. Using latent profile analysis (LPA) in a sample of infants enriched for ASD and ADHD, we first examined the number of distinct groups of 3-year-old children, based on ADHD and ASD symptomatology. To investigate early predictors of ASD and ADHD symptom profiles, we next examined differences in trajectories of infant behaviors among the LPA classes spanning general development, negative affect, attention, activity level, impulsivity, and social behavior. Participants included 166 infants at familial risk for ASD (n = 89), ADHD (n = 38), or low-risk for both (n = 39) evaluated at 12, 18, 24, and 36 months of age. A three-class solution was selected reflecting a Typically Developing (TD) class (low symptoms; n = 108), an ADHD class (high ADHD/low ASD symptoms; n = 39), and an ASD class (high ASD/ADHD symptoms; n = 19). Trajectories of infant behaviors were generally suggestive of a gradient pattern of differences, with the greatest impairment within the ASD class followed by the ADHD class. These findings indicate a mixture of overlapping and distinct early markers of preschool ASD- and ADHD-like profiles that can be difficult to disentangle early in life.

SUBMITTER: Miller M

PROVIDER: S-EPMC7891894 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Shared and distinct developmental pathways to ASD and ADHD phenotypes among infants at familial risk.

Miller Meghan M Austin Shane S Iosif Ana-Maria AM de la Paz Leiana L Chuang Annie A Hatch Burt B Ozonoff Sally S

Development and psychopathology 20201001 4

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are believed to share partially overlapping causal mechanisms suggesting that early risk markers may also overlap. Using latent profile analysis (LPA) in a sample of infants enriched for ASD and ADHD, we first examined the number of distinct groups of 3-year-old children, based on ADHD and ASD symptomatology. To investigate early predictors of ASD and ADHD symptom profiles, we next examined differences in trajecto ...[more]

PMID: 32933597

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Project description:BACKGROUND:Difficulties with executive functioning (EF) are common in individuals with a range of developmental disorders, including autism spectrum disorder (ASD). Interventions that target underlying mechanisms of EF early in development could be broadly beneficial, but require infant markers of such mechanisms in order to be feasible. Prospective studies of infants at high familial risk (HR) for ASD have revealed a surprising tendency for HR toddlers to show longer epochs of attention to faces than low-risk (LR) controls. In typical development, decreases in look durations towards the end of the first year of life are driven by the development of executive attention-a foundational component of EF. Here, we test the hypothesis that prolonged attention to visual stimuli (including faces) in HR toddlers reflects early differences in the development of executive attention. METHODS:In a longitudinal prospective study, we used eye-tracking to record HR and LR infants' looking behaviour to social and non-social visual stimuli at ages 9 and 15 months. At age 3 years, we assessed children with a battery of clinical research measures and collected parental report of effortful control (EC)-a temperament trait closely associated with EF and similarly contingent on executive attention. RESULTS:Consistent with previous studies, we found an attenuated reduction in peak look durations to faces between 9 and 15 months for the HR group compared with the LR group, and lower EC amongst the HR-ASD group. In line with our hypothesis, change in peak look duration to faces between 9 and 15 months was negatively associated with EC at age 3. CONCLUSIONS:We suggest that for HR toddlers, disruption to the early development of executive attention results in an attenuated reduction in looking time to faces. Effects may be more apparent for faces due to early biases to orient towards them; further, attention difficulties may interact with earlier emerging differences in social information processing. Our finding that prolonged attention to faces may be an early indicator of disruption to the executive attention system is of potential value in screening for infants at risk for later EF difficulties and for evaluation of intervention outcomes.

Project description:BackgroundShared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk.MethodsSocial-communication difficulties (N ≤ 5551, Social and Communication Disorders Checklist, SCDC) and combined hyperactive-impulsive/inattentive ADHD symptoms (N ≤ 5678, Strengths and Difficulties Questionnaire, SDQ-ADHD) were repeatedly measured in a UK birth cohort (ALSPAC, age 7 to 17 years). Genome-wide summary statistics on clinical ASD (5305 cases; 5305 pseudo-controls) and ADHD (4163 cases; 12,040 controls/pseudo-controls) were available from the Psychiatric Genomics Consortium. Genetic trait variances and genetic overlap between phenotypes were estimated using genome-wide data.ResultsIn the general population, genetic influences for SCDC and SDQ-ADHD scores were shared throughout development. Genetic correlations across traits reached a similar strength and magnitude (cross-trait rg ≤ 1, pmin = 3 × 10-4) as those between repeated measures of the same trait (within-trait rg ≤ 0.94, pmin = 7 × 10-4). Shared genetic influences between traits, especially during later adolescence, may implicate variants in K-RAS signalling upregulated genes (p-meta = 6.4 × 10-4). Uni-dimensionally, each population-based trait mapped to the expected behavioural continuum: risk-increasing alleles for clinical ADHD were persistently associated with SDQ-ADHD scores throughout development (marginal regression R2 = 0.084%). An age-specific genetic overlap between clinical ASD and social-communication difficulties during childhood was also shown, as per previous reports. Cross-dimensionally, however, neither SCDC nor SDQ-ADHD scores were linked to genetic risk for disorder.ConclusionsIn the general population, genetic aetiologies between social-communication difficulties and ADHD symptoms are shared throughout child and adolescent development and may implicate similar biological pathways that co-vary during development. Within both the ASD and the ADHD dimension, population-based traits are also linked to clinical disorder, although much larger clinical discovery samples are required to reliably detect cross-dimensional trait-disorder relationships.

Project description:Background and aimsDevelopmental disorders such as Autism Spectrum Disorder (ASD), Attention Deficit Hyperactivity Disorder (ADHD), and Developmental Dyslexia (DD) are reported to have more visual problems, oral language difficulties, and diminished reading skills in addition to their different diagnostic features. Moreover, these conditions also have increased internal noise and probably an impaired ability of external noise filtering. The aim of the present study was to compare the reading performance of these groups in the presence of external visual noise which disrupts the automatic reading processes through the degradation of letters.MethodsSixty-four children and adolescents in four groups, ASD, ADHD, DD, and TD, participated in the study. Two types of stimuli were used - unrelated words and pseudowords. The noise was generated by exchanging a fixed number of pixels between the black symbols and the white background distorting the letters. The task of the participants was to read aloud the words or pseudowords. The reading time for a single letter string, word or pseudoword, was calculated, and the proportion of errors was assessed in order to describe the reading performance.ResultsThe results obtained showed that the reading of unrelated words and pseudowords differs in the separate groups of participants and is affected differently by the added visual noise. In the no-noise condition, the group with TD had the shortest time for reading words and short pseudowords, followed by the group with ASD, while their reading of long pseudowords was slightly slower than that of the ASD group. The noise increase evoked variations in the reading of groups with ASD and ADHD, which differed from the no-noise condition and the control group with TD. The lowest proportion of errors was observed in readers with TD. The reading performance of the DD group was the worst at all noise levels, with the most prolonged reading time and the highest proportion of errors. At the highest noise level, the participants from all groups read the words and pseudowords with similar reading speed and accuracy.ConclusionsIn reading words and pseudowords, the ASD, ADHD, and DD groups show difficulties specific for each disorder revealed in a prolonged reading time and a higher proportion of errors. The dissimilarity in reading abilities of the groups with different development is most evident when the accuracy and reading speed are linked together.ImplicationsThe use of noise that degrades the letter structure in the present study allowed us to separate the groups with ASD, ADHD, and DD and disclose specifics in the reading process of each disorder. Error type analysis may provide a basis to improve the educational strategies by appropriately structuring the learning process of children with TD, ASD, ADHD, and DD.

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Shared and distinct developmental pathways to ASD and ADHD phenotypes among infants at familial risk.

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Shared and distinct developmental pathways to ASD and ADHD phenotypes among infants at familial risk.

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