The developmental neurobiology of autism spectrum disorder.
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ABSTRACT:
SUBMITTER: DiCicco-Bloom E
PROVIDER: S-EPMC6673916 | biostudies-literature | 2006 Jun
REPOSITORIES: biostudies-literature
Publications
The developmental neurobiology of autism spectrum disorder.
DiCicco-Bloom Emanuel E Lord Catherine C Zwaigenbaum Lonnie L Courchesne Eric E Dager Stephen R SR Schmitz Christoph C Schultz Robert T RT Crawley Jacqueline J Young Larry J LJ
The Journal of neuroscience : the official journal of the Society for Neuroscience 20060601 26
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Project description:Increasing evidence suggests that autism spectrum disorder (ASD) and many forms of developmental delay (DD) originate during fetal development. Preeclampsia may trigger aberrant neurodevelopment through placental, maternal, and fetal physiologic mechanisms.To determine whether preeclampsia is associated with ASD and/or DD.The Childhood Autism Risks from Genetics and the Environment (CHARGE) study is a population-based, case-control investigation of ASD and/or DD origins. Children from 20 California counties aged 24 to 60 months at the time of recruitment and living in catchment areas with a biological parent fluent in English or Spanish were enrolled from January 29, 2003, through April 7, 2011. Children with ASD (n?=?517) and DD (n?=?194) were recruited through the California Department of Developmental Services, the Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, and referrals. Controls with typical development (TD) (n?=?350) were randomly selected from birth records and frequency matched on age, sex, and broad geographic region. Physicians diagnosing preeclampsia were masked to neurodevelopmental outcome, and those assessing neurodevelopmental function were masked to preeclampsia status.Preeclampsia and placental insufficiency were self-reported and abstracted from medical records.The Autism Diagnostic Observation Schedule and Autism Diagnostic Interview-Revised were used to confirm ASD, whereas children with DD and TD were confirmed by Mullen Scales of Early Learning and Vineland Adaptive Behavior Scales and were free of autistic symptoms. Hypotheses were formulated before data collection.Children with ASD were twice as likely to have been exposed in utero to preeclampsia as controls with TD after adjustment for maternal educational level, parity, and prepregnancy obesity (adjusted odds ratio, 2.36; 95% CI, 1.18-4.68); risk increased with greater preeclampsia severity (test for trend, P?=?.02). Placental insufficiency appeared responsible for the increase in DD risk associated with severe preeclampsia (adjusted odds ratio, 5.49; 95% CI, 2.06-14.64).Preeclampsia, particularly severe disease, is associated with ASD and DD. Faulty placentation manifests in the mother as preeclampsia with vascular damage, enhanced systemic inflammation, and insulin resistance; in the placenta as oxygen and nutrient transfer restriction and oxidative stress; and in the fetus as growth restriction and progressive hypoxemia. All are potential mechanisms for neurodevelopmental compromise.
| S-EPMC4416484 | biostudies-literature
Project description:ObjectiveAlthough feeding problems are a common concern in children with autism spectrum disorder (ASD), few longitudinal studies have examined their persistence over time. The purpose of this study was to examine the developmental progression of feeding problems across four time points in preschoolers with ASD.MethodsGroup-based trajectory analyses revealed four distinct trajectories of feeding problems in our sample (N = 396).ResultsThe majority of children showed levels of feeding problems that were low from the outset and stable (Group 1; 26.3%) or moderate and declining over time (Group 2; 38.9%). A third group (26.5%) showed high levels of feeding problems as preschoolers that declined to the average range by school age. Few participants (8.3%) showed evidence of severe chronic feeding problems. Feeding problems were more highly correlated with general behavior problems than with autism symptom severity.ConclusionsOverall, our findings demonstrated that in our sample of children with ASD, most feeding problems remitted over time, but a small subgroup showed chronic feeding problems into school age. It is important to consider and assess feeding problems in ASD against the backdrop of typical development, as many children with ASD may show improvement with age.
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Project description:Fetal neuroinflammation and prenatal stress (PS) may contribute to lifelong neurological disabilities. Astrocytes and microglia, among the brain's non-neuronal "glia" cell populations, play a pivotal role in neurodevelopment and predisposition to and initiation of disease throughout lifespan. One of the most common neurodevelopmental disorders manifesting between 1-4 years of age is the autism spectrum disorder (ASD). A pathological glial-neuronal interplay is thought to increase the risk for clinical manifestation of ASD in at-risk children, but the mechanisms remain poorly understood, and integrative, multi-scale models are needed. We propose a model that integrates the data across the scales of physiological organization, from genome to phenotype, and provides a foundation to explain the disparate findings on the genomic level. We hypothesize that via gene-environment interactions, fetal neuroinflammation and PS may reprogram glial immunometabolic phenotypes that impact neurodevelopment and neurobehavior. Drawing on genomic data from the recently published series of ovine and rodent glial transcriptome analyses with fetuses exposed to neuroinflammation or PS, we conducted an analysis on the Simons Foundation Autism Research Initiative (SFARI) Gene database. We confirmed 21 gene hits. Using unsupervised statistical network analysis, we then identified six clusters of probable protein-protein interactions mapping onto the immunometabolic and stress response networks and epigenetic memory. These findings support our hypothesis. We discuss the implications for ASD etiology, early detection, and novel therapeutic approaches. We conclude with delineation of the next steps to verify our model on the individual gene level in an assumption-free manner. The proposed model is of interest for the multidisciplinary community of stakeholders engaged in ASD research, the development of novel pharmacological and non-pharmacological treatments, early prevention, and detection as well as for policy makers.
| S-EPMC10375982 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-02-27 | GSE111176 | GEO
Project description:Previous research has shown that individuals with autism spectrum disorder (ASD) and developmental coordination disorder (DCD) may have overlapping social and motor skill impairments. This study compares ASD, DCD, and typically developing (TD) youth on a range of social, praxis and motor skills, and investigates the relationship between these skills in each group. Data were collected on participants aged 8-17 (n = 33 ASD, n = 28 DCD, n = 35 TD). Overall, the clinical groups showed some similar patterns of social and motor impairments but diverged in praxis impairments, cognitive empathy, and Theory of Mind ability. When controlling for both social and motor performance impairments, the ASD group showed significantly lower accuracy on imitation of meaningful gestures and gesture to command, indicating a prominent deficit in these praxis skills in ASD. LAY SUMMARY: Individuals with autism spectrum disorder (ASD) and developmental coordination disorder (DCD) have social and motor skill impairments to varying degrees. This study compares ASD, DCD, and typically developing (TD) youth on a range of social, praxis, and motor skills. ASD and DCD shared similar patterns of gross and fine motor skills, but differed in skills related to making gestures. Specifically, our results also suggest that ASD has a prominent deficit in gesture performance and meaningful imitation compared to TD and DCD groups.
| S-EPMC9543450 | biostudies-literature
Project description:ImportanceMore than half of youth with autism spectrum disorders (ASDs) have sensory overresponsivity (SOR), an extreme negative reaction to sensory stimuli. However, little is known about the neurobiological basis of SOR, and there are few effective treatments. Understanding whether SOR is due to an initial heightened sensory response or to deficits in regulating emotional reactions to stimuli has important implications for intervention.ObjectiveTo determine differences in brain responses, habituation, and connectivity during exposure to mildly aversive sensory stimuli in youth with ASDs and SOR compared with youth with ASDs without SOR and compared with typically developing control subjects.Design, setting, and participantsFunctional magnetic resonance imaging was used to examine brain responses and habituation to mildly aversive auditory and tactile stimuli in 19 high-functioning youths with ASDs and 19 age- and IQ-matched, typically developing youths (age range, 9-17 years). Brain activity was related to parents' ratings of children's SOR symptoms. Functional connectivity between the amygdala and orbitofrontal cortex was compared between ASDs subgroups with and without SOR and typically developing controls without SOR. The study dates were March 2012 through February 2014.Main outcomes and measuresRelative increases in blood oxygen level-dependent signal response across the whole brain and within the amygdala during exposure to sensory stimuli compared with fixation, as well as correlation between blood oxygen level-dependent signal change in the amygdala and orbitofrontal cortex.ResultsThe mean age in both groups was 14 years and the majority in both groups (16 of 19 each) were male. Compared with neurotypical control participants, participants with ASDs displayed stronger activation in primary sensory cortices and the amygdala (P < .05, corrected). This activity was positively correlated with SOR symptoms after controlling for anxiety. The ASDs with SOR subgroup had decreased neural habituation to stimuli in sensory cortices and the amygdala compared with groups without SOR. Youth with ASDs without SOR showed a pattern of amygdala downregulation, with negative connectivity between the amygdala and orbitofrontal cortex (thresholded at z > 1.70, P < .05).Conclusions and relevanceResults demonstrate that youth with ASDs and SOR show sensorilimbic hyperresponsivity to mildly aversive tactile and auditory stimuli, particularly to multiple modalities presented simultaneously, and show that this hyperresponsivity is due to failure to habituate. In addition, findings suggest that a subset of youth with ASDs can regulate their responses through prefrontal downregulation of amygdala activity. Implications for intervention include minimizing exposure to multiple sensory modalities and building coping strategies for regulating emotional response to stimuli.
| S-EPMC4861140 | biostudies-literature
Project description:Current research suggests that autism spectrum disorder (ASD) is characterized by asynchronous neural oscillations. However, it is unclear whether changes in neural oscillations represent an index of the disorder or are shared more broadly among both affected and unaffected family members. Additionally, it remains unclear how early these differences emerge in development and whether they remain constant or change over time. In this study we examined developmental trajectories in spectral power in infants at high- or low-risk for ASD. Spectral power was extracted from resting EEG recorded over frontal regions of the scalp when infants were 6, 9, 12, 18 and 24 months of age. We used multilevel modeling to assess change over time between risk groups in the delta, theta, low alpha, high alpha, beta, and gamma frequency bands. The results indicated that across all bands, spectral power was lower in high-risk infants as compared to low-risk infants at 6-months of age. Furthermore high-risk infants showed different trajectories of change in spectral power in the subsequent developmental window indicating that not only are the patterns of change different, but that group differences are dynamic within the first two years of life. These findings remained the same after removing data from a subset of participants who displayed ASD related behaviors at 24 or 36 months. These differences in the nature of the trajectories of EEG power represent important endophenotypes of ASD.
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Project description:BackgroundMuch controversy exists regarding the clinical efficacy of behavioural and developmental interventions for improving the core symptoms of autism spectrum disorders (ASD). We conducted a systematic review to summarize the evidence on the effectiveness of behavioural and developmental interventions for ASD.Methods and findingsComprehensive searches were conducted in 22 electronic databases through May 2007. Further information was obtained through hand searching journals, searching reference lists, databases of theses and dissertations, and contacting experts in the field. Experimental and observational analytic studies were included if they were written in English and reported the efficacy of any behavioural or developmental intervention for individuals with ASD. Two independent reviewers made the final study selection, extracted data, and reached consensus on study quality. Results were summarized descriptively and, where possible, meta-analyses of the study results were conducted. One-hundred-and-one studies at predominantly high risk of bias that reported inconsistent results across various interventions were included in the review. Meta-analyses of three controlled clinical trials showed that Lovaas treatment was superior to special education on measures of adaptive behaviour, communication and interaction, comprehensive language, daily living skills, expressive language, overall intellectual functioning and socialization. High-intensity Lovaas was superior to low-intensity Lovaas on measures of intellectual functioning in two retrospective cohort studies. Pooling the results of two randomized controlled trials favoured developmental approaches based on initiative interaction compared to contingency interaction in the amount of time spent in stereotyped behaviours and distal social behaviour, but the effect sizes were not clinically significant. No statistically significant differences were found for: Lovaas versus special education for non-verbal intellectual functioning; Lovaas versus Developmental Individual-difference relationship-based intervention for communication skills; computer assisted instruction versus no treatment for facial expression recognition; and TEACCH versus standard care for imitation skills and eye-hand integration.ConclusionsWhile this review suggests that Lovaas may improve some core symptoms of ASD compared to special education, these findings are based on pooling of a few, methodologically weak studies with few participants and relatively short-term follow-up. As no definitive behavioural or developmental intervention improves all symptoms for all individuals with ASD, it is recommended that clinical management be guided by individual needs and availability of resources.
| S-EPMC2582449 | biostudies-literature
Project description:Previous studies have found alterations in 40 Hz oscillatory activity in response to auditory stimuli in adults with Autism Spectrum Disorder (ASD). The current study sought to examine the specificity and developmental trajectory of these findings by driving the cortex to oscillate at a range of frequencies in both children and adults with and without ASD. Fifteen participants with ASD (3 female, aged 6-23 years) and 15 age-matched controls (4 female, aged 6-25 years) underwent dense-array EEG as they listened to a carrier tone amplitude-modulated by a sinusoid linearly increasing in frequency from 0-100 Hz over 2 s. EEG data were analyzed for inter-trial phase coherence (ITPC) and single-trial power (STP). Older participants with ASD displayed significantly decreased ability to phase-lock to the stimulus in the low gamma frequency range relative to their typically developing (TD) counterparts, while younger ASD and TD did not significantly differ from each other. An interaction between age and diagnosis suggested that TD and ASD also show different developmental trajectories for low gamma power; TD showed a significant decrease in low gamma power with age, while ASD did not. Regardless of age, increased low gamma STP was significantly correlated with increased clinical scores for repetitive behaviors in the ASD group, particularly insistence on sameness. This study contributes to a growing body of evidence supporting alterations in auditory processing in ASD. Older ASD participants showed more pronounced low gamma deficits than younger participants, suggesting an altered developmental trajectory for neural activity contributing to auditory processing deficits that may also be more broadly clinically relevant. Future studies are needed employing a longitudinal approach to confirm findings of this cross-sectional study.
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Project description:Autism spectrum disorder (ASD) is marked by atypical trajectory of brain maturation, yet the developmental abnormalities in brain function remain unclear. The current study examined the effect of age on amplitude of low-frequency fluctuations (ALFF) in ASD and typical controls (TC) using a cross-sectional design. We classified all the participants into three age cohorts: child (<11 years, 18ASD/20TC), adolescent (11-18 years, 28ASD/26TC) and adult (≥18 years, 18ASD/18TC). Two-way analysis of variance (ANOVA) was performed to ascertain main effects and interaction effects on whole brain ALFF maps. Results exhibited significant main effect of diagnosis in ASD with decreased ALFF in the right precuneus and left middle occipital gyrus during all developmental stages. Significant diagnosis-by-age interaction was observed in the medial prefrontal cortex (mPFC) with ALFF lowered in autistic children but highered in autistic adolescents and adults. Specifically, remarkable quadratic change of ALFF with increasing age in mPFC presented in TC group was absent in ASD. Additionally, abnormal ALFF values in diagnosis-related brain regions predicted the social deficits in ASD. Our findings indicated aberrant developmental patterns of spontaneous brain activity associated with social deficits in ASD and highlight the crucial role of the default mode network in the development of disease.
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