Abstract

In the field of autism research, recent work has been devoted to studying both behavioral and neural markers that may aide in early identification of autism spectrum disorder (ASD). These studies have often tested infants who have a significant family history of autism spectrum disorder, given the increased prevalence observed among such infants. In the present study we tested infants at high- and low-risk for ASD (based on having an older sibling diagnosed with the disorder or not) at 6- and 12-months-of-age. We computed intrahemispheric linear coherence between anterior and posterior sites as a measure of neural functional connectivity derived from electroencephalography while the infants were listening to speech sounds. We found that by 12-months-of-age infants at risk for ASD showed reduced functional connectivity compared to low risk infants. Moreover, by 12-months-of-age infants later diagnosed with ASD showed reduced functional connectivity, compared to both infants at low risk for the disorder and infants at high risk who were not later diagnosed with ASD. Significant differences in functional connectivity were also found between low-risk infants and high-risk infants who did not go onto develop ASD. These results demonstrate that reduced functional connectivity appears to be related to genetic vulnerability for ASD. Moreover, they provide further evidence that ASD is broadly characterized by differences in neural integration that emerge during the first year of life.

Highlights

  • Autism spectrum disorder (ASD) is a developmental syndrome primarily characterized by deficits in social communication and interactions, and repetitive/restricted patterns of behaviors, interests, and/or activities, which are present, at least in part, from early in development [1]

  • Using coherence of gamma frequency activity as a metric of connectivity, we examined whether differences emerge during the first year of life, a period of development that precedes the onset of ASD symptoms, in infants at high or low risk for ASD as well as in the subset of those who go on to develop the disorder

  • A marginally significant difference was observed between HRA2 and high-risk for ASD (HRA)+ infants (t(20) = 1.74, p,0.1; two-tailed, p,0.05, one-tailed, Cohen’s d = 0.8) with higher coherence in the HRA2 group As in the results presented in the previous section, there was a main effect of condition (F(2,70) = 52.2 p,0.0001; Cohen’s f = 1.5)

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Summary

Introduction

Autism spectrum disorder (ASD) is a developmental syndrome primarily characterized by deficits in social communication and interactions, and repetitive/restricted patterns of behaviors, interests, and/or activities, which are present, at least in part, from early in development [1]. High frequency activity in the gamma range, for example, is thought to bind neural information from different networks, a process that is required for a number of perceptual and cognitive tasks and that is disrupted in several neurocognitive disorders including ASD [6]. Disruptions in the binding function of gamma activity may explain a wide range of language and social communication deficits that characterize ASD [7]. Behaviors that require the coordinated function of several brain regions may not be sufficiently integrated without the appropriate amount of gamma frequency activity

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