Eye tracking (ET) holds potential for the early detection of autism spectrum disorder (ASD). To overcome the difficulties of working with young children, developing a short and informative paradigm is crucial for ET. We investigated the fixation times of 37 ASD and 37 typically developing (TD) children ages 4-6 watching a 10-second video of a female speaking. ASD children showed significant reductions in fixation time at six areas of interest. Furthermore, discriminant analysis revealed fixation times at the mouth and body could significantly discriminate ASD from TD with a classification accuracy of 85.1%, sensitivity of 86.5%, and specificity of 83.8%. Our study suggests that a short video clip may provide enough information to distinguish ASD from TD children.
BackgroundSeveral lines of evidence indicate mitochondrial impairment in the pathophysiology of autism. As one of the most common biomarkers for mitochondrial dysfunction, mitochondrial DNA (mtDNA) copy number has also been linked to autism, but the relationship between mtDNA copy number and autism was still obscured. In this study, we performed a case–control study to investigate whether mtDNA copy number in peripheral blood cells is related to patients with autism.MethodsRelative mtDNA copy number in peripheral blood cells was measured by using real-time polymerase chain reaction method. The participants in this study included 78 patients with childhood autism and 83 typically developing children.ResultsWe observed children with autism had significantly elevated relative mtDNA copy number than healthy controls (Beta = −0.173, P = 0.0003). However, there were no significant correlations between mtDNA copy number and clinical features (paternal age, maternal age, age of onset, illness of duration, CARS score and ABC score) in childhood autism.ConclusionWe show that elevated mtDNA copy number in peripheral blood is associated with autism, indicating that there may be mitochondrial dysfunction in children with autism.
Telomeres are protective chromosomal structures that play a key role in preserving genomic stability. Epidemiologic studies have shown that the abnormal telomere length in leukocytes is associated with some mental disorders and age-related diseases. However, the association between leukocyte telomere length and autism has not been investigated. Here we investigated the possible association between relative telomere length (RTL) in peripheral blood leukocytes and childhood autism by using an established real-time polymerase chain reaction method. We observed significantly shorter RTL in patients with childhood autism than in controls (p = 0.006). Individuals with shorter RTL had a significantly increased presence of childhood autism compared with those who had long RTL. In patients, we found that family training interventions have a significant effect on telomere length (P = 0.012), but no correlations between RTL and clinical features (paternal age, maternal age, age of onset, illness of duration, CARS score and ABC score) were observed in this study. These results provided the first evidence that shorter leukocytes telomere length is significantly associated with childhood autism. The molecular mechanism underlying telomere length may be implicated in the development of autism.
Language impairment is common in children with autism spectrum disorders (ASDs). Previous research has shown that this disability may be, in part, due to atypical auditory processing of speech stimuli. However, how speech sounds are processed in children with ASD remains largely unknown. The present study assessed the developmental pattern of auditory information processing at the level of the brainstem in preschool children with ASD using speech‐evoked auditory brainstem response (speech‐ABR). Children with ASD (N = 15) and of typical developing (TD) (N = 20), both of preschool age, were enrolled. The speech‐ABRs recorded at two different time points (T1 and T2; 9.68 months apart on average) were virtually identical in the TD group. However, in the ASD group, the wave V latency of speech‐ABR was significantly shortened and the amplitudes of wave A and C were significantly larger at T2, compared to those recorded at T1 (10.78 months apart on average). Compared to the TD group, the wave V and A latencies were prolonged at T1, whereas the wave E amplitude decreased and wave F latency prolonged at T2. There was a positive partial correlation between the language performance and the wave A amplitude in the ASD group. These results indicate that auditory processing at the subcortical level is well‐developed in the TD preschool children, but is immature and abnormal in the children with ASD at the same ages. Thus, aberrant speech processing at the brainstem level may contribute significantly to the language impairment in children with ASD at preschool ages. Autism Res 2019, 12: 1022–1031. © 2019 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary Language impairment is common in children with autism spectrum disorders (ASDs). We investigated the developmental pattern of subcortical auditory processing by monitoring changes in the speech‐evoked auditory brainstem response (speech‐ABR) over a period of 10 months in preschool children. Our results show that subcortical auditory processing is impaired and immature in children with ASD compared with age‐matched, typically developing children. The results suggest that speech‐ABR may be used as an objective measure in evaluating the language performance of children with ASD. The results also suggest that aberrant speech processing at the level of the brainstem may contribute significantly to the language impairment in preschool children with ASD.
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