Jones Emily J H, Venema Kaitlin, Earl Rachel K, Lowy Rachel, Webb Sara J
Centre for Brain and Cognitive Development, Birkbeck, University of London, London, UK.
Center on Human Development and Disability, University of Washington, Seattle, WA, USA.
J Child Psychol Psychiatry. 2017 Mar;58(3):270-281. doi: 10.1111/jcpp.12650. Epub 2016 Nov 8.
As a neurodevelopmental disorder, symptoms of ASD likely emerge from a complex interaction between preexisting genetic vulnerabilities and the child's environment. One way to understand causal paths to ASD is to identify dimensional ASD-related traits that vary in the general population and that predispose individuals with other risk factors toward ASD. Moving beyond behavioral traits to explore underlying neurocognitive processes may further constrain the underlying genetics. Endophenotypes are quantitative, heritable, trait-related differences that are generally assessed with laboratory-based methods, can be identified in the general population, and may be more closely tied to particular causal chains that have a more restricted set of genetic roots. The most fruitful endophenotypes may be those observed in infancy, prior to the emergence of behavioral symptoms that they are hypothesized to cause. Social motivation is an ASD-related trait that is highly heritable. In this study, we investigate whether infant endophenotypes of social attention relate to familial risk for lower social motivation in the general population.
We examined whether infant social attention (measured using habituation, EEG power, and event-related potential tasks previously used in infants/toddlers with ASD) varies quantitatively with parental social motivation in 117 six-month-old and 106 twelve-month-old typically developing infants assessed cross-sectionally. To assess heritable aspects of social motivation, primary caregiver biological parents completed two self-report measures of social avoidance and discomfort that have shown high heritability in previous work.
Parents with higher social discomfort and avoidance had infants who showed shorter looks to faces but not objects; reduced theta power during naturalistic social attention; and smaller P400 responses to faces versus objects.
Early reductions in social attention are continuously related to lower parental social motivation. Alterations in social attention may be infant endophenotypes of social motivation traits related to ASD.
作为一种神经发育障碍,自闭症谱系障碍(ASD)的症状可能源于预先存在的遗传易感性与儿童环境之间的复杂相互作用。理解ASD因果路径的一种方法是识别在普通人群中变化的、与ASD相关的维度特征,这些特征使具有其他风险因素的个体易患ASD。超越行为特征去探索潜在的神经认知过程可能会进一步限制潜在的遗传学。内表型是定量的、可遗传的、与特征相关的差异,通常通过基于实验室的方法进行评估,可以在普通人群中识别,并且可能与具有更有限遗传根源的特定因果链更紧密相关。最有成效的内表型可能是在婴儿期观察到的,即在假设它们会导致的行为症状出现之前。社会动机是一种与ASD相关的高度可遗传的特征。在本研究中,我们调查了婴儿社会注意力的内表型是否与普通人群中社会动机较低的家族风险相关。
我们研究了117名6个月大的和106名12个月大的发育正常婴儿(采用横断面评估)的婴儿社会注意力(使用先前在患有ASD的婴幼儿中使用的习惯化、脑电图功率和事件相关电位任务进行测量)是否与父母的社会动机呈定量变化。为了评估社会动机的遗传方面,主要照顾者的亲生父母完成了两项关于社会回避和不适的自我报告测量,这些测量在先前的研究中显示出高遗传性。
社会不适和回避程度较高的父母所生的婴儿,对人脸的注视时间较短,但对物体的注视时间无差异;在自然主义的社会注意力过程中,θ波功率降低;与物体相比,对面孔的P400反应较小。
早期社会注意力的降低与父母较低的社会动机持续相关。社会注意力的改变可能是与ASD相关的社会动机特征的婴儿内表型。