Disentangling periodic and aperiodic neural activity in the first two years of life: Contributions of perinatal maternal distress on neurodevelopment and childhood psychopathology risk

项目摘要 认知依赖于高效而灵活的神经交流。神经元同步化中断可能 阻碍有效的神经通信，削弱支持参与的认知机制 注意力资源。中断的信息处理可以通过非周期指数来索引，该非周期指数 描述随着频率的增加而预期的功率指数下降。 脑电(EEG)功率谱。这种新的神经标记物与认知缺陷和 从幼年后期到老年的精神病理学。然而，我们不知道 非周期指数影响婴儿期的认知和行为发育。行为抑制和反应性 注意过程(即，注意偏向威胁、警觉)是两个核心风险因素，可能受 非周期神经活动的个体差异。早期注意偏差是一种认知机制 前瞻性地将BI与儿童焦虑联系起来。非周期指数越小，激发越强 大脑皮层回路中的抑制。这种神经活动模式可能会影响婴儿获取和处理的方式 环境输入，这可能会加强注意力偏向，增加BI的风险。非周期指数 轨迹也可能容易受到环境影响，例如母亲的痛苦(例如，感觉到的 压力、焦虑)，这可能是有针对性的预防努力的结果。拟议的K99研究将绘制 生命头两年的非周期指数的发展，识别注意力和行为 非周期指数的关联性，并描述非周期指数轨迹如何作为 母亲痛苦的波动。参与者将从正在进行的R01(Pérez-Edga，Buss，LoBue， MPI)，通过对气质的详细评估，考察了早期注意偏差如何对BI做出贡献 和生物心理社会风险(N=357)。利用这个丰富的表型和大样本，我们将绘制轨迹图 在生命的头两年(8、12、18和24个月)与注意力有关的非周期指数， 儿童精神病理学的行为风险和环境风险。拟议的R00研究将以此为基础 通过招募新的孕妇样本来调查基础知识是否协调 母亲的痛苦和促进健康的行为(如体力活动、睡眠质量)的波动 怀孕预示着婴儿会出现神经、认知和行为方面的困难。最终，非周期指数 脑电功率谱可作为注意力和行为的非侵入性和经济的生物标志物 风险，标志着以预防性服务为目标的关键神经功能障碍，NIMH优先考虑(战略目标 2.2)。在K99/R00“独立之路”奖的推动下，我的研究项目将研究如何 大脑成熟的功能轨迹与儿童精神疾病的注意和气质风险有关 混乱，重点是疾病风险的代际传播。

Project Summary Cognition depends on efficient and flexible neural communication. Disrupted neuronal synchronization may thwart efficient neural communication and undercut cognitive mechanisms that support engagement of attentional resources. Disrupted information processing can be indexed by the aperiodic exponent, which describes the expected exponential decrease in power across increasing frequencies of the electroencephalogram (EEG) power spectrum. This novel neural marker is associated with cognitive deficits and psychopathology from late childhood through old age. We do not know, however, whether changes in the aperiodic exponent affect cognitive and behavioral development in infancy. Behavioral inhibition (BI) and reactive attentional processes (i.e., attention bias to threat, vigilance) are two core risk factors that may be influenced by individual differences in aperiodic neural activity. Early attentional biases operate as a cognitive mechanism prospectively linking BI to childhood anxiety. A smaller aperiodic exponent indexes greater excitation relative to inhibition in cortical circuits. This pattern of neural activity may affect how infants access and process environmental input, which may potentiate attentional biases and increase risk for BI. Aperiodic exponent trajectories may be also susceptible to environmental influences, such as maternal distress (e.g., perceived stress, anxiety), that may be amenable to targeted prevention efforts. The proposed K99 study will chart the development of the aperiodic exponent across the first two years of life, identify the attentional and behavioral correlates of the aperiodic exponent, and describe how aperiodic exponent trajectories vary as a function of fluctuations in maternal distress. Participants will be drawn from an ongoing R01 (Pérez-Edgar, Buss, LoBue, MPIs) that examines how early attentional biases contribute to BI through a detailed assessment of temperament and biopsychosocial risk (N = 357). Leveraging this richly phenotyped and large sample, we will chart trajectories of the aperiodic exponent across the first two years of life (8, 12, 18, and 24 months) in relation to attentional, behavioral, and environmental risk for childhood psychopathology. The proposed R00 study will build on this foundational knowledge by recruiting a new sample of pregnant women to investigate whether coordinated fluctuations in a mothers’ distress and health-promoting behaviors (i.e., physical activity, sleep quality) while pregnant predict neural, cognitive, and behavioral difficulties in her infant. Ultimately, the aperiodic exponent of the EEG power spectrum may serve as a non-invasive and economical biomarker for attentional and behavioral risk, marking a key neural dysfunction to target with preventative services, a NIMH priority (Strategic Objective 2.2). Facilitated by this K99/R00 “Pathway to Independence” Award, my research program will examine how functional trajectories of brain maturation relate to attentional and temperamental risk for childhood mental disorder, with an emphasis on the intergenerational transmission of disease risk.