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

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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.