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Perinatal experiences during a critical developmental period program brain structure and function “for life,” thereby determining vulnerability to psychopathology and cognition in adulthood. Although these functional consequences are associated with alterations in HPA-axis activity and hippocampal structure and function, the underlying mechanisms remain unclear. The parent-offspring relationship (i.e., sensory and nutritional inputs by the mother) is key in mediating these lasting effects. This chapter discusses how early-life events, for example, the amount of maternal care, stress, and nutrition, can affect emotional and cognitive functions later in life. Interestingly, effects of perinatal malnutrition resemble the perinatal stress-induced long-term deficits. Because stress and nutrition are closely interrelated, it proposes that altered stress hormones and changes in specific key nutrients during critical developmental periods act synergistically to program brain structure and function, possibly via epigenetic mechanisms. Understanding how the adult brain is shaped by early experiences is essential to develop behavioural and nutritional preventive therapy.

Information on depression during childhood and adolescence is reviewed from a developmental psychopathology perspective. The chapter covers descriptive and diagnostic features, as well as considering key concerns in the assessment of depression from childhood through adolescence. Issues of developmental epidemiology, including prevalence rates, developmental trajectories, sex differences, and developmental patterns of sequential comorbidity, are reviewed. Multiple risks and vulnerabilities, with particular attention to the developmental relevance of these factors and processes in children and adolescence, are considered. Finally, future directions are emphasized, including continued investigation of transdiagnostic versus specific etiologies, employing multiple levels of analysis, and translating risk knowledge into personalization of evidence-based, developmentally sensitive assessment and intervention approaches.

Childhood sleep disruption is highly prevalent in today’s society due to multiple school and personal demands, clinical sleep disorders, and family schedules. Accumulating literature suggests that sleep disruption is associated with multiple behavioral, emotional, and cognitive deficits. Clearly, insults during childhood that affect learning and academic performance have great potential to impact educational achievement and subsequent career direction later in life. Although longitudinal studies are lacking and it is currently unclear whether sleep disruption truly causes cognitive deficits, small studies suggest that treating the underlying sleep disorder may improve cognitive ability. If so, poor sleep during the childhood years could have a major impact on public health. This chapter will review current literature that has investigated the associations between sleep disruption and cognition in children.

While key aspects of neural development occur prenatally in humans, the brain continues to show significant development postnatally. In this chapter, we review several aspects of brain development that continue well into childhood and adolescence. First, we discuss the continued sculpting of synaptic connections, including the extension of axons and dendrites, neurotransmitter function, synaptic pruning, and myelination. Second, we examine noninvasive indices of structural brain development, including regional volume and connectivity in the brain that may be more easily linked to changes in child behavior across development. Third, we briefly discuss broad developmental changes in functional activity of the brain and connectivity across regions. Finally, we discuss the evidence for postnatal neurogenesis, a relatively new discovery in postnatal brain development. We conclude that although prenatal events of brain development are critical, postnatal sculpting of the brain continues to play a central role in individual differences in behavior and developmental change.