Conclusion: Genetic and other neurobiological factors contribute to the development of MEB disorders in young people, but their relative contribution is influenced by environmental factors. Similarly, the effects of environmental manipulations are constrained by genetic and other neurobiological factors.
Thus, efforts to understand the neurological basis of cognitive, emotional, and behavioral development, and especially to understand how these neural substrates can be modified through environmental intervention, are clearly an important basis for prevention research. Although research efforts are justified for intervention strategies at all stages of development in young people, developmental neuroscience has provided overwhelming evidence for the particular importance of fetal and early postnatal development for establishing the fundamental anatomical and functional architecture of the human brain that will endure throughout life, as well as evidence for the existence of sensitive periods for environmental influences in infancy. Therefore, the prenatal period and early infancy warrant a relatively high level of focus in research efforts.
Recommendation 5-1: Research funders, led by the National Institutes of Health, should dedicate more resources to formulating and testing hypotheses of the effects of genetic, environmental, and epigenetic influences on brain development across the developmental span of childhood, with a special focus on pregnancy, infancy, and early childhood.
Greater collaboration between prevention researchers and developmental neuroscientists could provide a powerful scientific synergy. Theories of pathogenesis derived from developmental neuroscience should inform the design of preventive interventions, and prevention trials should be used to inform and evaluate hypotheses of causal mechanisms derived from developmental neuroscience. Likewise, prevention trials should be designed to identify, measure, and evaluate neurobiological effects as possible mediators in preventive interventions. Hypotheses about causal mechanisms generated from prevention research should be tested and expanded using basic and clinical neuroscience approaches.
Conclusion: Collaborations among prevention scientists and basic and clinical developmental neuroscientists could strengthen understanding of disease mechanisms and improve preventive interventions by mutually informing and testing hypotheses of causal mechanisms and theories of pathogenesis.