To improve the health and well-being of individuals, it has become clear that scientific discoveries must be translated into practical applications (Insel & Fernald, 2004; Moses, Dorsey, Matheson, & Thier, 2005). Historically, such discoveries, particularly in the health sciences, have begun at “the bench,” with basic research at the molecular or cellular level progressing to the “bedside” or clinical venue. Increasingly, both basic researchers and those who are involved directly in patient care recognize that the bench–bedside approach to translational research is best conceptualized as reciprocal in nature (Cicchetti & Hinshaw, 2002; Ialongo et al., 2006). That is, basic scientists can develop new tools for utilization with patients, and clinical researchers and clinicians can make novel assessments about the nature and progression of disease that can stimulate further basic research investigations (Zerhouni, 2005). This bidirectional process is consistent with one of the central tenets of developmental psychopathology, where knowledge on normative and atypical development is considered to be mutually informative (Cicchetti, 1993; Cicchetti & Toth, 1998, 2006; Rutter & Sroufe, 2000).Our work on this Editorial and Special Issue was partially supported by research grants from the National Institute of Drug Abuse, the National Institute of Mental Health, and the Spunk Fund, Inc.

The malleability of insecure and disorganized attachment among infants from maltreating families was investigated through a randomized preventive intervention trial. Findings from research on the effects of maltreatment on infant attachment were incorporated into the design and evaluation of the intervention. One-year-old infants from maltreating families (N = 137) and their mothers were randomly assigned to one of three intervention conditions: (a) infant–parent psychotherapy (IPP), (b) psychoeducational parenting intervention (PPI), and (c) community standard (CS) controls. A fourth group of infants from nonmaltreating families (N = 52) and their mothers served as an additional low-income normative comparison (NC) group. At baseline, mothers in the maltreatment group, relative to the nonmaltreatment group mothers, reported greater abuse and neglect in their own childhoods, more insecure relationships with their own mothers, more maladaptive parenting attitudes, more parenting stress, and lower family support, and they were observed to evince lower maternal sensitivity. Infants in the maltreatment groups had significantly higher rates of disorganized attachment than infants in the NC group. At postintervention follow-up at age 26 months, children in the IPP and PPI groups demonstrated substantial increases in secure attachment, whereas increases in secure attachment were not found for the CS and NC groups. Moreover, disorganized attachment continued to predominate in the CS group. These results were maintained when intent to treat analyses were conducted. The findings are discussed in terms of the utility of translating basic research into the design and evaluation of clinical trials, as well as the importance of preventive interventions for altering attachment organization and promoting an adaptive developmental course for infants in maltreating families.This research was supported by grants from the Administration of Children, Youth, and Families, the National Institute of Mental Health (MH54643), and the Spunk Fund, Inc.

A major focus in developmental psychopathology is on understanding developmental mechanisms and, armed with this information, intervening to improve children's outcomes. Translational research attempts to bridge the distance between understanding and intervention. In the collaborations that have formed the core of our research network on early experience, stress, and prevention science, we have focused on translating basic research on early experiences and stress neurobiology into preventive interventions for neglected and abused children. Our experiences in attempting to move from bench to bedside have led us to recognize the many challenges that face translational researchers. This review provides a brief synopsis of the animal model literature on early experience and stress neurobiology from which we glean several key bridging issues. We then review what is currently known about the impact of childhood neglect and abuse on stress neurobiology in human adults and children. Next, we describe how this work has informed the evaluation of our preventive interventions with maltreated children. Finally, we discuss several considerations that should facilitate a more complete integration of basic research on early experience and stress neurobiology into preventive intervention strategies.This paper reflects the work of the Early Experience, Stress and Prevention Science Network (R21 MH65046), whose members are Mary Dozier, Philip Fisher, Nathan Fox, Megan Gunnar, Seymour Levine, Charles Neal, Seth Pollak, Paul Plotsky, Mar Sanchez, and Delia Vazquez. Preparation of this manuscript was supported by a Senior Scientist Award (K05 MH66208) to Megan Gunnar, and by MH59780 and MH65046, NIMH, U.S. PHS; MH46690, NIMH and ORMH, U.S. PHS; and DA17592, NIDA, NIH, U.S. PHS to Philip Fisher.

Through a translational approach, dynamic skill theory enhances the understanding of the variation in the behavioral and cognitive presentations of a high-risk population—maltreated children. Two studies illustrate the application of normative developmental constructs from a dynamic skills perspective to samples of young maltreated and nonmaltreated children. Each study examines the emotional and cognitive development of maltreated children with attention to their developing world view or negativity bias and cognitive skills. Across both studies, maltreated children demonstrate negativity bias when compared to their nonmaltreated counterparts. Cognitive complexity demonstrated by the maltreated children is dependent upon a positive or negative context. Positive problem solving is more difficult for maltreated children when compared to their nonmaltreated counterparts. Differences by maltreatment type, severity, timing of the abuse, and identity of the perpetrator are also delineated, and variation in the resulting developmental trajectories in each case is explored. This translation of dynamic skill theory, as applied to maltreated children, enhances our basic understanding of their functioning, clarifies the nature of their developmental differences, and underscores the need for early intervention.This research was supported by grants from the National Institute of Mental Health, the Roche Relief Fund, the Spencer Foundation, and the Spunk Fund, Inc. We are especially grateful to Tracy McCabe and Pamela Raya for their assistance and to the child and families who participated in these investigations.

Understanding why interparental difficulties pose a risk to children in families experiencing domestic violence is an urgent task for ameliorating childhood psychopathology, particularly in light of the paucity of knowledge on the unfolding mediating mechanisms and the potentiating and protective conditions that underlie the multiplicity of pathways between domestic violence and child maladjustment. Toward addressing this significant gap, this paper examines how the emotional security theory (EST) may foster advances in our understanding of the genesis, course, and treatment of children's psychological problems in families experiencing domestic violence. Following an overview of the theoretical assumptions and significance of translating the emotional security theory to high-risk contexts, we address how children's difficulties in preserving security may emerge in the face of domestic violence and accompanying forms of severe family adversity, and illustrate the implications of emotional insecurity for childhood psychopathology in homes characterized by domestic violences. In the final section, we address how the EST may be useful in informing public policy and intervention initiatives designed to reduce the burden of mental illness.This research was supported by a National Institute of Mental Health award (R01 MH071256) to Patrick T. Davies and Dante Cicchetti. Marcia A. Winter was supported by a National Institute of Mental Health fellowship (F31 MH068057).

There is a pressing need for the early and accurate identification of young children at risk for language and other developmental disabilities and the provision of timely, age-appropriate intervention, as mandated by Part C of the Individuals with Disabilities Education Act. Research has shown that early intervention is effective for many language impaired children in different etiological groups, and can reduce the functional impact of persistent disorders on children and their families. Yet, the accurate identification of infants and toddlers at risk for language impairment remains elusive, especially for late-talking children without obvious genetic or neurological conditions. In this paper, the need for translational research on basic processes in early language development in typical and atypical populations and the contextual factors that affect them are discussed, along with current challenges and future directions for its successful implementation. Implications of this research for clinical evidence-based practice are also considered.Partial support during the writing of this paper was provided by NIH Grant RO1HD044068. I am grateful to Dante Cicchetti for his thoughtful feedback on a prior version of this paper.

Building upon methods and research utilized with normative populations, we examine extant assumptions regarding the effects of child maltreatment on memory. The effects of stress on basic memory processes is examined, and potential neurobiological changes relevant to memory development are examined. The impact of maltreatment-related sequelae (including dissociation and depression) on basic memory processes as well as false memories and suggestibility are also outlined. Although there is a clear need for additional research, the investigations that do exist reveal that maltreated children's basic memory processes are not reliably different from that of other, nonmaltreated children.Preparation of this article was supported by a grant from the National Institute of Mental Health to the authors.

Studies using narratives with children and parents offer ways to study affective meaning-making processes that are central in many theories of developmental psychopathology. This paper reviews theory regarding affective meaning making, and argues that narratives are particularly suited to examine such processes. The review of narrative studies and methods is organized into three sections according to the focus on child, parent, and parent–child narratives. Within each focus three levels of analysis are considered: (a) narrative organization and coherence, (b) narrative content, and (c) the behavior/interactions of the narrator(s). The implications of this research for developmental psychopathology and clinical work are discussed with an emphasis on parent–child jointly constructed narratives as the meeting point of individual child and parent narratives.

A model of the development of hostile attributional style and its role in children's aggressive behavior is proposed, based on the translation of basic science in ethology, neuroscience, social psychology, personality psychology, and developmental psychology. Theory and findings from these domains are reviewed and synthesized in the proposed model, which posits that (a) aggressive behavior and hostile attributions are universal human characteristics, (b) socialization leads to the development of benign attributions, (c) individual differences in attributional style account for differences in aggressive behavior, and (d) interventions to change attributions have the potential to alter antisocial development. Challenges for future research are described.

There is increasing evidence that with the onset of adolescence, girls experience higher rates of depression than boys. However, a comprehensive understanding of the risk factors contributing to this emerging gender difference has yet to be attained. Previous studies indicate that both self-discrepancy, the perception that one is failing to attain an important personal goal, and ruminative coping, a tendency to passively and repetitively focus on one's failure and the causes and consequences of that failure, contribute to depression and that adolescent girls are more likely to manifest each than adolescent boys. In this translational study we tested the hypothesis that, whereas both actual:ideal discrepancy and ruminative coping style would independently predict depression in adolescent girls, the combination of high levels of actual:ideal discrepancy and ruminative coping would predict more severe depressive symptoms. Analyses of cross-sectional data in a sample of 223 girls ranging from 7th through 12th grades revealed a significant main effect for ruminative coping style and a trend for actual:ideal discrepancy, as well as the predicted interaction effect. We discuss the implications of this integrative psychosocial model for the etiology, treatment, and prevention of depression in adolescent girls.This work was funded by the following grants to A. A. Papadakis: the Duke University Women's Studies Program Ernestine Friedl Research Award, the Society for the Psychology of Women Hyde Graduate Student Research Grant, and the Duke University Graduate School Summer Research Fellowship; and grants to T. J. Strauman from the National Institute of Mental Health (MH59106, MH67447). Support was also provided by the National Institute of Child Health and Human Development (5-T32-HD007376) and the Duke University Initiative on Child and Family Health. We thank Ann Aspnes, Janina Brodsky, Kimberly Burdette, Tsu-Yin Chang, Lindsay Derman, Hillary Hays, Caitlin Hogan, Cara Kimberg, Patricia Kuo, Lori Kwapil, Ruby Lekwauwa, Megan McCrudden, Ellen McGinnis, Amy Noll McLean, Keri-Ann O'Leary, Rebecca Parrish, Dana Torpey, Emily Traupman, Carolyn Yarian, and Natalie Zervas for their invaluable assistance in conducting this study. We are grateful to the students, teachers, and administration of the schools and summer camp who generously participated in this research.

Abnormalities in attention have long been viewed as one of the fundamental underlying cognitive deficits in schizophrenia, likely contributing both to formation of some types of symptoms and particularly to the substantial work and social impairments that often accompany schizophrenia. Yet, the precise nature of the attentional deficits in schizophrenia remains poorly understood. Translating advances in cognitive psychology to clinical research brings paradigms with greater analytic power to the study of attention in schizophrenia. In particular, these paradigms should shed light on whether the attentional dysfunction in schizophrenia is best conceptualized as arising from limitations in amount or allocation of processing capacity or from more specific structural bottlenecks that do not allow certain processes to be carried out in two tasks simultaneously. Certain types of dual-task paradigms are particularly well suited to make distinctive predictions, particularly those involving a psychological refractory period paradigm. The background and design of a series of ongoing studies of prodromal, first-episode, and chronic schizophrenia patients are described that are addressing the developmental course of attentional dysfunction in this disorder. These refined paradigms should substantially increase our understanding of the specific forms of attentional impairment characterizing schizophrenia and their connections to symptom development and functional outcome.

Schizophrenia has long been approached from a translational perspective; however, new findings from the past decade have radically affected the dominant accounts of this illness. It is now possible to derive a consistent account of one contributing cause of schizophrenia across multiple levels of analysis, from genes to receptors, functional neuroanatomy, cognition, and symptoms. To this end, we summarize the data attributing the disorganization symptoms of schizophrenia to a failure of executive, prefrontal cortical processes. We describe the hypothesis that this failure reflects an impairment in N-methyl-D-aspartate (NMDA) glutamatergic neurotransmission, that is likely to involve both the dysregulated function of NMDA synapses, as well as the physical loss of NMDA synapses, particularly in prefrontal cortex. Dysregulation in NMDA synaptic function can be in turn attributed to polymorphisms in a variety of genes (regulator of G-protein signaling 4, dystrobrevin binding protein 1, neuregulin-1, d-amino acid oxidase activator, and others) that have been linked to schizophrenia and are likely to impact NMDA-mediated synaptic neuroplasticity. Although the science of schizophrenia is not yet at a point where any domain or set of findings provides strong constraints across other levels of analysis, the further development of evidence for this chain of causation can provide increasingly strong tests of the NMDA synapse deficit theory.This work was supported by Grant MH069675 from the National Institute of Health. The authors thank Scott Sponheim and Irving Gottesman for their perspectives and insights on various aspects of the manuscript.

Advances in molecular biology, neuroimaging, genetic epidemiology, and developmental psychopathology have provided a unique opportunity to explore the interplay of genes, brain, and behavior within a translational research framework. Herein, we begin by outlining an experimental strategy by which genetic effects on brain function can be explored using neuroimaging, namely, imaging genetics. We next describe some major findings in imaging genetics to highlight the effectiveness of this strategy for delineating biological pathways and mechanisms by which individual differences in brain function emerge and potentially bias behavior and risk for psychiatric illness. We then discuss the importance of applying imaging genetics to the study of psychopathology within a developmental framework. By beginning to move toward a systems-level approach to understanding pathways to behavioral outcomes as they are expressed across development, it is anticipated that we will move closer to understanding the complexities of the specific mechanisms involved in the etiology of psychiatric disease. Despite the numerous challenges that lie ahead, we believe that developmental imaging genetics has potential to yield highly informative results that will ultimately translate into public health benefits. We attempt to set out guidelines and provide exemplars that may help in designing fruitful translational research applications that incorporate a developmental imaging genetics strategy.This research was supported in part by funding from the United Kingdom National Programme on Forensic Mental Health Research and Development (to E.V.), the Medical Research Council Grant G0401170 (to E.V.), the National Institute of Mental Health Grants K01-MH001957 (to D.E.W.) and K01-MH072837 (to A.R.H.), as well as an NARSAD Young Investigator Award (to A.R.H.).

Research has shown that both prenatal alcohol and tobacco exposure are associated with increased risk of significant adverse medical, developmental, and behavioral outcomes including substance abuse. Research on the outcomes of prenatal exposure to illicit drugs (PNDE) has also found increased physical and behavioral problems for gestationally drug-exposed children. However, a clear picture has not emerged on whether the consequences of PNDE are independent from those associated with having a substance abusing parent and whether PNDE increases vulnerability to drug abuse. Because of its typical co-occurrence with factors inherent in having a drug-abusing parent, PNDE is at least a marker of significant increased risk for a range of negative outcomes including greater vulnerability to substance abuse. Although a review of the relevant research literatures indicates that the direct consequences of PNDE appear to be generally both subtle and nonglobal, PNDE does appear to have negative developmental and behavioral outcomes, and there is evidence that it is a modest direct contributor to increased substance abuse vulnerability.The viewpoints expressed in this article do not necessarily represent the National Institutes of Health or the Department of Health and Human Services. The authors thank Vincent Smeriglio for the information and suggestions he provided. The views expressed in this article do not necessarily represent his views.

The role of biobehavioral sciences is critically evaluated within the model for translational research proposed in the NIH Roadmap. Concern is expressed regarding the lack of specification and representation of intervening disciplines along the translational chain from assessment to treatment to outcome. The implications of this model on the future of developmental psychopathology are discussed. A new model is proposed that emphasizes the role of biobehavioral sciences in translational research focusing on psychiatric disorders.The preparation of this manuscript was supported in part by a grant from the National Institutes of Health (MH 067446).