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      The impact of developmental timing for stress and recovery

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          Abstract

          Stress can have lasting effects on the brain and behavior. Delineating the impact of stress on the developing brain is fundamental for understanding mechanisms through which stress induces persistent effects on behavior that can lead to psychopathology. The growing field of translational developmental neuroscience has revealed a significant role of the timing of stress on risk, resilience, and neuroplasticity. Studies of stress across species have provided essential insight into the mechanisms by which the brain changes and the timing of those changes on outcome. In this article, we review the neurobiological effects of stress and propose a model by which sensitive periods of neural development interact with stressful life events to affect plasticity and the effects of stress on functional outcomes. We then highlight how early-life stress can alter the course of brain development. Finally, we examine mechanisms of buffering against early-life stress that may promote resilience and positive outcomes. The findings are discussed in the context of implications for early identification of risk and resilience factors and development of novel interventions that target the biological state of the developing brain to ultimately ameliorate the adverse consequences of stress during childhood and adolescence.

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          Most cited references 93

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          Prior juvenile diagnoses in adults with mental disorder: developmental follow-back of a prospective-longitudinal cohort.

          If most adults with mental disorders are found to have a juvenile psychiatric history, this would shift etiologic research and prevention policy to focus more on childhood mental disorders. Our prospective longitudinal study followed up a representative birth cohort (N = 1037). We made psychiatric diagnoses according to DSM criteria at 11, 13, 15, 18, 21, and 26 years of age. Adult disorders were defined in the following 3 ways: (1) cases diagnosed using a standardized diagnostic interview, (2) the subset using treatment, and (3) the subset receiving intensive mental health services. Follow-back analyses ascertained the proportion of adult cases who had juvenile diagnoses and the types of juvenile diagnoses they had. Among adult cases defined via the Diagnostic Interview Schedule, 73.9% had received a diagnosis before 18 years of age and 50.0% before 15 years of age. Among treatment-using cases, 76.5% received a diagnosis before 18 years of age and 57.5% before 15 years of age. Among cases receiving intensive mental health services, 77.9% received a diagnosis before 18 years of age and 60.3% before 15 years of age. Adult disorders were generally preceded by their juvenile counterparts (eg, adult anxiety was preceded by juvenile anxiety), but also by different disorders. Specifically, adult anxiety and schizophreniform disorders were preceded by a broad array of juvenile disorders. For all adult disorders, 25% to 60% of cases had a history of conduct and/or oppositional defiant disorder. Most adult disorders should be reframed as extensions of juvenile disorders. In particular, juvenile conduct disorder is a priority prevention target for reducing psychiatric disorder in the adult population.
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            Stress and hippocampal plasticity.

             B McEwen (1998)
            The hippocampus is a target of stress hormones, and it is an especially plastic and vulnerable region of the brain. It also responds to gonadal, thyroid, and adrenal hormones, which modulate changes in synapse formation and dendritic structure and regulate dentate gyrus volume during development and in adult life. Two forms of structural plasticity are affected by stress: Repeated stress causes atrophy of dendrites in the CA3 region, and both acute and chronic stress suppresses neurogenesis of dentate gyrus granule neurons. Besides glucocorticoids, excitatory amino acids and N-methyl-D-aspartate (NMDA) receptors are involved in these two forms of plasticity as well as in neuronal death that is caused in pyramidal neurons by seizures and by ischemia. The two forms of hippocampal structural plasticity are relevant to the human hippocampus, which undergoes a selective atrophy in a number of disorders, accompanied by deficits in declarative episodic, spatial, and contextual memory performance. It is important, from a therapeutic standpoint, to distinguish between a permanent loss of cells and a reversible atrophy.
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              In vivo evidence for post-adolescent brain maturation in frontal and striatal regions.

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                Author and article information

                Contributors
                Journal
                Neurobiol Stress
                Neurobiol Stress
                Neurobiology of Stress
                Elsevier
                2352-2895
                19 February 2015
                January 2015
                19 February 2015
                : 1
                : 184-194
                Affiliations
                Sackler Institute for Developmental Psychobiology, Weill Cornell Medical College, 1300 York Ave, New York, NY 10065, USA
                Author notes
                []Corresponding author. dyg9003@ 123456nyp.org
                Article
                S2352-2895(15)00023-5
                10.1016/j.ynstr.2015.02.001
                4363736
                25798454
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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