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Jamie Hanson

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Early-life stress is a contributor to mental disorders across the lifespan. Epidemiological studies have demonstrated that early-life stress contributes not just to risk of mental disorders but substantially to the risk of physical disease as well. It is also clear that stress during early development has distinct effects upon the nervous system when compared to trauma and stress experienced in adulthood. Developmental stress has the capacity to program and canalize the nervous system in ways that can profoundly alter how it responds to future insults. These effects can be observed at molecular, neuroanatomical, functional and behavioral levels. These changes, mediated through alterations in neuroendocrine and neuroimmune reactivity, can have complex and lasting consequences for multiple organ systems that range beyond the brain to the gut and to the cardiovascular system. Changes in cognition and behavior resulting from early-life stress also contribute to social pathologies such as delinquency, decreased school performance, and increased incarceration. For these reasons, arriving at a mechanistic understanding of how stress programs the brain in early life is a first order concern with significant implications for public health, public policy and neuroscience. This Research Topic will examine the many ways in which early-life stress programs the brain and consequently the body across the lifespan. Further, we will examine factors, which may prove protective against early life stress. We will include contributions from intersecting disciplines that seek to advance our understanding of how early life stress changes the nervous system from basic science, clinical and community perspectives. Section 1: Introduction & Setup (CHARGE: Basic introduction, but with a vague nod to the “allostatic curve and excitotoxicity” model). Early life stress (ELS) is prevalent and is associated with multiple hazards to development (namely heightened risk for many forms of psychopathology The amygdala has been the focus of a great deal of attention in research aimed at understanding the effects of early life stress. Essential functions of the amygdala A majority of past studies have shown increased amygdala activation to social-emotional stimuli. Neural adaptation to chronic hyperactivity has been termed allostasis and is associated with well-understood changes in medial temporal lobe structures. Projecting cells of the amygdala show increased dendritic volume and complexity in animal models, which has been hypothesized to underlie the increased amygdala volume after a single episode of depression in humans (McEwen, 2005). Differences in dendritic complexity can account for differences in the volume of regions in the amygdala (Cooke et al, 2007), so we expect overall amygdala volume to parallel dendritic changes in the allostatic load model. Since amygdala volume is decreased in chronic depression, McEwen (2005) suggested that chronic overload might eventually lead to amygdala atrophy. An important implication of this model is that excitotoxic damage could eventually lead to cell death in the amygdala at older ages. Consistent with this, the first stereological study found decreased primary cell numbers in amygdalar tissues from adults with autism (Schumann & Amaral, 2006).