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      Immune and Neuroendocrine Mechanisms of Stress Vulnerability and Resilience

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      Neuropsychopharmacology
      Springer Nature

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          Abstract

          Diagnostic criteria for mood disorders including major depressive disorder (MDD) largely ignore biological factors in favor of behavioral symptoms. Compounding this paucity of psychiatric biomarkers is a need for therapeutics to adequately treat the 30-50% of MDD patients who are unresponsive to traditional antidepressant medications. Interestingly, MDD is highly prevalent in patients suffering from chronic inflammatory conditions, and MDD patients exhibit higher levels of circulating pro-inflammatory cytokines. Together, these clinical findings suggest a role for the immune system in vulnerability to stress-related psychiatric illness. A growing body of literature also implicates the immune system in stress resilience and coping. In this review, we discuss the mechanisms by which peripheral and central immune cells act on the brain to affect stress-related neurobiological and neuroendocrine responses. We specifically focus on the roles of pro-inflammatory cytokine signaling, peripheral monocyte infiltration, microglial activation, and hypothalamic-pituitary-adrenal axis hyperactivity in stress vulnerability. We also highlight recent evidence suggesting that adaptive immune responses and treatment with immune modulators (exogenous glucocorticoids, humanized antibodies against cytokines) may decrease depressive symptoms and thus represent an attractive alternative to the current antidepressant treatments.

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          The role of inflammation in depression: from evolutionary imperative to modern treatment target.

          Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.
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            Ordinary magic. Resilience processes in development.

            The study of resilience in development has overturned many negative assumptions and deficit-focused models about children growing up under the threat of disadvantage and adversity. The most surprising conclusion emerging from studies of these children is the ordinariness of resilience. An examination of converging findings from variable-focused and person-focused investigations of these phenomena suggests that resilience is common and that it usually arises from the normative functions of human adaptational systems, with the greatest threats to human development being those that compromise these protective systems. The conclusion that resilience is made of ordinary rather than extraordinary processes offers a more positive outlook on human development and adaptation, as well as direction for policy and practice aimed at enhancing the development of children at risk for problems and psychopathology.
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              Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress.

              Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.
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                Author and article information

                Journal
                Neuropsychopharmacology
                Neuropsychopharmacology
                Springer Nature
                0893-133X
                1740-634X
                June 13 2016
                June 13 2016
                : 42
                : 1
                : 62-80
                Article
                10.1038/npp.2016.90
                5143517
                27291462
                8ed0ecf1-77a0-4d80-a0a1-1691b26e02f7
                © 2016
                History

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