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Journal ArticleDOI

Stress and the brain: from adaptation to disease

TLDR
In response to stress, the brain activates several neuropeptide-secreting systems, which eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators as mentioned in this paper.
Abstract
In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.

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Is dysregulation of the HPA-axis a core pathophysiology mediating co-morbid depression in neurodegenerative diseases?

TL;DR: The current state of knowledge regarding HPA-axis pathology in Alzheimer’s, PD and HD is summarized, differentiating between prodromal and later stages of disease progression when evidence is available.
Journal ArticleDOI

Corticosteroid receptors and neuroplasticity.

TL;DR: The picture that emerges is that the balance (or imbalance) between MR/GR activation influences not only cell birth and death, but also other forms of neuroplasticity, and researchers should be able to better define new targets for therapeutic intervention in stress-related disorders.
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The Corticotropin-Releasing Factor Family: Physiology of the Stress Response.

TL;DR: This review focuses on the physiology of CRF-related peptides and their cognate receptors and describes the major molecular features covering aspects of gene expression and regulation, structural properties, and molecular interactions, as well as mechanisms of signal transduction and their surveillance.
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Cellular and molecular basis for stress-induced depression

TL;DR: It is shown that chronic restraint stress induces the selective loss of p11, a multifunctional protein binding to 5-HT receptors, in layer II/III neurons of the prelimbic cortex (PrL), as well as depression-like behaviors, both of which are reversed by selective serotonin reuptake inhibitors (SSRIs) and the tricyclic class of antidepressant agents.
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The Social Determinants of Mental Health: Implications for Research and Health Promotion

TL;DR: It is argued that combining evidence and ideas from a number of disciplines, including public health research and psychiatry, presents an opportunity to understand the relationship better with social determinants of health better, and so inform complementary strategies in treatment, prevention and health promotion.
References
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Journal ArticleDOI

Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene

TL;DR: Evidence of a gene-by-environment interaction is provided, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
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How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
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Epigenetic programming by maternal behavior.

TL;DR: It is shown that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible, suggesting a causal relation among epigenomicState, GR expression and the maternal effect on stress responses in the offspring.
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Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants

TL;DR: It is shown that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants, suggesting that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neuroGenesis in the hippocampus.
Journal ArticleDOI

A Syndrome produced by Diverse Nocuous Agents

Hans Selye
- 01 Jul 1936 - 
TL;DR: If the organism is severely damaged by acute non-specific nocuous agents such as exposure to cold, surgical injury, production of spinal shock, excessive muscular exercise, or intoxications with sublethal doses of diverse drugs, a typical syndrome appears, the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed.
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