Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment.

By C. Pariante, Andrew H. Miller. Biological Psychiatry, 2001

1,162 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/7e1ab854f53ee694313f78e09f2e3c83743aa4a1

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Citations in the corpus

Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “…by increased cortisol concentrations following dexamethasone (DEX) administration in the DEX suppression test (DST) and the DEX-CRH test and decreased glucocorticoid-mediated inhibition of in vitro immune responses are well described in patients with major depression (Pariante and Miller, 2001).”
Neurobehavioral Effects of Interferon-α in Cancer Patients: Phenomenology and Paroxetine Responsiveness of Symptom Dimensions (2002, background): “1995 ), and antidepressants have been shown to facilitate inhibitory feedback on cytokine secretion by endogenous glucocorticoids (”
The stress system in the human brain in depression and neurodegeneration. (2005, background): “In addition, antidepressant drugs attenuate the synthesis of CRH by stimulation and/or upregulation of corticosteroid receptor expression (Reus et al., 1997; Fischer et al., 1990; Brady et al., 1991, 1992; Delbende et al., 1991; Reul et al., 1993; Nemeroff, 1996; Yau et al., 1995, 2002; Pariante and”
Adverse childhood experiences, allostasis, allostatic load, and age-related disease. (2012, background): “In contrast, elevation in cortisol levels and impaired compensatory mechanisms, such as pituitary hyper-responsiveness to CRH and/or reduced glucocorticoid receptor sensitivity, may contribute to increasing the risk of depression in maltreated individuals [24,25,133].”
Work stress precipitates depression and anxiety in young, working women and men (2007, background): “Persistently elevated stress hormone levels may have direct neurotoxic effects on the brain, particularly in the hippocampus (Sapolsky et al. 1986), and can induce down-regulation of the glucocorticoid receptor, which impairs affect regulation (Avitsur et al. 2001; Pariante & Miller, 2001).”
Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, positive): “Decreased feedback regulation of HPA axis function by glucocorticoids is believed to be mediated, in part, by alterations in the glucocorticoid receptor (GR) (50).”
The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression (2009, background): “Long-term treatment with some antidepressants has direct effects on the GR leading to enhanced GR function and increased GR expression and normalization of the hypothalamic-pituitary-adrenal (HPA)-axis (Pariante and Miller 2001; Fitzgerald et al. 2006).”
Brain-gut interactions in inflammatory bowel disease. (2013, background): “Perhaps acute stress may inhibit the HPA which would increase glucocorticoid resistance and reduce the endogenous immune response which can lead to a flare (127).”
The role of FKBP5, a co-chaperone of the glucocorticoid receptor in the pathogenesis and therapy of affective and anxiety disorders. (2009, background): “In fact, an impaired signaling via corticosteroid-activated GR, leading to an impaired negative feedback regulation and thus to partial glucocorticoid resistance appears to be one of the most robust biological abnormalities observed in mood disorders (Pariante and Miller, 2001).”
Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “…monoaminergic systems and the hypothalamic-pituitary adrenal (HPA)-axis, changes in growth factors and neuropeptides, alterations in glutamate neurotransmission, and decreased neurogenesis (Heim et al., 1997, Charney, 1998, Berman et al., 2000, Pariante and Miller, 2001, Duman and Monteggia, 2006).”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “Special interest has been recently paid to natural compounds such as curcumin (a derivative of the curry spice, turmeric), which has been shown to decrease NF-kB activation in the PBMCs of patients with pancreatic cancer (Dhillon et al, 2008); a tocopherol (a form of Vitamin E), which has been shown”
Prenatal developmental origins of behavior and mental health: The influence of maternal stress in pregnancy. (2017, background): “proinflammatory state affects glucocorticoid gene expression and function (Pariante and Miller, 2001), stimulates activity of the HPA axis (Tsigos and Chrousos, 2002), and attenuates the noradrenaline and serotonin content in the brain (Leonard, 2001) and may, thus, have an pathophysiological role i”
The Bargaining Model of Depression (2002, background): “Pariante and Miller (2001) summarize these findings in their review of the role of glucocorticoid receptors and stress hormones in major depression: Hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis in patients with major depression is one of the most consistent findings in biological…”
Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. (2007, background): “Indeed, depressed patients exhibit increased concentrations of CRH in CSF, increased CRH mRNA and protein in the paraventricular nucleus of the hypothalamus (postmortem samples), and a blunted ACTH response to CRH challenge (likely reflecting downregulation of pituitary CRH receptors) (Nemeroff, 199”
Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment (2004, background): “, and an impaired negative feedback of this system due to glucocorticoid receptor insensitivit”
When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. (2011, methodology): “Indeed, altered glucocorticoid receptor signaling has been proposed as a major factor in the pathogenesis of the disorder (8, 27).”