The HPA axis in major depression: classical theories and new developments.

By C. Pariante, Stafford Lightman. Trends in Neurosciences, 2008

1,997 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/d24168260d7c0c8e5d6a94f131010d60d0dd4b4b

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Citations in the corpus

Stress and depression: old questions, new approaches (2015, background): “It has long been observed that depressed adult patients show several indicators of dysregulation of the HPA axis — some state-dependent but others trait-like — including altered basal levels of cortisol, disrupted homeostatic mechanisms of the HPA axis evidenced in abnormal responses to an exogenous”
Exercise and mental health. (2017, background): “HPA dysfunction seen in anxiety or depression can be characterized by heightened or reduced cortisol production, hypersecretion of corticotrophin releasing hormone [95] and compromised sensitivity to glucocorticoids [96].”
Reinforcement Learning in non-stationary environments: An intrinsically motivated stress based memory retrieval performance (SBMRP) model (2014, background): “Nature had designed biological stress system within the organism (e.g. Hypothalamic-Pituitary-Adrenal (HPA) Axis [7]) to effectively solve uncertainty in non-stationary en- 978-1-4799-2072-3/14/$31.00 ©2014 IEEE 1728 vironment problem.”
Brain-gut interactions in inflammatory bowel disease. (2013, background): “Patients with major depression have increased concentrations of the HPA axis hormones, ACTH and cortisol, as well as increases in the cerebrospinal fluid measures of CRF (111,112).”
Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “The role of corticotropin releasing hormone (CRH) and the HPA-axis in major depression and in cytokine-induced depression has been investigated extensively (Arborelius et al., 1999, Capuron et al., 2003b, Pariante and Lightman, 2008, Raison et al., 2010a) .”
Identifying the women at risk of antenatal anxiety and depression: A systematic review (2016, background): “As both systems are over-stimulated during normal pregnancy, this may make mothers more susceptible to depression in the context of previous exposure to childhood maltreatment (Danese et al., 2007; Heim et al., 2008; Pariante et al., 2014; Pariante and Lightman, 2008; RobertsonBlackmore et al., 2013”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “…with major depression have been found to show increased concentrations of the HPA axis hormones, ACTH and cortisol, as well as increases in the CSF measures of the HPA axis-regulatory neuropeptide, corticotrophin-releasing hormone (CRH) (Pariante and Miller, 2001; Pariante and Lightman, 2008).”
Depression and Hypothalamic-Pituitary-Adrenal Activation: A Quantitative Summary of Four Decades of Research (2011, background): “Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis during depression has been called one of the most reliable findings in all of biological psychiatry (1).”
Stress-related and basic determinants of hair cortisol in humans: A meta-analysis. (2016, critical): “Beyond anxiety disorders, our metaanalytic findings failed to reveal a significant effect of mood disorders on HCC, which is surprising and does not correspond to previous evidence suggesting hyperactivity of the HPA axis, particularly in major depression (Pariante and Lightman, 2008).”
Developing constructs for psychopathology research: research domain criteria. (2010, positive): “…in response to stress have been well characterized (Charney, Grillon, & Bremner, 1998), and the HPA axis has been linked to a range of psychopathologies, including posttraumatic stress disorder, major depressive disorder, bipolar disorder, and schizophrenia (see e.g., Pariante & Lightman, 2008).”
The Bidirectional Relationship of Depression and Inflammation: Double Trouble (2020, background): “Some subsets of T cells even undergo apoptosis upon receiving a glucocorticoid signal (Pariante and Lightman, 2008).”
Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders (2018, background): “The pathophysiology of depression is complex and includes social environmental stress factors; genetic and biological processes, such as the overdrive of the HPA axis, inflammation (31), and disturbances in monamine neurotransmission as described above (91).”
A Unified Model of Depression (2016, positive): “Dysregulation of the hypothalamicpituitary-adrenal (HPA) axis is one of the most consistent biological correlates of severe depression (see Pariante & Lightman, 2008; Stetler & Miller, 2011) and may be linked to serotonergic or noradrenergic dysfunction (given the important role of these…”
Interleukin (IL)-6, tumour necrosis factor alpha (TNF-α) and soluble interleukin-2 receptors (sIL-2R) are elevated in patients with major depressive disorder: a meta-analysis and meta-regression. (2012, background): “…suggests thatdysregulation of thehypothalamicpituitary-adrenal (HPA) axis plays an indispensible role in the pathogenesis of endogenous depression (Pariante and Lightman, 2008), the impact of inflammationon the occurrence of depression was firstly recognized at the early 1990s (Maes et al.,…”