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13 results

  • Chapter 10 - Mood Disorders and Stress-Related Disorders

  • Edited by Allan Young, Institute of Psychiatry, King's College London, Marsal Sanches, Baylor College of Medicine, Texas, Jair C. Soares, McGovern Medical School, The University of Texas, Mario Juruena, King's College London
  • Book:
    Clinical Textbook of Mood Disorders
    Published online:
    16 May 2024
    Print publication:
    23 May 2024, pp 103-115

  • Summary

    This chapter outlines the current research on the stress response and how chronic stress can lead to the dysfunction of neuroendocrine and immune responses and ultimately contribute to the development of psychiatric disorders. The chapter aims to provide an understanding of the pathways involved in the stress response, in particular the HPA axis and the role of cortisol, exploring the role of HPA hyperactivity as a contributor to major depressive disorder. The chapter reviews the impact of the stress response in bipolar and post-traumatic stress disorder, concluding with a summary of our current understanding of the interplay of mood disorders with early life stress.

  • Chapter 1 - Mood Disorders in the Twenty-First Century

  • Edited by Allan Young, Institute of Psychiatry, King's College London, Marsal Sanches, Baylor College of Medicine, Texas, Jair C. Soares, McGovern Medical School, The University of Texas, Mario Juruena, King's College London
  • Book:
    Clinical Textbook of Mood Disorders
    Published online:
    16 May 2024
    Print publication:
    23 May 2024, pp 1-9

  • Summary

    Mood disorders are among the most prevalent and potentially severe mental disorders. These conditions are associated with important psychological morbidity and functional impact, as well as elevated rates of suicide. While the past several decades have produced valuable contributions to the understanding of the pathophysiology of mood disorders, currently available treatments at times fail to produce full remission and restore patient’s premorbid level of function. Nevertheless, promising new agents and novel therapeutic targets are currently under investigation. The twenty-first century is looking at an individualized approach for the management of mood disorders, with the proper integration of evidence-based, effective biological and psychosocial therapeutic modalities.

Clinical Textbook of Mood Disorders
  • Edited by Allan Young, Marsal Sanches, Jair C. Soares, Mario Juruena
  • Published online:
    16 May 2024
    Print publication:
    23 May 2024
  • Mood disorders affect around 1 in 5 people, but the diagnosis and management of these conditions can be challenging. This practical handbook presents a comprehensive overview of these disorders, as well as detailed guidelines for their treatment. The handbook takes a transdisciplinary approach to mood disorders, focusing not only on the biological aspects but also on psychosocial features of importance for optimal diagnosis and management. Content covers nosological considerations, historical aspects, peculiarities along the lifespan, and the associations between mood disorders and other conditions, with a focus on their implications for the optimal management of patients. Practical and evidence-based information is discussed on the role of guidelines related to treatment in selected population groups, including youth, the elderly, and women. With a practical, reader-friendly approach, this book will be invaluable for mental health professionals involved in the treatment of patients with mood disorders, including trainees from different mental health areas.

  • Assessment of the hypothalamic–pituitary–adrenal axis activity: glucocorticoid receptor and mineralocorticoid receptor function in depression with early life stress – a systematic review

  • Cristiane Von Werne Baes, Sandra M. de Carvalho Tofoli, Camila Maria S. Martins, Mario F. Juruena
  • Journal:
    Acta Neuropsychiatrica / Volume 24 / Issue 1 / February 2012
    Published online by Cambridge University Press:
    24 June 2014, pp. 4-15

  • Objective: The mechanisms involved in the dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, especially in the functioning of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) in depressed patients, are not well elucidated. The objective of this study was to conduct a systematic review of articles that assess the HPA axis activity from GR and MR in depressed patients and healthy controls with or without early life stress.

    Methods: We conducted a systematic review of articles in PubMed, SCOPUS and SciELO published between 2000 and 2011, using the following search terms: child abuse, depression, HPA axis, dexamethasone, prednisolone, fludrocortisone and spironolactone. Thirty-four papers were selected for this review.

    Results: Most studies identified in this review used the dexamethasone/corticotropin-releasing hormone test and dexamethasone suppression test. In these studies, hypercortisolaemia was associated with depression. We identified three studies with the Prednisolone suppression test, only one study with the use of fludrocortisone and one with spironolactone. This review found nine studies that evaluated the HPA axis in individuals with early life stress.

    Conclusions: The majority of the studies assessed in this review show that early life stress leads to permanent changes in the HPA axis and may lead to development of depression in adults. The most consistent findings in the literature show increased activity of the HPA axis in depression associated with hypercortisolaemia and reduced inhibitory feedback. These findings suggest that this dysregulation of the HPA axis is partially attributable to an imbalance between GR and MR. Evidences have consistently showed that GR function is impaired in major depression, but few studies have assessed the activity of MR in depression and early life stress.

  • An integrative science approach: neuroscience in the DSM-V and ICD-11

  • Mario Francisco Juruena
  • Journal:
    Acta Neuropsychiatrica / Volume 23 / Issue 4 / August 2011
    Published online by Cambridge University Press:
    24 June 2014, pp. 143-144
    • Article
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  • Molecular mechanisms of glucocorticoid receptor sensitivity and relevance to affective disorders

  • Mario F Juruena, Anthony J Cleare, Moisés E Bauer, Carmine M Pariante
  • Journal:
    Acta Neuropsychiatrica / Volume 15 / Issue 6 / December 2003
    Published online by Cambridge University Press:
    24 June 2014, pp. 354-367

  • Changes in the hypothalamic–pituitary–adrenocortical (HPA) system are characteristic of depression, and in the majority of these patients these result in HPA axis hyperactivity. This is further supported by the reduced sensitivity to the inhibitory effects of the glucocorticoid, dexamethasone (DEX), on the production of adrenocorticotropic hormone (ACTH) and cortisol, during the DEX suppression test and the DEX-corticotropin-releasing hormone (DEX/CRH) test. Because the effects of glucocorticoids are mediated by intracellular receptors including, most notably, the glucocorticoid receptor (GR), several studies have examined the number and/or function of GRs in depressed patients. These studies have consistently demonstrated that GR function is impaired in major depression, resulting in reduced GR-mediated negative feedback on the HPA axis and increased production and secretion of CRH in various brain regions postulated to be involved in the causality of depression. This article summarizes the literature on GR in depression and on the impact of antidepressants on the GR in clinical and preclinical studies, and supports the concept that impaired GR signaling is a key mechanism in the pathogenesis of depression, in the absence of clear evidence of decreased GR expression. The data also indicate that antidepressants have direct effects on the GR, leading to enhanced GR function and increased GR expression. Hypotheses regarding the mechanism of these receptor changes involve non-steroid compounds that regulate GR function via second messenger pathways, such as cytokines and neurotransmitters. Moreover, we present recent evidence suggesting that membrane steroid transporters such as the multidrug resistance (MDR) p-glycoprotein, which regulate access of glucocorticoids to the brain, could be a fundamental target of antidepressant treatment. Research in this field will lead to new insights into the pathophysiology and treatment of affective disorders.

  • Prednisolone suppression test in depression: prospective study of the role of HPA axis dysfunction in treatment resistance

  • Mario F. Juruena, Carmine M. Pariante, Andrew S. Papadopoulos, Lucia Poon, Stafford Lightman, Anthony J. Cleare
  • Journal:
    The British Journal of Psychiatry / Volume 194 / Issue 4 / April 2009
    Published online by Cambridge University Press:
    02 January 2018, pp. 342-349
    Print publication:
    April 2009
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  • Background

    People with severe depressive illness have raised levels of cortisol and reduced glucocorticoid receptor function.

    Aims

    To obtain a physiological assessment of hypothalamic–pituitary–adrenal (HPA) axis feedback status in an in-patient sample with depression and to relate this to prospectively determined severe treatment resistance.

    Method

    The prednisolone suppression test was administered to 45 in-patients with depression assessed as resistant to two or more antidepressants and to 46 controls, prior to intensive multimodal in-patient treatment.

    Results

    The patient group had higher cortisol levels than controls, although the percentage suppression of cortisol output after prednisolone in comparison with placebo did not differ. Nonresponse to in-patient treatment was predicted by a more dysfunctional HPA axis (higher cortisol levels postprednisolone and lower percentage suppression).

    Conclusions

    In patients with severe depression, HPA axis activity is reset at a higher level, although feedback remains intact. However, prospectively determined severe treatment resistance is associated with an impaired feedback response to combined glucocorticoid and mineralocorticoid receptor activation by prednisolone.