HPA axis and cognitive dysfunction in mood disorders

Author(s):  
Rebecca Strawbridge ◽  
Allan H. Young
Psychiatry ◽  
2009 ◽  
Vol 8 (3) ◽  
pp. 97-101 ◽  
Author(s):  
Stuart Watson ◽  
Paul Mackin
Keyword(s):  

2019 ◽  
Vol 62 (5) ◽  
pp. 1416-1426 ◽  
Author(s):  
Jacqueline Laures-Gore ◽  
Dalia Cahana-Amitay ◽  
Tony W. Buchanan

Purpose The current study investigated diurnal cortisol dynamics in adults with and without aphasia, along with subjective reports of stress and measures of language production. Dysregulation of cortisol, a common biomarker of stress, is associated with cognitive dysfunction in different clinical populations. However, little is known about the consequences of stress-induced cortisol disturbances for stroke survivors, including those with aphasia. Method Nineteen participants with aphasia and 14 age-matched neurotypical adults were tested. Saliva samples were collected from participants to assess the cortisol awakening response, a marker of the integrity of the hypothalamic-pituitary-adrenal (HPA) axis. Participants also completed 2 subjective stress questionnaires. Language was evaluated using 3 short, picture description narratives, analyzed for discourse (dys)fluency and productivity markers. Results In contrast to neurotypical participants, adults with aphasia did not show the predictable cortisol awakening response. Participants with aphasia also showed an unusual heightened level of cortisol upon awakening. Additionally, neurotypical participants demonstrated an association between intact language performance and the cortisol awakening response, whereas the participants with aphasia did not, although they did perceive the language tasks as stressful. Conclusion This study indicates that the functionality of the HPA axis, as indexed by cortisol, contributes to optimal language performance in healthy adults. The absence of an awakening response among participants with aphasia suggests that stroke leads to dysregulation of the HPA axis, although the degree to which this impairment affects language deficits in this population requires further investigation.


2016 ◽  
Vol 27 (4) ◽  
pp. 397-409 ◽  
Author(s):  
Ivan Zaletel ◽  
Dragana Filipović ◽  
Nela Puškaš

AbstractThe hippocampus is a brain structure involved in the regulation of hypothalamic-pituitary-adrenal (HPA) axis and stress response. It plays an important role in the formation of declarative, spatial and contextual memory, as well as in the processing of emotional information. As a part of the limbic system, it is a very susceptible structure towards the effects of various stressors. The molecular mechanisms of structural and functional alternations that occur in the hippocampus under chronic stress imply an increased level of circulating glucocorticoids (GCs), which is an HPA axis response to stress. Certain data show that changes induced by chronic stress may be independent from the GCs levels, opening the possibility of existence of other poorly explored mechanisms and pathways through which stressors act. The hippocampal GABAergic parvalbumin-positive (PV+) interneurons represent an especially vulnerable population of neurons in chronic stress, which may be of key importance in the development of mood disorders. However, cellular and molecular hippocampal changes that arise as a consequence of chronic stress still represent a large and unexplored area. This review discusses the current knowledge about the PV+ interneurons of the hippocampus and the influence of chronic stress on this intriguing population of neurons.


CNS Spectrums ◽  
2015 ◽  
Vol 21 (5) ◽  
pp. 362-366 ◽  
Author(s):  
Roger S. McIntyre ◽  
Hanna O. Woldeyohannes ◽  
Joanna K. Soczynska ◽  
Nadia A. Maruschak ◽  
Ida K. Wium-Andersen ◽  
...  

BackgroundCognitive dysfunction is common in major depressive disorder (MDD) and a critical determinant of health outcome. Anhedonia is a criterion item toward the diagnosis of a major depressive episode (MDE) and a well-characterized domain in MDD. We sought to determine the extent to which variability in self-reported cognitive function correlates with anhedonia.MethodA post hoc analysis was conducted using data from (N=369) participants with a Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR)-defined diagnosis of MDD who were enrolled in the International Mood Disorders Collaborative Project (IMDCP) between January 2008 and July 2013. The IMDCP is a collaborative research platform at the Mood Disorders Psychopharmacology Unit, University of Toronto, Toronto, Canada, and the Cleveland Clinic, Cleveland, Ohio. Measures of cognitive function, anhedonia, and depression severity were analyzed using linear regression equations.ResultsA total of 369 adults with DSM-IV-TR–defined MDD were included in this analysis. Self-rated cognitive impairment [ie, as measured by the Adult ADHD Self-Report Scale (ASRS)] was significantly correlated with a proxy measure of anhedonia (r=0.131, p=0.012). Moreover, total depression symptom severity, as measured by the total Montgomery–Åsberg Depression Rating Scale (MADRS) score, was also significantly correlated with self-rated measures of cognitive dysfunction (r=0.147, p=0.005). The association between anhedonia and self-rated cognitive dysfunction remained significant after adjusting for illness severity (r=0.162, p=0.007).ConclusionsThese preliminary results provide empirical data for the testable hypothesis that anhedonia and self-reported cognitive function in MDD are correlated yet dissociable domains. The foregoing observation supports the hypothesis of overlapping yet discrete neurobiological substrates for these domains.


2000 ◽  
Vol 177 (5) ◽  
pp. 390-395 ◽  
Author(s):  
Richard McQuade ◽  
Allan H. Young

BackgroundThe hypercortisolaemia and dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis associated with mood disorders have been attributed to a breakdown in the glucocorticoid-receptor-mediated negative feedback mechanism regulating HPA activity. Reinstating normal feedback may be therapeutic in mood disorders.AimsTo review the evidence for the involvement of the glucocorticoid receptor in the pathogenesis and treatment of mood disorders.MethodMedline and hand searches were carried out, selecting literature relevant to psychiatrists and psychopharmacologists.ResultsA dysfunction in glucocorticoid receptors is integral to the HPA abnormalities of mood disorders. Antidepressant and mood-stabilising drugs can up-regulate glucocorticoid receptors, restoring glucocorticoid function. Preliminary clinical studies targeting the glucocorticoid receptor are encouraging.ConclusionsDrugs designed specifically to up-regulate glucocorticoid receptors may be integral to future strategies in treating mood disorders.


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