HPA axis function in depression and dementia: A review

O’Brien, John; Ames, David; Schweitzer, Isaac

doi:10.1002/gps.930081103

Cited by 29 publications

(7 citation statements)

References 101 publications

(78 reference statements)

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“…corticosterone) secretion by binding to inhibitory glucocorticoid receptors throughout the HPA axis. Disorders that include exaggerated stress responsiveness as a symptom, such as anxiety and depression disorders are typically associated with a diminished suppressiblility of the HPA axis, a condition termed HPA non-suppression (Halbreich et al, 1989; O’Brien et al, 1993). Due to the relationship between stress response and HPA non-suppression, DEX administration is often used to determine if a dysfunction of negative feedback within the HPA axis is responsible for exaggerations of the stress response.…”

Section: Discussionmentioning

confidence: 99%

“…The relationship between glucocorticoids and stress response is also reflected in the observation that psychological disorders such as generalized anxiety and depression are commonly associated with dysfunctions of the HPA axis (O’Brien et al, 1993). These diseases involve inappropriate, often exaggerated responses of this system to environmental stressors (Young et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…These diseases involve inappropriate, often exaggerated responses of this system to environmental stressors (Young et al, 2004). Symptoms of these disorders, including an exaggerated stress responses, are often normalized following successful clinical treatment, which includes exercise therapy (O’Brien et al, 1993; Salmon, 2001). The HPA axis is thought to be one of the systems through which these benefits of physical exercise are mediated (Biddle et al, 2000; Fox, 1999; Salmon, 2001)…”

Section: Introductionmentioning

confidence: 99%

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Selection for intrinsic endurance modifies endocrine stress responsiveness

et al. 2010

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Physical exercise dampens an individual's stress response and decreases symptoms of anxiety and depression disorders. While the extrinsic relationship of exercise and psychological state are established, their intrinsic relationship is unresolved. We investigated the potential intrinsic relationship of exercise with stress responsiveness using NIH rats bidirectionally selected for intrinsic endurance capacity. Selection resulted in two populations, one with high intrinsic endurance (high capacity runners; HCR) and one with low intrinsic endurance (low capacity runners; LCR). Animals from these populations were subjected to the elevated plus maze (EPM) and novel environment to assess levels of anxiety-like behavior, and to restraint stress to determine stress responsiveness. Pre-test plasma corticosterone levels and the response of plasma corticosterone to exposure to the EPM and restraint were analyzed using ELISA. A dexamethasone suppression test was performed to assess negative feedback tone of corticosterone release. Pre-test plasma corticosterone levels were similar between LCR and HCR, and these populations had similar behavioral and corticosterone responses to the EPM. Following restraint, HCR animals exhibited more anxiotypic behavior than LCR animals on the EPM, and exhibited an increase in plasma corticosterone following EPM and restraint that was not observed in LCR animals. HCR animals also exhibited more anxiotypic behavior in the novel environment compared to LCR animals. Plasma corticosterone levels were equally reduced in both populations following dexamethasone administration. Overall, our data suggest a positive genetic relationship between exercise endurance and stress responsiveness, which is at odds with the established extrinsic relationship of these traits.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Selection for intrinsic endurance modifies endocrine stress responsiveness

et al. 2010

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“…Similarly, there are six such studies for stroke disease and five have found depression to increase subsequent stroke (Thomas et al, 2003a). Such findings suggest there are close pathophysiological links between depression and vascular disease, which may involve the frequently reported abnormalities in the hypothalamic pituitary adrenal (HPA) axis (O'Brien et al, 1993) and the immune-inflammatory response in both depression (Kronfol, 2002) and vascular disease (Ridker et al, 2002).…”

Section: Depression and Vascular Diseasementioning

confidence: 95%

Criteria are needed for research in vascular depression

Thomas¹

2004

Int. Psychogeriatr.

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There has been longstanding interest in the relationship of depression to vascular disease and this has received renewed interest since the publication of the “vascular depression” hypothesis by Alexopoulos and colleagues (Alexopoulos et al., 1997). They proposed that cerebrovascular disease (CVD) predisposed, precipitated or perpetuated late-life depression by its impact on frontal-subcortical circuits (FSC). However, whilst several lines of research strongly support this proposal, we still have no useful working criteria for vascular depression, assuming such a nosological entity exists.

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“…Both the dementia of AD and depression are associated with functional abnormalities of the HPA axis (O'Brien et al 1993). There are higher CSF cortisol concentrations in AD patients than in controls (Peskind et al 2001).…”

Section: The Effect Of Psychological Stress At the Physiological Levementioning

confidence: 98%

The role of stress and anxiety in the onset of familial Creutzfeldt-Jakob Disease (CJD): Review

Gigi

2009

Stress

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Creutzfeldt-Jakob Disease (CJD) is considered to be a sudden and fatal degenerative brain disorder that leads to death within a few months. In the last decade, we have studied the course of familial CJD (fCJD) among Jews of Libyan descent, one of the largest clusters of fCJD in the world. Recently, we published results that included the identification of abnormal anxiety levels in healthy CJD E200K mutation carriers that were significantly different from those of healthy non-carriers from the same families. All participants were first-degree relatives of patients known to have been carriers of the E200K mutation and had died from CJD, and none of the participants was aware of his/her genetic make-up. In the current review, it is suggested that an abnormality in anxiety levels among the healthy fCJD mutation carriers may reflect the clinical presentation of the disease onset especially during and after any stressful experience. This hypothesis is supported by a summary of relevant literature, dealing with psychological, physiological, and cellular aspects.

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HPA axis function in depression and dementia: A review

Cited by 29 publications

References 101 publications

Selection for intrinsic endurance modifies endocrine stress responsiveness

Selection for intrinsic endurance modifies endocrine stress responsiveness

Criteria are needed for research in vascular depression

The role of stress and anxiety in the onset of familial Creutzfeldt-Jakob Disease (CJD): Review

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