Effects of major depression on the cognitive function of younger and older subjects

Tarbuck, Andrew; Paykel, Eugene S.

doi:10.1017/s0033291700036187

Cited by 106 publications

(75 citation statements)

References 52 publications

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“…Relationships between depression and a decrease in performance (e.g. reduction in speed of response, impaired decision-making) on cognitive tests have also been reported by other investigators [198,199,200,201]. …”

Section: Resultssupporting

confidence: 69%

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

Guidi

Fava

Bech

et al. 2010

Psychother Psychosom

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Background: A comprehensive assessment of the wide spectrum of depressive symptomatology, particularly in its subclinical forms, is lacking in standard rating scales. There is also an emerging need for instruments that can detect small differences in therapeutic studies and have good sensitivity. The purpose of this paper is to review the clinimetric characteristics of Paykel’s Clinical Interview for Depression (CID) and to examine the results of the studies in which the interview has been used. Methods: Published reports which involved the use of the CID were identified by searching the following electronic databases: Medline, PsychINFO, EMBASE, and Web of Science. A manual search of the literature was also performed. Results: The initial strategies yielded 169 published reports for potential inclusion in the review: 98 are discussed here. The CID has been used extensively in a variety of studies, including descriptive studies, classification by means of factor analysis and cluster analysis, and predictor variables of response to treatment or relapse. The CID has also been used as an outcome measure in several controlled clinical trials and follow-up studies of pharmacotherapy and psychotherapy of affective disorders. It has been shown to be valid and reliable, to discriminate depressives from controls, or different subgroups of depressed patients, and to reflect changes during the course of treatment, particularly when individual symptoms are considered. Conclusions: Evidence from these studies highlights the utility of the CID in clinical research and practice. Its clinimetric characteristics, particularly the broad evaluation of affective symptomatology and the sensitivity to change, make it an instrument of choice in therapeutic trials.

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Section: Resultssupporting

confidence: 69%

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

Guidi

Fava

Bech

et al. 2010

Psychother Psychosom

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“…As this measure involves a number of cognitive operations including processing speed, it is unclear if one can conclude from Purcell et al's (1997) study that younger depressed patients do not show cognitive slowing. Tarbuck & Paykel (1995) reported that older depressed patients (mean age 69 years) were slower than younger depressed patients (mean age 41 years) on a choice reaction time (RT) measure. However, RT improved to a similar extent in both groups following recovery, indicating that both age and depression may affect information processing speed, but these variables do not interact to produce cognitive slowing in older depressed but not younger depressed.…”

Section: Introductionmentioning

confidence: 99%

Evidence of an early information processing speed deficit in unipolar major depression

2002

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“…These results strongly suggest that down-regulation of 5-HT 1A receptors, caused by either genetic or stress-related processes, may significantly contribute to the development of mood disorders in humans. Specifically, a hippocampal deficit in 5-HT 1A receptors could contribute to the cognitive abnormalities often seen in people with mood disorders (16)(17)(18)(19).…”

mentioning

confidence: 99%

Impaired hippocampal-dependent learning and functional abnormalities in the hippocampus in mice lacking serotonin _1A receptors

Sarnyai

Sibille²,

Pavlides³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

350

191

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The hippocampus is a major limbic target of the brainstem serotonergic neurons that modulate fear, anxiety, and learning through postsynaptic serotonin 1A receptors (5-HT1A receptors). Because chronic stress selectively down-regulates the 5-HT 1A receptors in the hippocampus, we hypothesized that mice lacking these receptors may exhibit abnormalities reminiscent of symptoms of stress-related psychiatric disorders. In particular, a hippocampal deficit in the 5-HT1A receptor could contribute to the cognitive abnormalities often seen in these disorders. To test whether a deficit in 5-HT 1A receptors impairs hippocampus-related functions, we studied hippocampal-dependent learning and memory, synaptic plasticity in the hippocampus, and limbic neuronal excitability in 5-HT1A-knockout (KO) mice. 5-HT1A-KO animals showed a deficit in hippocampal-dependent learning and memory tests, such as the hidden platform (spatial) version of the Morris water maze and the delayed version of the Y maze. The performance of KO mice was not impaired in nonhippocampal memory tasks such as the visible platform (nonspatial) version of the Morris water maze, the immediate version of the Y maze, and the spontaneous-alternation test of working memory. Furthermore, paired-pulse facilitation in the dentate gyrus of the hippocampus was impaired in 5-HT 1A-KO mice. Finally, 5-HT1A-KO mice, as compared with wild-type animals, displayed higher limbic excitability manifested as lower seizure threshold and higher lethality in response to kainic acid administration. These results demonstrate that 5-HT1A receptors are required for maintaining normal hippocampal functions and implicate a role for the 5-HT 1A receptor in hippocampal-related symptoms, such as cognitive disturbances, in stress-related disorders.A deficiency of postsynaptic serotonin 1A (5-HT 1A ) has been implicated in mood disorders, such as depression and posttraumatic stress disorder and panic disorder (1-4). In particular, a receptor deficiency has been reproducibly found in the limbic systems of people with mood disorders (3, 5). Decreased 5-HT1A receptor binding was found in the brains of depressed suicide victims (6), and recent brain-imaging studies performed with positron-emission tomography have revealed decreased 5-HT 1A -receptor densities in the medial temporal lobe and other limbic brain regions of patients with major depression (7,8). Also, chronic stress, which is well known to be a major factor in the development of mood disorders, has been shown to lead to a specific down-regulation of 5-HT 1A receptors in the hippocampus of experimental animals (9-15). These results strongly suggest that down-regulation of 5-HT 1A receptors, caused by either genetic or stress-related processes, may significantly contribute to the development of mood disorders in humans. Specifically, a hippocampal deficit in 5-HT 1A receptors could contribute to the cognitive abnormalities often seen in people with mood disorders (16-19).The serotonergic system seems to play a role in behaviors that invo...

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Effects of major depression on the cognitive function of younger and older subjects

Cited by 106 publications

References 52 publications

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

Evidence of an early information processing speed deficit in unipolar major depression

Impaired hippocampal-dependent learning and functional abnormalities in the hippocampus in mice lacking serotonin _1A receptors

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Effects of major depression on the cognitive function of younger and older subjects

Cited by 106 publications

References 52 publications

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

The Clinical Interview for Depression: A Comprehensive Review of Studies and Clinimetric Properties

Evidence of an early information processing speed deficit in unipolar major depression

Impaired hippocampal-dependent learning and functional abnormalities in the hippocampus in mice lacking serotonin 1A receptors

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Product

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Impaired hippocampal-dependent learning and functional abnormalities in the hippocampus in mice lacking serotonin _1A receptors