Neuropsychological Deficits in Psychotic Versus Nonpsychotic Major Depression and No Mental Illness

Schatzberg, Alan F.; Posener, Joel A.; DeBattista, Charles; Kalehzan, B. Michelle; Rothschild, Anthony J.; Shear, Paula K.

doi:10.1176/appi.ajp.157.7.1095

Cited by 182 publications

(113 citation statements)

References 23 publications

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“…Patients with major depression also are particularly impaired on verbal learning and episodic memory tasks (Austin et al 1999;Sweeney et al 2000), while implicit memory performances seem spared (Danion et al 1995;Ilsley et al 1995). However, no memory deficit was observed in drug-free major depression (Schatzberg et al 2000;Porter et al 2003). This could suggest that deficits are related to antidepressant medications.…”

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 90%

“…Cognitive deficits appear particularly pronounced in elderly patients and among major depression patients with severe illness, or with melancholic/ psychotic features (Beats et al 1996;Schatzberg et al 2000). However, the relationship between cognitive performances and major depression melancholic subtype disappeared after covarying for Hamilton score (Austin et al 1999) and could thus implicate severity itself rather than subtype.…”

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 99%

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Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

226

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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Section: Cognitive Deficits In Major Depressionmentioning

confidence: 90%

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

226

126

View full text Add to dashboard Cite

show abstract

“…For example, depressed individuals have been observed to display more errors on incongruent stimuli (Lockwood et al, 2002;Schatzberg et al, 2000). Other studies do not find differences in error rates but do find that in general, depressed individuals react slower than never-depressed individuals on the task (Degl 'Innocenti et al, 1998).…”

Section: Introductionmentioning

confidence: 97%

Pupillary assessment and computational modeling of the Stroop task in depression

Siegle

Steinhauer

Thase

2004

International Journal of Psychophysiology

134

124

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Depressed individuals frequently display disruptions in selective attention, but the time course and specificity of these difficulties are not well-understood. To better understand the nature of attentional disruptions in depression, 28 healthy adults and 23 unmedicated depressed adults completed a Stroop color-naming task using a long inter-stimulus interval and pupil dilation was recorded as a measure of cognitive load. Both groups took longer to name the color for incongruent than congruent trials. Pupil dilation was also larger for incongruent trials than for congruent trials across groups, which suggested that pupil dilation reflected cognitive load on the task. Though the groups did not differ in the magnitude of Stroop effect in pupil dilation, depressed individuals displayed decreased pupil dilation in the seconds following stimuli relative to controls. Computational neural network modeling further suggested that observed effects were consistent with decreased prefrontal cortex activity, associated with decreased cognitive control. ᮊ

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“…However, this inhibition is attenuated in patients with psychotic depression suggesting impaired MR function in these patients (Lembke et al, 2013). Importantly, psychotically depressed patients show the most severe cognitive deficits (Schatzberg et al, 2000). Furthermore, there is evidence of decreased MR expression in the hippocampus and prefrontal cortex in depressed patients (Klok et al, 2011a;Medina et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Mineralocorticoid Receptor Stimulation Improves Cognitive Function and Decreases Cortisol Secretion in Depressed Patients and Healthy Individuals

Otte

Wingenfeld

Kuehl

et al. 2014

Neuropsychopharmacol

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Memory and executive function are often impaired in patients with major depression, while cortisol secretion is increased. Mineralocorticoid receptors (MR) are abundantly expressed in the hippocampus and in the prefrontal cortex, brain areas critical for memory, executive function, and cortisol inhibition. Here, we investigated whether MR stimulation with fludrocortisone (1) improves memory and executive function and (2) decreases cortisol secretion in depressed patients and healthy individuals. Twenty-four depressed patients without medication and 24 age-, sex-, and education-matched healthy participants received fludrocortisone (0.4 mg) or placebo in a randomized, double-blind, within-subject cross-over design. We measured verbal memory, visuospatial memory, executive function, psychomotor speed, and salivary cortisol secretion during cognitive testing between 1400 and 1700 hours. For verbal memory and executive function, we found better performance after fludrocortisone compared with placebo across groups. No treatment effect on other cognitive domains emerged. Depressed patients performed worse than healthy individuals in psychomotor speed and executive function. No group effect or group Â treatment interaction emerged on other cognitive domains. Fludrocortisone decreased cortisol secretion across groups and there was a significant correlation between cortisol inhibition and verbal memory performance. Our data suggest a crucial role of MR in verbal memory and executive function and demonstrate the possibility to improve cognition in depressed patients and healthy individuals through MR stimulation.

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Neuropsychological Deficits in Psychotic Versus Nonpsychotic Major Depression and No Mental Illness

Cited by 182 publications

References 23 publications

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Pupillary assessment and computational modeling of the Stroop task in depression

Mineralocorticoid Receptor Stimulation Improves Cognitive Function and Decreases Cortisol Secretion in Depressed Patients and Healthy Individuals

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