Cognitive impairment in major depression: association with salivary cortisol.
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Cognitive impairment in major depression: association with salivary cortisol. / Hinkelmann, Kim; Moritz, Steffen; Botzenhardt, Johannes; Terfehr, Kirsten; Wiedemann, Klaus; Kellner, Michael; Otte, Christian.
In: BIOL PSYCHIAT, Vol. 66, No. 9, 9, 2009, p. 879-885.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Cognitive impairment in major depression: association with salivary cortisol.
AU - Hinkelmann, Kim
AU - Moritz, Steffen
AU - Botzenhardt, Johannes
AU - Terfehr, Kirsten
AU - Wiedemann, Klaus
AU - Kellner, Michael
AU - Otte, Christian
PY - 2009
Y1 - 2009
N2 - BACKGROUND: Cognitive deficits and elevated cortisol are hallmarks of depression. Cortisol acts via mineralocorticoid and glucocorticoid receptors, which have their highest density in the hippocampus, a brain area closely related to cognitive function. Several studies have separately examined cortisol secretion and cognitive deficits in depression. However, only few studies have assessed their association in the same patients producing inconclusive results. METHODS: We examined 52 medication-free patients with major depression (37 women, 15 men; mean age 35 +/- 11 years; Hamilton Depression Scale mean score 27 +/- 5) and 50 healthy control subjects, matched for age, gender, and years of education. We applied several neuropsychological tests. Salivary cortisol levels were measured on the same day at 08:00, 12:00, 16:00, and 22:00 hours. RESULTS: Compared with healthy subjects, patients had significantly higher cortisol levels and were impaired in verbal memory, visuospatial memory, working memory, and selective attention. In depressed patients, but not in healthy control subjects, we found a negative correlation between salivary cortisol levels (area under the curve) and hippocampus-related neuropsychological domains (verbal memory, visuospatial memory) and executive function. CONCLUSIONS: Cognitive deficits, especially those closely related to hippocampus function, appear to be related to cortisol secretion in depressed patients. Elevated cortisol may downregulate mineralocorticoid and glucocorticoid receptors in the hippocampus, which could, in part, be responsible for cognitive deficits in depressed patients.
AB - BACKGROUND: Cognitive deficits and elevated cortisol are hallmarks of depression. Cortisol acts via mineralocorticoid and glucocorticoid receptors, which have their highest density in the hippocampus, a brain area closely related to cognitive function. Several studies have separately examined cortisol secretion and cognitive deficits in depression. However, only few studies have assessed their association in the same patients producing inconclusive results. METHODS: We examined 52 medication-free patients with major depression (37 women, 15 men; mean age 35 +/- 11 years; Hamilton Depression Scale mean score 27 +/- 5) and 50 healthy control subjects, matched for age, gender, and years of education. We applied several neuropsychological tests. Salivary cortisol levels were measured on the same day at 08:00, 12:00, 16:00, and 22:00 hours. RESULTS: Compared with healthy subjects, patients had significantly higher cortisol levels and were impaired in verbal memory, visuospatial memory, working memory, and selective attention. In depressed patients, but not in healthy control subjects, we found a negative correlation between salivary cortisol levels (area under the curve) and hippocampus-related neuropsychological domains (verbal memory, visuospatial memory) and executive function. CONCLUSIONS: Cognitive deficits, especially those closely related to hippocampus function, appear to be related to cortisol secretion in depressed patients. Elevated cortisol may downregulate mineralocorticoid and glucocorticoid receptors in the hippocampus, which could, in part, be responsible for cognitive deficits in depressed patients.
M3 - SCORING: Zeitschriftenaufsatz
VL - 66
SP - 879
EP - 885
JO - BIOL PSYCHIAT
JF - BIOL PSYCHIAT
SN - 0006-3223
IS - 9
M1 - 9
ER -