Abstract
Hypothalamo-pituitary-adrenal (HPA)-axis hyperactivity is well established in a large proportion of both Alzheimer's disease (AD) patients and idiopathic depression patients, resulting in, e.g. increased cerebrospinal fluid (CSF) cortisol levels. We hypothesized that HPA-axis activity in depressed AD patients is even more increased than in non-depressed AD patients, resulting in higher CSF cortisol levels. Cortisol levels were measured in post mortem CSF of depressed and non-depressed AD patients and in controls. Cortisol levels in AD patients were more than double those of controls, while no significant differences were found between depressed and non-depressed AD patients. These results suggest a different pathogenetic mechanism in depression in AD than in idiopathic depression.
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