Abstract

Background: Depression is frequently encountered in Parkinson’s disease (PD). In addition, more than half of the PD patients have a disturbed dexamethasone suppression test, which is associated with increased activity of corticotropin-releasing hormone (CRH) neurons. We recently found an increase in CRH neuron number, CRH–messenger RNA, and vasopressin colocalization in CRH neurons in the paraventricular nucleus (PVN) of depressed patients, which may be involved in the pathogenesis of depression. Methods: The number of neurons expressing CRH was determined in the PVN of 6 depressed PD patients with a high score (≥ 13) on the Hamilton Depression Rating Scale, 6 nondepressed PD patients, and 6 controls. Results: The three groups did not differ in the number of neurons expressing CRH. Conclusions: We hypothesize that activation of CRH neurons in the PVN, as we recently observed in idiopathic depression, does not play an essential role in depression in PD.

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