1. ¹Department of Psychiatry, Maastricht University Hospital, Maastricht, The Netherlands
2. ²Institute of Brain and Behaviour, Maastricht University, Maastricht, The Netherlands
3. ³Department of Neurology, Maastricht University Hospital, Maastricht, The Netherlands

Correspondence: Dr AFG Leentjens, Department of Psychiatry, Maastricht University Hospital, PO Box 5800, Maastricht 6202 AZ, The Netherlands, Tel: +31 43 3877443, Fax: +31 43 3875444, E-mail: a.leentjens@np.unimaas.nl

Received 7 June 2005; Revised 2 August 2005; Accepted 22 August 2005; Published online 5 October 2005.

Abstract

The serotonergic hypothesis for depression in Parkinson's disease (PD) states that the reduced cerebral serotonergic activity that occurs in PD constitutes a biological risk factor for depression. The aim of our study was to assess the serotonergic hypothesis of depression in PD patients using an experimental approach. In a double-blind, randomized order, placebo-controlled crossover design, the response on the Profile of Mood States (POMS) questionnaire to acute tryptophan depletion (ATD) was studied in 15 PD nondepressed patients and 15 control subjects, without a prior personal or family history of depression. PD patients had lower (worse) baseline scores on the sadness, fatigue and vigor subscales of the POMS, in both ATD and the placebo condition, but not on the tension and anger subscales. There was however neither a significe between group effect, nor significe within-group effect due to ATD. We could find no evidence of a specific serotonergic vulnerability of PD patients for depression. Therefore, our results do not support the serotonergic hypothesis for depression in PD.