ORIGINAL ARTICLE Monoamine transporter availability in Parkinson’ s disease patients with or without depression Swen Hesse & Philipp M. Meyer & Karl Strecker & Henryk Barthel & Florian Wegner & Christian Oehlwein & Ioannis Ugo Isaias & Johannes Schwarz & Osama Sabri Received: 20 September 2007 / Accepted: 25 September 2008 / Published online: 27 November 2008 # Springer-Verlag 2008 Abstract Purpose Depression is a common symptom in patients suffering from Parkinson’ s disease (PD) and markedly reduces their quality of life. As post-mortem studies have shown, its presence may reflect extensive cell loss in the midbrain and brainstem with imbalances in monoaminergic neurotransmitters. However, in vivo evidence of specific monoaminergic deficits in depressed PD patients is still sparse. Therefore, we studied PD patients with depression (PD+D) and without depression (PD-D) using high-resolu- tion single-photon emission computed tomography (SPECT) and the monoamine transporter marker [ 123 I]FP-CIT. Methods A magnetic resonance imaging-based region-of- interest analysis was applied to quantify the specific-to- nondisplaceable [ 123 I]FP-CIT binding coefficient V 3 ″ in the striatum, thalamus and midbrain/brainstem regions. Results PD+D patients had significantly lower V 3 ″ compared with PD-D patients in the striatum (p<0.001), thalamus (p=0.002), and midbrain/brainstem (p=0.025). Only PD+D patients without selective serotonin reuptake inhibitor (SSRI) treatment showed lower thalamic and midbrain V 3 ″ than controls (p<0.001, p=0.029). In a small sub-group of SSRI- treated PD+D patients neither thalamic V 3 ″ nor midbrain/ brainstem V 3 ″ differed from those in PD-D patients (p=0.168, p=0.201) or controls (p=0.384, p=0.318). Conclusion Our data indicate that depression in PD is associated with a more pronounced loss of striatal dopa- mine transporter availability that is most likely secondary to increased dopaminergic degeneration. In addition, de- pressed PD patients have a lower availability of midbrain/ brainstem monoamine transporters than nondepressed PD patients. These findings provide in vivo evidence in support of the known post-mortem data demonstrating more exten- sive nerve cell loss in PD with depression and indicate that SPECT imaging can help to identify pathophysiological changes underlying nonmotor symptoms in this common movement disorder. Keywords SPECT . Dopamine . Serotonin . Striatum . Midbrain Introduction In Parkinson’ s disease (PD), nonmotor symptoms often accompany or even precede motor symptoms and have a strong impact on the quality of life [1]. Up to 45% of PD patients develop depression [2, 3]. The precise pathophysiology underlying depression in PD is not clear. The role of (mesocorticolimbic and mesostriatocortical) dopaminergic dysfunction, which strongly correlates with bradykinesia and rigidity [4] in developing depressive symptoms, needs to be further elucidated [5], not least since there is a lack of consistency Eur J Nucl Med Mol Imaging (2009) 36:428–435 DOI 10.1007/s00259-008-0979-7 The results of this study were partly presented at the Amersham Healthcare User Meeting during the 40 th Annual Meeting of the German Society of Nuclear Medicine 2002 in Freiburg, Germany, and at the 54 th Annual Congress of the Society of Nuclear Medicine 2007 in Washington, DC, USA. S. Hesse (*) : P. M. Meyer : H. Barthel : O. Sabri Department of Nuclear Medicine, University of Leipzig, Stephanstraße 11, 04103 Leipzig, Germany e-mail: Swen.Hesse@medizin.uni-leipzig.de K. Strecker : F. Wegner : I. U. Isaias : J. Schwarz Department of Neurology, University of Leipzig, Leipzig, Germany C. Oehlwein Specialized Parkinson’ s Disease Outpatient Centre, Gera, Germany