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Comorbidity of depression, or depressive symptoms and Parkinson's disease (PD), is a common condition with a high prevalence,1 which may start developing before the formal clinical diagnosis of PD during the so-called premotor (non-motor or preclinical or prodromal) stage of the disease. Such association may be further strengthened during the progression of continuous neuronal loss and disease. The underlying pathophysiological mechanisms of the association between depression and PD are not clearly understood, and it is hypothesised that changes in brain pathology, neurotransmitter signalling pathways and, particularly, abnormalities of dopaminergic, noradrenergic and serotoninergic projections may substantially contribute to its development.1 Psychological factors, life stresses and internal perception of PD as a devastating neurodegenerative condition with no effective cure may also contribute to the development of depression in patients with PD. Commonly observed key PD symptoms, such as rigidity, bradykinesia and hypomimia, may add complexity in clinical differentiation between depression or depressive symptoms and PD.
Vriend et al2 use dopamine transporter (DaT) imaging with Iodine-123-fluoropropyl (FP)-carbomethoxy-3 β-(4-iodophenyltropane) (CIT) [123I]FP-CIT (DaTSCAN or DaTscan) in patients with PD with associated depressive …
Competing interests IDG is employee of GE Healthcare, the manufacturer of [123I]FP-CIT.
Provenance and peer review Commissioned; internally peer reviewed.
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