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Despite a growing body of evidence suggests that abnormal iron metabolism plays an important role in the pathogenesis of Parkinson's disease (PD), few studies explored its role in non-motor symptoms (NMS) of PD. The present study aimed to investigate the relationship between abnormal iron metabolism and NMS of PD. Seventy PD patients and 64 healthy controls were consecutively recruited to compare serum iron, ceruloplasmin, ferritin, and transferrin levels. We evaluated five classic NMS, including depression, anxiety, pain, sleep disorder, and autonomic dysfunction in PD patients using the Hamilton Depression Scale (HAMD), the Hamilton Anxiety Scale (HAMA), the short form of the McGill Pain Questionnaire, the Pittsburgh Sleep Quality Index and the Scale for Outcomes in Parkinson's disease for Autonomic Symptoms, respectively. Hierarchical multiple regression analysis was used to investigate the correlations between abnormal iron metabolism and NMS. No differences in serum ceruloplasmin and ferritin levels were examined between PD patients and healthy controls, but we observed significantly decreased serum iron levels and increased serum transferrin levels in PD patients in comparison with healthy controls. After eliminating confounding factors, HAMD scores and HAMA scores were both negatively correlated with serum iron levels and positively correlated with serum transferrin levels. In summary, abnormal iron metabolism might play a crucial role in the pathogenesis of depression and anxiety in PD. Serums levels of iron and transferrin could be peripheral markers for depression and anxiety in PD.

Object: To detect the cerebral metabolic bases of Parkinson's disease (PD) patients with anxiety., Methods: Totally 28 idiopathic PD patients without depression (17-item Hamilton Depression Rating Scale, HAMD score <14) were enrolled in our study. All subjects were classified into PD with anxiety (PD-A) (n=13) and PD without anxiety (PD-NA) (n=15) by cutoff score of 11 according to Hamilton Anxiety Rating Scale (HAMA). Besides, age- and gender- matched healthy controls (HCs) (n=15) were selected. A resting-state F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) scan was applied to estimate cerebral metabolic activity. All statistical analyses were performed using IBM SPSS Statistics V20.0.0 software, while statistical parametric mapping software (SPM) was used to analyze the FDG-PET images., Results: PD-A showed decreased glucose metabolism in the bilateral orbitofrontal cortex (OFC, BA10 and BA11) when compared with PD-NA. Significant decrease of cerebral glucose metabolism in the bilateral OFC, bilateral supplementary motor area (SMA, BA6), bilateral dorsal anterior cingulate cortex (dACC, BA32), right dorsolateral prefrontal cortex (dlPFC, BA9), right ventrolateral prefrontal cortex (vlPFC, BA44), right putamen and left caudatum was detected in PD-A compared with HCs. There was significant reduced glucose metabolism of the bilateral SMA in PD-NA when compared with HCs (uncorrected p<0.005)., Conclusion: The anxiety of PD was associated with the metabolic reductions of PFC and striatal areas. OFC, part of PFC, could be taken as a characteristic feature for anxiety in PD. This metabolic pattern suggested that deficits of prefrontostriatal pathways might affect anxiety mood in PD., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Object Anxiety disorders are very common in Parkinson’s disease (PD), but neural mechanisms underlying these symptoms still remain elusive. In the present study, we aim to investigate the neural substrates in anxiety disorders in PD. Methods The present study comprised 48 PD patients and 19 healthy subjects. According to a Hamilton Anxiety Rating Scale cutoff score of 12, we divided PD patients into PD with anxiety groups (n = 15) and PD without anxiety groups (n = 33). Patients with apparent depressive symptoms and cognitive decline were excluded. All subjects were evaluated for demographic and clinical characteristics and performed 3.0 T MRI scans. The alterations of neural activity were examined utilizing resting-state fMRI (rs-fMRI) combined with the amplitude of low-frequency fluctuations (ALFF) approach. Results Results of the analysis of covariance indicated that PD patients with anxiety displayed increased ALFF mainly in right cerebellar posterior lobe (CPL), bilateral brainstem and right orbitofrontal gyrus (OFG). Subsequently, the Spearman correlation demonstrated negative correlation between ALFF values in right cerebellum_9 and the Hamilton Anxiety Rating Scale scores. Conclusion Our findings demonstrated that anxiety disorders in PD were associated with increased activities in anxiety-related brain regions, including OFG, brainstem and CPL, using the ALFF approach. [ABSTRACT FROM AUTHOR]