Depressive symptoms are common in Parkinson's disease (PD), but the pathophysiology and neural basis underlying depression in PD is not well understood. Abnormal functional connectivity of the amygdala with various cortical and subcortical areas has been observed in major depressive disorder, indicating that dysfunction of the corticolimbic network may be involved in the pathogenesis of major depressive disorder. However, little is known about alterations of amygdala functional connectivity in depressed PD patients. In the present study, 20 depressed PD patients, 40 nondepressed PD patients, and 43 matched healthy controls underwent neuropsychological tests and resting-state functional MRI scanning. Between-group differences in amygdala functional connectivity network were examined using t tests. Compared to the nondepressed PD patients, depressed PD patients showed increased left amygdala functional connectivity with the bilateral mediodorsal thalamus, right amygdala functional connectivity with the left superior temporal gyrus, and left calcarine gyrus. Compared to the healthy controls, the depressed PD group also showed increased left amygdala functional connectivity with the bilateral mediodorsal thalamus, but decreased left amygdala functional connectivity with the left putamen, left inferior frontal gyrus, and the right cerebellum, as well as decreased right amygdala functional connectivity with the left inferior orbitofrontal gyrus, the left gyrus rectus, and the right putamen. The increased connectivity between limbic regions and decreased connectivity between the corticolimbic networks may reflect impaired high-order cortical regulatory effects on the emotion-related limbic areas, which may lead to mood dysregulation. Our study should advance the understanding of neural mechanisms underlying depression in PD.

Depressive symptoms are common in Parkinson’s disease (PD), but the neurophysiological mechanisms of depression in PD are poorly understood. The current study attempted to examine disrupted spontaneous local brain activities and functional connectivities that underlie the depression in PD. We recruited a total of 20 depressed PD patients (DPD), 40 non-depressed PD patients (NDPD) and 43 matched healthy controls (HC). All the subjects underwent neuropsychological tests and resting-state fMRI scanning. The between-group differences in the amplitude of low frequency fluctuations (ALFF) of BOLD signals were examined using post-hoc tests after the analysis of covariance. Compared with the NDPD and HC, the DPD group showed significantly increased ALFF in the left median cingulated cortex (MCC). The functional connectivity (FC) between left MCC and all the other voxels in the brain were then calculated. Compared with the HC and NDPD group, the DPD patients showed stronger FC between the left MCC and some of the major nodes of the default mode network (DMN), including the post cingulated cortex/precuneus, medial prefrontal cortex, inferior frontal gyrus, and cerebellum. Correlation analysis revealed that both the ALFF values in the left MCC and the FC between the left MCC and the nodes of DMN were significantly correlated with the Hamilton Depression Rating Scale score. Moreover, higher local activities in the left MCC were associated with increased functional connections between the MCC and the nodes of DMN in PD. These abnormal activities and connectivities of the limbic-cortical circuit may indicate impaired high-order cortical control or uncontrol of negative mood in DPD, which suggested a possible neural mechanism of the depression in PD.

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Much is known concerning the underlying mechanisms of Parkinson’s disease (PD) with depression, but our understanding of this disease at the neural-system level remains incomplete. This study used resting-state functional MRI (rs-fMRI) and independent component analysis (ICA) to investigate intrinsic functional connectivity (FC) within and between large-scale neural networks in 20 depressed PD (dPD) patients, 35 non-depressed PD (ndPD) patients, and 34 healthy controls (HC). To alleviate the influence caused by ICA model order selection, this work reported results from analyses at 2 levels (low and high model order). Within these two analyses, similar results were obtained: 1) dPD and ndPD patients relative to HC had reduced FC in basal ganglia network (BGN); 2) dPD compared with ndPD patients exhibited increased FC in left frontoparietal network (LFPN) and salience network (SN), and decreased FC in default-mode network (DMN); 3) dPD patients compared to HC showed increased FC between DMN and LFPN. Additionally, connectivity anomalies in the DMN, LFPN and SN correlated with the depression severity in patients with PD. Our findings confirm the involvement of BGN, DMN, LFPN and SN in depression in PD, facilitating the development of more detailed and integrative neural models of PD with depression.

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A novel empirical mode decomposition method was adopted to investigate the dissociative or interactive neural impact of depression and motor impairments in Parkinson’s disease (PD). Resting-state fMRI data of 59 PD subjects were first decomposed into characteristic frequency bands, and the main effects of motor severity and depression and their interaction on the energy of blood-oxygen-level-dependent signal oscillation in specific frequency bands were then evaluated. The results show that the severity of motor symptoms is negatively correlated with the energy in the frequency band of 0.10–0.25 Hz in the bilateral thalamus, but positively correlated with 0.01–0.027 Hz band energy in the bilateral postcentral gyrus. The severity of depression, on the other hand, is positively correlated with the energy of 0.10–0.25 Hz but negatively with 0.01–0.027 Hz in the bilateral subgenual gyrus. Notably, the interaction between motor and depressive symptoms is negatively correlated with the energy of 0.10–0.25 Hz in the substantia nigra, hippocampus, inferior orbitofrontal cortex, and temporoparietal junction, but positively correlated with 0.02–0.05 Hz in the same regions. These findings indicate unique associations of fMRI band signals with motor and depressive symptoms in PD in specific brain regions, which may underscore the neural impact of the comorbidity and the differentiation between the two PD-related disorders.