Dataset Information

Impaired interhemispheric synchrony in Parkinson's disease with depression.

ABSTRACT: The alterations of interhemispheric resting-state functional connectivity (FC) in Parkinson's disease (PD) with depression remain unclear, so we aimed to explore the differences of interhemispheric FC between PD with and without depression. Twenty-one depressed PD (DPD) patients, 49 non-depressed PD (NDPD) patients and 50 matched healthy controls (HC) participated in this study. Resting-state functional magnetic resonance imaging (fMRI) data were analyzed with the voxel-mirrored homotopic connectivity (VMHC) approach. The DPD patients showed lower VMHC values in the bilateral dorsolateral prefrontal cortex (DLPFC) and calcarine cortex compared to both NDPD and HC groups, and further receiver operating characteristic curves (ROC) analyses revealed that the VMHC in these two brain areas could be used as biomarkers to distinguish DPD from NDPD and from HC. The pooled PD patients (both DPD and NDPD) exhibited decreased VMHC in the bilateral putamen, middle occipital gyrus (MOG), postcentral gyrus (PoCG), paracentral lobule (PCL) and cerebellum posterior lobe when compared with HC. Decreased VMHC values within the DLPFC and calcarine cortex appeared to be unique features for DPD and might be used as potential neuroimaging markers to distinguish DPD patients from NDPD and HC groups. These findings may underlie the neural mechanisms of depression in PD.

SUBMITTER: Zhu Y

PROVIDER: S-EPMC4893739 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Impaired interhemispheric synchrony in Parkinson's disease with depression.

Zhu Yajing Y Song Xiaopeng X Xu Mingze M Hu Xiao X Li Erfeng E Liu Jiajia J Yuan Yonggui Y Gao Jia-Hong JH Liu Weiguo W

Scientific reports 20160606

The alterations of interhemispheric resting-state functional connectivity (FC) in Parkinson's disease (PD) with depression remain unclear, so we aimed to explore the differences of interhemispheric FC between PD with and without depression. Twenty-one depressed PD (DPD) patients, 49 non-depressed PD (NDPD) patients and 50 matched healthy controls (HC) participated in this study. Resting-state functional magnetic resonance imaging (fMRI) data were analyzed with the voxel-mirrored homotopic connec ...[more]

PMID: 27265427

Similar Datasets

Project description:A key feature of normal neonatal EEG at term age is interhemispheric synchrony (IHS), which refers to the temporal co-incidence of bursting across hemispheres during trace alternant EEG activity. The assessment of IHS in both clinical and scientific work relies on visual, qualitative EEG assessment without clearly quantifiable definitions. A quantitative measure, activation synchrony index (ASI), was recently shown to perform well as compared to visual assessments. The present study was set out to test whether IHS is stable enough for clinical use, and whether it could be an objective feature of EEG normality. We analyzed 31 neonatal EEG recordings that had been clinically classified as normal (n = 14) or abnormal (n = 17) using holistic, conventional visual criteria including amplitude, focal differences, qualitative synchrony, and focal abnormalities. We selected 20-min epochs of discontinuous background pattern. ASI values were computed separately for different channel pair combinations and window lengths to define them for the optimal ASI intraindividual stability. Finally, ROC curves were computed to find trade-offs related to compromised data lengths, a common challenge in neonatal EEG studies. Using the average of four consecutive 2.5-min epochs in the centro-occipital bipolar derivations gave ASI estimates that very accurately distinguished babies clinically classified as normal vs. abnormal. It was even possible to draw a cut-off limit (ASI~3.6) which correctly classified the EEGs in 97% of all cases. Finally, we showed that compromising the length of EEG segments from 20 to 5 min leads to increased variability in ASI-based classification. Our findings support the prior literature that IHS is an important feature of normal neonatal brain function. We show that ASI may provide diagnostic value even at individual level, which strongly supports its use in prospective clinical studies on neonatal EEG as well as in the feature set of upcoming EEG classifiers.

Project description:A full understanding of Parkinson's Disease etiopathogenesis and of the causes of the preferential vulnerability of nigrostriatal dopaminergic neurons is still an unsolved puzzle. A multiple-hit hypothesis has been proposed, which may explain the convergence of familial, environmental and idiopathic forms of the disease. Among the various determinants of the degeneration of the neurons in Substantia Nigra pars compacta, in this review we will focus on the endotoxicity associated to dopamine dyshomeostasis. In particular, we will discuss the relevance of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL) in the catechol-induced neurotoxicity. Indeed, the synergy between the catechol and the aldehyde moieties of DOPAL exacerbates its reactivity, resulting in modification of functional protein residues, protein aggregation, oxidative stress and cell death. Interestingly, αSynuclein, whose altered proteostasis is a recurrent element in Parkinson's Disease pathology, is considered a preferential target of DOPAL modification. DOPAL triggers αSynuclein oligomerization leading to synapse physiology impairment. Several factors can be responsible for DOPAL accumulation at the pre-synaptic terminals, i.e. dopamine leakage from synaptic vesicles, increased rate of dopamine conversion to DOPAL by upregulated monoamine oxidase and decreased DOPAL degradation by aldehyde dehydrogenases. Various studies report the decreased expression and activity of aldehyde dehydrogenases in parkinsonian brains, as well as genetic variants associated to increased risk in developing the pathology. Thus, we discuss how the deregulation of these enzymes might be considered a contributing element in the pathogenesis of Parkinson's Disease or a down-stream effect. Finally, we propose that a better understanding of the impaired dopamine metabolism in Parkinson's Disease would allow a more refined patients stratification and the design of more targeted and successful therapeutic strategies.

Project description:Apathy is a common and disabling complication of Parkinson's disease characterized by reduced goal-directed behaviour. Several studies have reported dysfunction within prefrontal cortical regions and projections from brainstem nuclei whose neuromodulators include dopamine, serotonin and noradrenaline. Work in animal and human neuroscience have confirmed contributions of these neuromodulators on aspects of motivated decision-making. Specifically, these neuromodulators have overlapping contributions to encoding the value of decisions, and influence whether to explore alternative courses of action or persist in an existing strategy to achieve a rewarding goal. Building upon this work, we hypothesized that apathy in Parkinson's disease should be associated with an impairment in value-based learning. Using a four-armed restless bandit reinforcement learning task, we studied decision-making in 75 volunteers; 53 patients with Parkinson's disease, with and without clinical apathy, and 22 age-matched healthy control subjects. Patients with apathy exhibited impaired ability to choose the highest value bandit. Task performance predicted an individual patient's apathy severity measured using the Lille Apathy Rating Scale (R = -0.46, P < 0.001). Computational modelling of the patient's choices confirmed the apathy group made decisions that were indifferent to the learnt value of the options, consistent with previous reports of reward insensitivity. Further analysis demonstrated a shift away from exploiting the highest value option and a reduction in perseveration, which also correlated with apathy scores (R = -0.5, P < 0.001). We went on to acquire functional MRI in 59 volunteers; a group of 19 patients with and 20 without apathy and 20 age-matched controls performing the Restless Bandit Task. Analysis of the functional MRI signal at the point of reward feedback confirmed diminished signal within ventromedial prefrontal cortex in Parkinson's disease, which was more marked in apathy, but not predictive of their individual apathy severity. Using a model-based categorization of choice type, decisions to explore lower value bandits in the apathy group activated prefrontal cortex to a similar degree to the age-matched controls. In contrast, Parkinson's patients without apathy demonstrated significantly increased activation across a distributed thalamo-cortical network. Enhanced activity in the thalamus predicted individual apathy severity across both patient groups and exhibited functional connectivity with dorsal anterior cingulate cortex and anterior insula. Given that task performance in patients without apathy was no different to the age-matched control subjects, we interpret the recruitment of this network as a possible compensatory mechanism, which compensates against symptomatic manifestation of apathy in Parkinson's disease.

Dataset Information

Impaired interhemispheric synchrony in Parkinson's disease with depression.

Publications

Impaired interhemispheric synchrony in Parkinson's disease with depression.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets